[Senate Hearing 107-628]
[From the U.S. Government Publishing Office]
S. Hrg. 107-628
ALZHEIMER'S DISEASE, 2002
=======================================================================
HEARING
before a
SUBCOMMITTEE OF THE
COMMITTEE ON APPROPRIATIONS UNITED STATES SENATE
ONE HUNDRED SEVENTH CONGRESS
SECOND SESSION
__________
SPECIAL HEARING
APRIL 30, 2002--WASHINGTON, DC
__________
Printed for the use of the Committee on Appropriations
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______
COMMITTEE ON APPROPRIATIONS
ROBERT C. BYRD, West Virginia, Chairman
DANIEL K. INOUYE, Hawaii TED STEVENS, Alaska
ERNEST F. HOLLINGS, South Carolina THAD COCHRAN, Mississippi
PATRICK J. LEAHY, Vermont ARLEN SPECTER, Pennsylvania
TOM HARKIN, Iowa PETE V. DOMENICI, New Mexico
BARBARA A. MIKULSKI, Maryland CHRISTOPHER S. BOND, Missouri
HARRY REID, Nevada MITCH McCONNELL, Kentucky
HERB KOHL, Wisconsin CONRAD BURNS, Montana
PATTY MURRAY, Washington RICHARD C. SHELBY, Alabama
BYRON L. DORGAN, North Dakota JUDD GREGG, New Hampshire
DIANNE FEINSTEIN, California ROBERT F. BENNETT, Utah
RICHARD J. DURBIN, Illinois BEN NIGHTHORSE CAMPBELL, Colorado
TIM JOHNSON, South Dakota LARRY CRAIG, Idaho
MARY L. LANDRIEU, Louisiana KAY BAILEY HUTCHISON, Texas
JACK REED, Rhode Island MIKE DeWINE, Ohio
Terrence E. Sauvain, Staff Director
Charles Kieffer, Deputy Staff Director
Steven J. Cortese, Minority Staff Director
Lisa Sutherland, Minority Deputy Staff Director
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Subcommittee on Departments of Labor, Health and Human Services, and
Education, and Related Agencies
TOM HARKIN, Iowa, Chairman
ERNEST F. HOLLINGS, South Carolina ARLEN SPECTER, Pennsylvania
DANIEL K. INOUYE, Hawaii THAD COCHRAN, Mississippi
HARRY REID, Nevada JUDD GREGG, New Hampshire
HERB KOHL, Wisconsin LARRY CRAIG, Idaho
PATTY MURRAY, Washington KAY BAILEY HUTCHISON, Texas
MARY L. LANDRIEU, Louisiana TED STEVENS, Alaska
ROBERT C. BYRD, West Virginia MIKE DeWINE, Ohio
Professional Staff
Ellen Murray
Jim Sourwine
Mark Laisch
Adrienne Hallett
Erik Fatemi
Bettilou Taylor (Minority)
Mary Dietrich (Minority)
Sudip Shrikant Parikh (Minority)
Candice Rogers (Minority)
Administrative Support
Carole Geagley
C O N T E N T S
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Page
Opening statement of Senator Tom Harkin.......................... 1
Opening statement of Senator Arlen Specter....................... 2
Statement of Richard J. Hodes, M.D., Director, National Institute
on Aging, National Institutes of Health, Department of Health
and Human Services............................................. 3
Prepared statement........................................... 5
Statement of Orien Reid, Chair, board of directors, Alzheimer's
Association.................................................... 11
Prepared statement........................................... 13
Statement of Marilyn Albert, Ph.D., Chair, Medical and Scientific
Advisory Committee, Alzheimer's Association.................... 15
Prepared statement........................................... 16
Statement of Carol Gratz, New Hampton, IA, East Central Iowa
Chapter, Alzheimer's Association............................... 19
Statement of Gene Gratz, New Hampton, IA, East Central Iowa
Chapter, Alzheimer's Association............................... 21
Prepared statement........................................... 21
Statement of David Hyde Pierce, actor............................ 23
Prepared statement........................................... 24
ALZHEIMER'S DISEASE, 2002
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TUESDAY, APRIL 30, 2002
U.S. Senate,
Subcommittee on Labor, Health and Human
Services, and Education, and Related Agencies,
Committee on Appropriations,
Washington, DC.
The subcommittee met at 9:09 a.m., in room SD-106, Dirksen
Senate Office Building, Hon. Tom Harkin (chairman) presiding.
Present: Senators Harkin and Specter.
opening statement of senator tom harkin
Senator Harkin. The hearing of the Senate Labor, Health and
Human Services, and Education Appropriations Subcommittee will
come to order. I welcome everyone here this morning. I thank
you for the tremendous turnout.
This is the third year in a row that this subcommittee has
held a hearing on Alzheimer's disease specifically, either with
me as chairman or my friend Arlen Specter. I think that is as
clear a sign as any that there are no party lines when it comes
to preventing and curing Alzheimer's. This is an equal
opportunity disease, striking men and women of all races and
all backgrounds, so it is fitting that Democrats and
Republicans have worked arm in arm to confront it.
The fact that we have held so many hearings on Alzheimer's
also shows how urgently we need answers. A poll released this
morning shows that 57 percent of Americans are personally
worried about getting this disease, and for good reason. There
are currently 4 million people in the United States with
Alzheimer's and by the year 2050 that number is expected to
rise to about 14 million. We will be paying $357 billion a year
in health care costs. That is, unless science can find a way to
prevent or delay this disease.
Fortunately, thanks in large part to this subcommittee's
effort to double funding at NIH, led by Senator Specter and me,
that goal is in sight. Researchers are finally closing in on
what causes Alzheimer's. They are using cutting-edge brain
imaging to figure out how to diagnose it, and they are studying
everything from folic acid and statins to Advil and gingko
biloba to see if any of these drugs and supplements can help
delay it.
On another front, this Nation has finally recognized the
importance of family caregivers in helping people with
Alzheimer's. This disease takes an enormous toll on caregivers,
not only financially but also emotionally and physically. This
subcommittee funds two programs to address this need, the
Family Caregiver Support Program and the Alzheimer's Matching
Grant Program, and we will continue to give them high priority.
We are fortunate to have an outstanding panel of witnesses
here today to discuss these issues. I of course extend a
special welcome to Carol and Gene Gratz of New Hampton, Iowa.
It takes a lot of time and courage to come to Washington and
prepare for a hearing like this, and I want to thank you and
Kris for being here and for helping remind us what it means to
battle Alzheimer's and what is involved in caring for a loved
one who has been stricken with this disease.
This same goes for the hundreds of patients, family
members, and friends in the audience, who are here as part of
the Alzheimer's Association's Capitol Hill Day. Your personal
stories are worth more than a hundred statistics to Senators
and Congressmen that you visit today. I commend you for your
advocacy. We need you here and we need you talking to all of
your Congressmen and Senators here in Washington.
So before we turn to our witnesses, I would yield to my
colleague, the ranking member, Senator Specter, for his opening
remarks.
opening statement of senator arlen specter
Senator Specter. Thank you very much, Mr. Chairman, and
thank you for your leadership on the effort to cure Alzheimer's
and on matters of medical treatment in general.
Thank you, ladies and gentlemen, for coming here today.
This kind of an outpouring of support in one of the Senate's
biggest hearing rooms is noted in this city and this country
and really around the world.
I thank the Pennsylvania Alzheimer's Association for the
Humanitarian Award which I received in this room at the outset
of the session. It was interesting to pose for a moment or two
for a so-called photo op. I did not realize there were so many
cameras in the audience. It is just too bad we cannot take
enough time to have everyone photographed individually with
Senator Harkin----
Senator Harkin. So goes life.
Senator Specter [continuing]. And I might sneak into the
corner of a picture or two. But we have very, very important
work to do.
Senator Harkin has noted that he and I and this
subcommittee, have led the fight on increasing funding for the
National Institutes of Health and Alzheimer's. When we started
our effort to double the NIH funding, we asked the Budget
Committee for $1 billion, were turned down, took it to the
floor, and lost 63 to 37. So Tom and I got out our sharp
pencils and found $1 billion among the priorities.
Having lost on our effort to increase the funding by $1
billion, and then the next year we asked for $2 billion. That
is the way things are done in Washington. We got turned down
again, and once again we found the money as a matter of
priorities.
On this last vote it was 96 to 4 in favor of increasing NIH
funding. Through the leadership of this subcommittee, the
funding has almost doubled from $12 billion to $23 billion.
This year President Bush has taken the lead in asking for $3.4
billion more. So you can see we are on the move.
Last year Alzheimer's was funded at almost $600 million,
and this year we are looking for $650 million. I know that you
ladies and gentlemen are looking for $1 billion and, frankly,
so are we.
I regret that I cannot be present at the news conference
later. Today happens to be an exceptionally busy day. They are
all busy days around here, but today is an exceptionally busy
day because we are going to introduce legislation that will
allow nuclear transplantation. Some people call it therapeutic
cloning, but that is a misnomer because it gives the impression
that it is cloning. Everybody is against reproductive cloning.
You certainly would not want to create another Arlen Specter.
But if you wanted to create another Tom Harkin, then there
would be an argument, an argument in favor.
But very, very seriously, since stem cells came upon the
scene in November 1998 this subcommittee has held a series of
hearings, 14 in number, to encourage their use because they can
be inserted into the brain, and perhaps will be the ultimate
answer to Alzheimer's. Now with this nuclear transplantation
there is a procedure so that a person suffering from
Alzheimer's, Parkinson's, or other maladies, will not reject
the cells.
We have got a tough fight on our hands because there are
people who want to criminalize cell transplantation. Later this
morning we are going to be having a news conference and I am
going to have to excuse myself at about 10 o'clock to attend
that conference. However, Senator Harkin and I are blessed with
fellow Senators here, Senator Taylor, Senator Ellen, and I will
be following very closely what we are doing here and fighting
very hard to move toward that billion dollars for Alzheimer's
and more funding for NIH.
Thank you all for being here and for your battle. Thank
you, Mr. Chairman. Thank you, Senator Specter.
STATEMENT OF RICHARD J. HODES, M.D., DIRECTOR, NATIONAL
INSTITUTE ON AGING, NATIONAL INSTITUTES OF
HEALTH, DEPARTMENT OF HEALTH AND HUMAN
SERVICES
Senator Harkin. Our first witness this morning will be Dr.
Richard Hodes. Dr. Hodes, if you could take the witness table,
please. Dr. Hodes is the Director of the National Institute on
Aging, the lead Institute at NIH on Alzheimer's disease. Dr.
Hodes received his bachelor's degree from Yale University, his
M.D. from Harvard. He held numerous posts in the National
Cancer Institute before being named Director of the National
Institute on Aging in 1993.
Dr. Hodes has testified several times before this
subcommittee. We certainly welcome him back. So Dr. Hodes, we
have your written testimony. It will be made a part of the
record in its entirety. If you could sum it up for us, I would
certainly appreciate it.
Dr. Hodes. Thank you, Mr. Chairman, Senator Specter. It is
a privilege to be back before this committee once more, joining
the Alzheimer's Association and all present here. I will take
these few minutes to summarize for you the progress in
Alzheimer's research over the past year. The chairman has
adequately summarized the magnitude of the problem and the
urgency that faces us and the Nation with an increased number
of older people at risk for Alzheimer's disease.
The very positive news is that progress over the past years
has been extraordinary. I use the one figure that is in the
written testimony as well to illustrate the nature of the
process by which basic discovery is translated into application
for clinical interventions. Over the past year research on risk
factors for Alzheimer's disease has made important progress.
Some of the progress was again enumerated in the introduction
and has identified factors such as high cholesterol, blood
pressure, high homocysteine levels, factors which we are used
to thinking of as risk factors for cardiovascular disease and
which also appear to be risk factors for Alzheimer's.
The importance of this identification is that it provides
targets for modifiable risk factors, and then in fact these are
translated into clinical prevention trials currently underway.
Similarly, the discovery of Alzheimer's genes has provided
great clues into the mechanisms underlying that process. We
have now identified three genes which are responsible for the
early onset familial forms of Alzheimer's, as well as one gene,
APOE4, that appears to be a risk factor for the common variety
of that disease. In the past year it has become evident that an
additional four genes are likely to be involved in Alzheimer's
and their identification and characterization will again
provide new targets for intervention.
Imaging has allowed us for the first time to identify
changes in the brain at most early stages, and this is an
advance that is critical if we are going to learn how to
intervene before irreparable damage has been done to the brain
and to follow the effect of therapies by looking at changes in
brain structure and function through these imaging techniques.
The past years have provided for the first time animal
experimental models of Alzheimer's, which again have proved
extraordinarily useful in identifying the mechanisms that
mediate the disease and providing ways to test therapies in
animal models before their introduction to humans, once
identified as being promising and safe. This currently leads to
the translation of the information about secretases, for
example, the proteins which are important in generating the
plaques that characterize Alzheimer's disease, and drugs to
inhibit the formation of these amyloid peptides, as well as
what you have heard about before, the use of some immunologic
approaches to try to clear or prevent the formation of the
lesions that characterize Alzheimer's disease.
These all pass through stages of drug development,
preclinical testing, and into clinical trials. Whereas a few
years ago there were no trials that were targeted at
intervening to prevent rather than treat disease, we are now
supporting 18 major clinical trials, 7 of which are
preventions.
Overall, these past years have seen extraordinary progress.
As recently as 15 years ago, we knew essentially nothing about
the genetics or underlying molecular basis for Alzheimer's
disease. Now we have an extensive knowledge that has been
translated into useful information.
As recently as 10 years ago, we knew very little about the
early risk factors and our ability to identify early stages of
Alzheimer's through imaging was really in its infancy. Over the
past 5 years only have we been able to translate this into
prevention studies. In the past year alone, we have learned
through animal models to recreate ever more valid and
legitimate experimental systems which mimic both the anatomic
lesions and the memory deficit of Alzheimer's disease, and
these again have provided new and increasing opportunities for
intervention.
prepared statement
We have a promise beyond what we expected a few years ago
and as we continue in this promise to prevent and treat
Alzheimer's disease we continue as well to recognize the need
to care for those with Alzheimer's and those many caregivers
who are also affected, and so research on trying to ease the
burden to caregivers as well as the present quality of life of
those afflicted is a part of our research agenda as well.
Again, I thank you for the opportunity once more to appear
before you and look forward to answering questions that you
might have. Thank you.
[The statement follows:]
Prepared Statement of Dr. Richard J. Hodes
Senator Harkin and Members of the Committee: Thank you for inviting
me to appear before you today to discuss Alzheimer's disease (AD), an
issue of interest and concern to us all. I am Dr. Richard Hodes,
Director of the National Institute on Aging (NIA), the lead federal
agency for Alzheimer's disease research. I am delighted to be here this
morning to tell you about the progress we are making toward
understanding, treating, and preventing AD.
As you know, AD is a major public health issue for the United
States, and it has a devastating impact on individuals, families, the
health care system, and society as a whole. Approximately 4 million
Americans are currently battling the disease, with annual costs
estimated to exceed $100 billion. Moreover, the rapid aging of the
American population threatens to increase this burden several-fold in
the coming decades. However, despite the grim statistics, we have made,
and are making, tremendous progress.
Until very recently, preventing or curing AD was considered, at
best, a distant possibility. Our understanding of AD's underlying
biology was limited, and for this reason it was difficult even to
predict what might be effective as a treatment or preventive.
Today, the picture is considerably brighter. Through laboratory and
population-based scientific studies, we have identified a number of
risk factors for AD, including both genetic and possible lifestyle
factors. Research supported by the NIA, the National Institute of
Neurological Disorders and Stroke (NINDS), and the National Institute
of Mental Health (NIMH) has identified several genes that can cause AD,
thereby helping us identify pathways affecting its development or
progression, which will lead to better molecular predictors of the
disease even before it is clinically apparent. The development and
refinement of powerful imaging techniques that target anatomical,
molecular, and functional processes in the brain will give us an
improved ability to diagnose AD early, while the patient can still take
an active role in decision-making. These techniques, along with better
neuropsychological tests, are also enabling us to identify people who
are at very high risk of one day developing the disease and to
determine just how the disease starts in brain. This knowledge, in
turn, may allow early intervention in persons long before the disease
affects their level of functioning.
Most importantly, we are making significant advances toward
effectively treating, or even preventing, AD. NIA is currently
supporting 18 AD clinical trials, seven of which are large-scale
prevention trials. These trials are testing agents such as estrogen,
anti-inflammatory drugs, and anti-oxidants for their effects on slowing
progress of the disease, delaying AD's onset, or preventing it
altogether. We eagerly await the results of these trials.
As we search for effective preventive interventions and treatments
for AD, it is becoming clear that, rather than seeking only a ``magic
bullet'' that will, by itself, prevent or cure the disease, we may be
able to identify a number of potential interventions that together can
be used to reduce risk. Several recent studies have highlighted this.
For example, a recent study in the New England Journal of Medicine
\1\ indicates that elevated blood levels of the amino acid
homocysteine, already considered a risk factor for cardiovascular
disease, are associated with an increased risk of developing AD. The
relationship between AD and homocysteine is of particular interest
because blood levels of homocysteine can be reduced, for example, by
increasing intake of folic acid (or folate) and vitamins B6 and B12.
And, in fact, in a separate study in the Journal of Neuroscience,\2\
NIA researchers show that folic acid may protect AD transgenic mice
against death of neurons in one of the brain regions most affected in
AD. NIA has ongoing clinical trials of these substances to test whether
supplementation can slow the rate of cognitive decline in cognitively
normal men as well as in women at increased risk for developing heart
disease. A pilot clinical trial to determine effective treatment levels
of folate/B6/B12 for lowering plasma homocysteine levels in persons
with AD is ongoing, and a full-scale clinical trial on people diagnosed
with AD is due to start in 2003. Other studies have indicated that the
use of statins, the most common type of cholesterol-lowering drugs, may
lower the risk of developing AD. A clinical trial to determine whether
statins slow the rate of disease progression in AD patients is planned
for fall 2002.
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\1\ S. Sesdradri, A. Beiser, J. Selhub, et al., ``Plasma
Homocysteine As A Risk Factor For Dementia and Alzheimer's Disease,'' N
Eng J Med, 346:7, pp. 476-483.
\2\ I. Kruman, T.S. Kumaravel, A. Lohani, W. Pedersen, R.G. Cutler,
Y. Kruman, N. Haughey, J. Lee, M. Evans, and M.P. Mattson, ``Folic Acid
Deficiency and Homocysteine Impair DNA Repair in Hippocampal Neurons
and Sensitize Them To Amyloid Toxicity in Experimental Models of
Alzheimer's Disease,'' Journal of Neuroscience, 22:5, pp. 1752-1762.
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Another promising area of study is the role of mentally stimulating
activities throughout life as a factor capable of maintaining cognitive
health or even reducing the risk of cognitive decline or AD. Through
its Advanced Cognitive Training for Independent and Vital Elderly
(ACTIVE) study, NIA is currently exploring whether three specific
interventions (on memory, reasoning, and speed of processing) can
maintain or improve functioning in unimpaired, community-dwelling older
adults. In addition, NIA-supported researchers recently found that more
frequent participation in activities such as reading, doing crossword
puzzles, or playing card games is associated with a reduced risk of
later developing AD.\3\
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\3\ Wilson RS, Mendes de Leon CF, Barnes LL et al., ``Participation
in Cognitively Stimulating Activities and Risk of Incident Alzheimer
Disease,'' JAMA 287: 742-748.
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In addition to these exciting clinical findings, NIA-supported
investigators are beginning to unravel AD's complex etiology. For
example, until very recently, just four of the approximately 30,000
genes in the human genome were conclusively known to affect the
development of AD pathology. Three of these genes cause early onset AD,
and only one is associated with the more common form of the disease,
late-onset AD (LOAD). Recent genetic studies suggest that as many as
four additional and as yet unidentified genes may also be risk factors
for LOAD, and regions in several different chromosomes have been
identified as likely locations for these genes. Finding new risk factor
genes will help identify pathways affecting the development or
progression of AD and may eventually lead to better predictors of the
disease even before it is diagnosed.
To facilitate the identification of the remaining AD risk factor
genes, NIA is planning an expansion of its National Cell Repository. A
national resource for research on AD, the Repository was created to
collect and distribute DNA, cells, and information from families with
multiple members with AD and related dementias. Its activities include
the production of a catalog of cell lines and DNA samples that are
available for qualified scientists to study. The expansion will allow
researchers to more rapidly identify the underlying genetic mechanisms
and environmental risk factors that interact to cause the more common
late-onset form of AD. Understanding these mechanisms will provide
opportunities for the design of effective diagnostic, therapeutic, and
preventive interventions.
The process of translating basic science findings into clinical
interventions is a challenging but critical component of AD research.
For example, a promising finding gained through basic research efforts
was the ability of an immunization strategy to prevent or reverse
formation of amyloid plaques in mouse models of AD. In collaboration
with NINDS, NIA has issued a Request for Applications (RFA) and funded
a number of studies to better understand the science underlying the
vaccine approach. Similarly, NIA-funded studies are providing exciting
new evidence on the identity of the snipping enzyme that cuts the
amyloid beta molecule out of its precursor protein, and ways to blunt
its activity. These interventions may be capable of preventing the
formation of amyloid plaques.
In addition, NIA-supported researchers have recently made a
surprising discovery about the role of amyloid plaques in AD pathology.
In one study, investigators found that amyloid beta oligomers, or small
precursor components of amyloid plaques, inhibited brain mechanisms
thought to be involved in memory formation in rats.\4\ In another,
scientists used an immunization strategy to treat plaque-containing AD
transgenic mice. Although the amount of plaques in the mice's brains
remained constant, the mice very quickly regained cognitive
functioning.\5\ These findings suggest that amyloid plaques themselves
may not be responsible for AD's cognitive symptoms, and that a related
pathology--perhaps a precursor molecule such as the amyloid beta
oligomer--is the true culprit. This insight, in turn, may lead to the
development of new and effective treatments for the disease.
---------------------------------------------------------------------------
\4\ Walsh DM et al. Naturally secreted oligomers of amyloid
protein potently inhibit hippocampal long-term potentiation
in vivo. Nature 416: 535-539, 2002.
\5\ Dodart J-C et al. Immunization reverses memory deficits without
reducing brain A burden in Alzheimer's disease model. Nature
Neuroscience 2002: Advance online publication.
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Although the findings are still preliminary, these studies
illustrate the importance of continued basic research to help us
understand the mechanisms behind AD development and pathology, and the
ways in which basic research findings can suggest new prevention and
treatment strategies.
Scientists funded by NIA, NINDS, and NIMH are also developing and
refining powerful imaging techniques that hold promise of earlier and
more accurate diagnosis of AD, as well as improved identification of
people who are at risk of developing the disease and a more complete
understanding of normal and abnormal age-related changes in the brain.
For example, recent studies suggest that positron emission tomography
(PET) scanning of metabolic changes in the brain and magnetic resonance
imaging (MRI) scanning of structural brain changes may be useful tools
for predicting future decline associated with AD and other
neurodegenerative diseases.
Researchers have also developed a new way of using functional MRI
(fMRI), a technique for visualizing activity of brain structures, that
is both easier on the person being tested and capable of imaging
smaller structures in the brain than has been possible in the past.
Using this new technique, investigators assessed the hippocampus, an
area of the brain involved in memory formation, in people between 20
and 88 years of age. They found that activity in certain regions of the
hippocampus declines normally with age, but that decline in a specific
region, the entorhinal cortex, is abnormal and may reflect an illness
or condition such as AD. They conclude that some age-related memory
loss is normal, due to ordinary hippocampal changes, but that
individuals with dysfunction in the entorhinal cortex may be at
increased risk of progressing to full-blown AD.\6\ These studies, if
confirmed by ongoing longitudinal observation of the patients, hold the
promise, for the first time, of being able to distinguish between the
subtle brain changes that occur with normal aging and those that are a
harbinger of clinical AD.
---------------------------------------------------------------------------
\6\ Small SA et al. Imaging hippocampal function across the human
life span: Is memory decline normal or not? Annals of Neurology 51:
290-295, 2002.
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These methodologies may also be useful for evaluating the efficacy
of drugs in stemming the progression of AD or preventing its onset
altogether. However, these and other emerging imaging techniques, while
promising, require further testing and analysis before they can be
routinely adopted in the clinical setting.
Another very important area of research involves easing the burden
on caregivers of AD patients. In a sense, the AD ``patient'' is not
only the person with the disease, but the entire family unit. Most
Americans with AD are cared for outside the institutional setting by an
adult child or in-law, a spouse, another relative, or a friend. The
financial costs of this care can be devastating to families; the
average lifetime cost per person for patients with AD is approximately
$174,000.\7\ In addition to these financial burdens, caregivers
frequently experience emotional stress and physical strain.
---------------------------------------------------------------------------
\7\ Ernst, RL and Hay, JW The US economic and social costs of
Alzheimer's disease revisited. American Journal of Public Health 84:
1262-1264, 1994.
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NIA is investing in new approaches to assist these caregivers. A
first priority is to assess the magnitude of the problem. For example,
the ongoing Aging, Demographic, and Memory Study (ADAMS) has been
designed to assess dementia and AD among Americans, the burden on
caregivers, the economic cost of dementia to families and to society,
and the burden of dementia over the course of the illness.
NIA is also supporting a study of a combined behavioral and drug
intervention on patients with mild AD. In this study, caregivers will
be key participants in the behavioral intervention, and the researchers
hypothesize that this participation will reduce caregivers'
psychological stress. In addition, NIA is supporting a large, multi-
site clinical trial, REACH (Resources for Enhancing Alzheimer's
Caregiver Health), to examine the effectiveness of various
interventions to strengthen family members' capacity to care for
individuals with AD. Thus far, the study has recruited over 1,200
caregiver/care recipient pairs at six different sites across the
country to participate in 12 different interventions. REACH is designed
to show us what works to support caregivers and at what cost; we
anticipate that the first findings from this trial may be available
within the next several years. The NIMH is supporting a major project
called the Clinical Anti-psychotic Trial of Intervention Effectiveness
for Alzheimer's Disease (CATIE-AD) designed to help identify effective
treatments for behavioral problems in AD, to help reduce the burden of
care for both providers and families.
Fifteen years ago, we did not know any of the genes that could
cause AD, and we had no idea of the biological pathways that were
involved in the development of brain pathology. Now, we know the 3
major genes for early-onset disease and one of the major risk factor
genes for late-onset disease, and we have extensive knowledge of
pathways leading to the development of AD's characteristic amyloid
plaques in the brain. Ten years ago, we could not model the disease in
animals. Today, transgenic mice are an invaluable resource for modeling
amyloid plaque development in the brain and in testing possible
therapies. Five years ago, we did not have any prevention trials funded
and had no ways of identifying persons at high risk for the disease.
Now, we have seven ongoing prevention trials, and scientists are
identifying persons at high risk for developing AD by imaging,
neuropsychological tests, and structured clinician interviews. And as
recently as one year ago, we did not understand anything about how
plaques and tangles relate to each other. Now, through the creation of
the first double transgenic mouse to produce both plaques and tangles,
we know that plaques in the brain can influence the development of
tangles in brain regions susceptible in AD. Recent findings also
suggest that there are some common mechanisms of disease in a number of
neurodegenerative disorders, which will further inform research in AD.
It is difficult to predict the pace of science or to know with
certainty what the future will bring. However, the progress we have
already made will help us speed the pace of discovery, unravel the
mysteries of AD's pathology, and develop safe, effective preventions
and treatments, to the benefit of older Americans.
Thank you for giving me this opportunity to share with you our
progress on Alzheimer's disease. I would be happy to answer any
questions you may have.
Senator Harkin. Dr. Hodes, thank you very much.
I am going to ask you to stay, if you could, and we will
have the next panel up.
I will yield to Senator Specter. He does have to leave.
Senator Specter. Thank you, Mr. Chairman. I appreciate the
opportunity to ask a few questions of you, Dr. Hodes, at this
time because I am going to have to excuse myself, as I said
earlier.
The funding for Alzheimer's, as well as the funding for all
of the other National Institutes of Health, depends to a
significant extent on the sense of the Congress, really the
sense of the American people, as to how well the money is being
spent and what are the results. We have had estimates on
Parkinson's, for example, that we may be within 5 years of a
cure.
While I know it is difficult to make a quantitative
evaluation, I would be interested, to the extent that is
consistent with your scientific methodology, if you can give us
some estimate as to a time line for a cure on Alzheimer's?
Dr. Hodes. Well, I apologize for the fact that I think I
cannot responsibly quote a specific time in terms of years. But
I can certainly share an exceptional sense of optimism
projecting from the pace of discovery as summarized over these
past 15 years. This pace is bringing us closer to interventions
and cures than we ever dreamed possible a few years ago.
The fact that we were able to bring into clinical trials
interventions which have the promise for preventing disease is
extraordinary. I can tell you that the results of some of these
ongoing prevention trials, for example, will be coming to
fruition over the next 3 to 5 years. That is not an estimate of
when we know we will have success, but it is an estimate of
when we should have the first results on some of the large-
scale prevention trials which have real promise of success.
Senator Specter. So you are saying, in terms of prevention,
the prospects are good that the scientific research has a
realistic possibility of preventing Alzheimer's?
Dr. Hodes. Yes. I think that we have over these past years
uncovered now multiple potential targets. We have identified
risk factors and learned how to modify those risk factors. Some
of these risk factors are behavioral, some of them are
biochemical and genetic. The more targets we have for
intervention, the greater the chance that one or more of them
is going to be successful. And yes, the pace of progress over
these past years gives good reason to propose a realistic
vision of a cure and/or prevention for Alzheimer's disease over
the years to come.
Senator Specter. When we talk about raising the funding
this year by approximately $50 million, from $600 to $650
million, what tangible evidence can you give Senator Harkin and
myself as ammunition to deal with our colleagues in the Senate
as to why that increase ought to be given? What can you tell us
that we can pass on to the other Members of the Senate?
Dr. Hodes. I can provide some general statements and then
some rather more specific. In the general sense, the greatest
argument for a continued increase in funding is the quality of
scientific opportunities. Each discovery, be it in genetics, in
risk factors, in relief of caregivers, creates opportunities,
which then need to be followed by additional research.
In particular, as basic research has provided opportunities
for treatment and prevention, we have come to a stage of
carrying out multiple clinical trials. Now, if we were to carry
out only one clinical trial at a time, awaiting its result
before going on to the next, I think this would be an
unpardonable delay in eventually reaching success. So our
approach has been to capitalize on the funding that has been
made available to fund all of the most outstanding
opportunities for clinical trials.
Clinical trials, for prevention in particular, require the
inclusion of thousands of individuals followed for several
years. They are expensive studies. Each of these studies may
cost in the range of $25 to $50 million. In order to carry out
those several, each of which is responsive to outstanding
current scientific opportunities, an increase in budget would
be enormously helpful and important.
Senator Specter. Okay. The billion dollar question. Dr.
Hodes, what can you accomplish with $1 billion that you cannot
accomplish with $650 million?
Dr. Hodes. Well, we would be able, simply arithmetically,
by that comparison to support 50 percent more research than we
do. Fifty percent more research would easily be carried out by
supporting uncompromised quality of both basic science to try
to produce the opportunities for translation in the years to
come as well as an increased speed of expeditiously following
up on current opportunities to follow all of the candidate
interventions for both treatment and prevention.
Senator Specter. Dr. Hodes, I would like you to give some
thought when you go back to your office, to your laboratory, to
see if you can quantify more specifically. I appreciate the
answers you have given, but we started funding Alzheimer's with
$3.9 million in 1976 and now it is up to $600 million and you
want to go to $1 billion. To the extent that you could give
some hard estimates or some hard information--for example my
colleagues can understand that you could possibly get 50
percent more research from $1 billion versus $650 million. That
kind of arithmetic is about the limit of our capability.
But see if you cannot give us something really tangible, as
tangible as possible.
Dr. Hodes. Absolutely. I would be pleased to provide
concrete examples.
[The information follows:]
Recent research advances have created important new opportunities
for research that will accelerate progress toward interventions for
early diagnosis, treatment, and prevention of AD.
Recent scientific advances, largely the result of NIH-supported
research, have illuminated significant genetic and cellular mechanisms
that underlie AD. For example, four genes that affect the development
of AD have already been identified, and recent studies suggest that for
late-onset AD (the more common form of the disease) there may be at
least four more risk factor genes. Efforts to pinpoint their exact
location will help identify pathways affecting the development or
progression of AD and may eventually lead to better predictors of the
disease even before it is clinically apparent.
In addition, scientists are developing and refining powerful
imaging techniques that target anatomical, molecular, and functional
processes in the brain. These new techniques hold promise of earlier
and more accurate diagnosis of AD, as well as improved identification
of people who are at risk of developing the disease. For example,
recent studies suggest that positron emission tomography (PET) scanning
of metabolic changes in the brain and magnetic resonance imaging (MRI)
scanning of structural brain changes may be useful tools for predicting
future decline associated with AD and other neurodegenerative diseases.
Researchers have also developed a new method of functional MRI (fMRI),
a technique for visualizing activity of brain structures, that is both
easier on the person being tested and capable of imaging smaller
structures in the brain than has been possible in the past. These
methodologies may also be useful for evaluating the efficacy of drugs
in stemming the progression of AD or preventing its onset altogether.
However, these and other emerging imaging techniques, while promising,
require further testing and analysis before they can be routinely
adopted in the clinical setting.
Research findings at the molecular level have created new and
unprecedented opportunities for translation of basic research into
clinical applications. The process is necessarily deliberate; as new
target molecules are identified, interventions must be developed,
tested in animal models for safety and efficacy, and only then moved
into human trials. At the same time, clinical trials are needed today
to test treatment interventions that have already shown promise in
animal models, including promising new vaccines that ``wash'' amyloid
from the brain and treatments that target enzymes called secretases,
which begin the formation of amyloid plaques in the brain by snipping a
protein into fragments that re-form as plaques. This research area is
of tremendous interest to researchers in industry and academia as well
as at other NIH Institutes, and this interest is leading to expanded
opportunities for partnership.
Trials are also needed for interventions that prevent AD onset or
progression. Examination of a number of possible AD preventives is
underway--for example, the AD Prevention Trial using vitamin E and
donepezil, as well as trials testing the effect of estrogen, anti-
inflammatory drugs, and antioxidants. Candidate interventions that
lower amyloid burden in animal models of AD are being identified with
increasing frequency. Targeting specific abnormal cellular pathways
uncovered by recent discoveries, including plaque and tangle formation
and death of brain cells, are pointing to design of new interventions
to prevent the onset of AD. Prevention trials are among the most costly
of research projects, but, if successful, the payoff in terms of
reduced disease and disability will be significant.
Critical opportunities that could be supported with increased funds
in fiscal year 2003 include:
(1) Epidemiology studies to identify additional genetic causes and
risk factors for AD, information that will provide new targets for
treatment and prevention.
(2) Testing of new methods for early diagnosis of AD, based on
imaging and markers of early brain changes. Early diagnosis is critical
to effective treatment and prevention, before onset of symptoms and
death of brain cells.
(3) Pre-clinical trials in newly created animal models of AD, which
permit rapid testing of potential treatments based on new genetic and
molecular targets.
(4) Clinical trials of AD prevention. Candidates for prevention,
based on human epidemiology and animal model studies, require clinical
trials. These include anti-inflammatory agents, anti-oxidants,
estrogen, statins, immunization with amyloid peptide, and secretase
inhibitors.
(5) Development of interventions to reduce caregiver burden and
strengthen family members' capacity to care for AD patients.
It must be noted that this estimate is based on our assessment of
scientific opportunities over the next five years, without
consideration of economic constraints or other competing priorities of
the Federal government. This level of support must be integrated with
other research efforts of the NIH.
Senator Specter. Thank you very much, Dr. Hodes.
Thank you, Mr. Chairman.
Senator Harkin. Thank you, Senator Specter.
I just noticed, looking at the record, we have got it
pretty even. When I was chairman we almost doubled it and when
you were chairman we almost doubled it. That is pretty good.
Senator Specter. It looks like if we have another change in
chairmanships we will double it again.
Let me tell you ladies and gentlemen, while I prefer to be
chairman to ranking, when Senator Harkin and I shift the gavel
it is seamless, absolutely seamless. It keeps going the same
way.
Senator Harkin. That is true, absolutely.
Thank you very much, Dr. Hodes.
I would like to call up our next panel if I could then.
Orien Reid, Chair of the National Board of Directors; Dr.
Marilyn Albert; Carol and Gene Gratz; and David Hyde Pierce. We
will go in that order, and I would first recognize Ms. Orien
Reid, the Chair of the National Board of Directors of the
Alzheimer's Association.
Ms. Reid was a consumer reporter on television and radio
for 26 years and recently formed a media consulting business.
Ms. Reid earned her bachelor of arts degree from Park College
and a master's degree from the Atlanta University School of
Social Work. She lives in Laverock, Pennsylvania. I am not sure
I know where that is, but it sounds like a nice place to be.
Ms. Reid. Suburban Philadelphia.
Senator Specter. One additional comment about Ms. Reid, Mr.
Chairman. She is a very, very familiar figure on Philadelphia
television and when she speaks people listen.
Senator Harkin. Politicians listen, right?
Senator Specter. So do statesmen.
STATEMENT OF ORIEN REID, CHAIR, BOARD OF DIRECTORS,
ALZHEIMER'S ASSOCIATION
Ms. Reid. Thank you. Thank you, Senators. Thank you, thank
you so much.
Senator Specter. Adlai Stevenson defined a statesman as a
dead politician.
Ms. Reid. Well, I am not ready to die.
Thank you so much. Thank you, Senator Specter.
Senator Harkin. Orien Reid, welcome. All your statements
will be made part of the record in their entirety. If you would
just sum it up for us, I would appreciate it. Again, I thank
you for your great leadership.
Ms. Reid. I certainly will. Thank you so much for inviting
me to testify at this very important hearing today. As you
noted, I serve as Chair of the National Board of Directors of
the Alzheimer's Association.
I am here this morning to speak for my own family because,
you see, today is a very special day. It is my mother's
birthday, and had she not been killed by Alzheimer's disease
she would be 86 years old today. So I just feel her spirit with
me today and I want to speak for her and for my grandmother, my
aunt, and my uncle, all of whom had Alzheimer's disease.
I also speak for the hundreds of families, Alzheimer's
families who are gathered in this room today, and for the
millions of families like us. We are here today to thank you
for your consistent leadership on issues that matter to the
Alzheimer's community. We are here to tell you that we support
your continued efforts to increase funding for Alzheimer's
research and services. We know that you are on our side. We are
here to enlist others to support your effort to increase
medical research funding in general and specifically for
Alzheimer's disease.
Now, I would like to submit and present to you for the
record the Alzheimer's national public policy program to
conquer Alzheimer's disease. You will have that. Today
Alzheimer's advocates from across the country will deliver this
national program personally to their own Senators and
Representatives.
My request today is an urgent one. It is to ask you to
increase appropriations for Alzheimer's research by $200
million this year and to a billion dollars a year as soon as
possible.
We thank you for your support of our goal, which in
particular we are very happy that you chose to reflect it as
part of the language of your committee report last year. We
have seen your commitment to Alzheimer's disease research
funding through the years.
The problem is we are running out of time to find an end to
this disease. It is time now. The time is now for Congress to
make this investment. The two experts in Alzheimer's research
that I have sitting here will tell you about, and Dr. Hodes has
just told you about, some of the scientific opportunities that
exist today. If we are going to prevent the 14 million baby
boomers from getting Alzheimer's disease, we have got to do
something today.
The experts know the science, but I along with 19 million
other caregivers know what it is like to live with this
disease. I watched Alzheimer's disease destroy my mother, a
beautiful woman with a beautiful mind, a woman who counseled
eminent leaders like Dr. Martin Luther King Junior and the
former Mayor of Atlanta, Maynard Jackson.
My family and I made major sacrifices and I do not regret
that a bit. But what I do regret is the fact that this disease
robbed my children of their childhood. It also took the money
that I had saved for their college education and it left scars
that continue to affect their lives. Today my children and I
all live in fear because we do not want to live this nightmare
all over again. I am only 16 years younger than my mother was
when she was diagnosed with this disease. It is also very
disconcerting to me to learn that African Americans may be at a
higher risk for Alzheimer's disease. That does not make me feel
comfortable.
Today there are 14 million baby boomers in the United
States who will get Alzheimer's disease if we do not find a way
to stop it. We cannot save Medicare if 14 million baby boomers
get Alzheimer's disease because the cost of treating people
with Alzheimer's disease is estimated to climb from $31.9
billion in 2000 up to $49.3 billion in 2010, just 8 years away,
even though Medicare does not pay for most of the long-term
care.
We cannot preserve Medicare and Medicaid if we do not find
a way to stop this disease. That can only be done through
research.
In addition to research, there are some important programs
before your committee. We are happy to hear that you are going
to continue your support of the family caregiver support
program and we urge you to continue your support to expand the
Alzheimer's matching grant program to all 50 States, to reach
rural, underserved, and minority populations.
PREPARED STATEMENT
You can see how your support has helped thousands of their
families with Alzheimer's disease. As my beloved friend Maureen
Reagan used to say, she hoped that we would be the last
generation to face this disease without hope. You are our only
hope so that we will not have to. Please help us.
Thank you.
[The statement follows:]
Prepared Statement of Orien Reid
Senator Harkin, Senator Specter and other members of the
Subcommittee: Thank you very much for inviting me to testify today at
this very important hearing. I serve as chair of the Board of Directors
of the Alzheimer's Association. I am here to speak for my own family--
my mother, my aunt, my uncle, and my grandmother--all of whom had
Alzheimer's disease. I also speak for the hundreds of Alzheimer
families gathered in this room today, and for the millions of families
like us across the country.
We are here to thank you for your constant leadership on issues
that matter to the Alzheimer community, and to tell you that we support
you in your continued efforts to increase funding for Alzheimer
research and services. We know you are on our side. We are here to
enlist others to support your effort to increase medical research
funding in general, and specifically for Alzheimer's disease.
I would like to present to you and submit for the record the
Association's National Public Policy Program to Conquer Alzheimer's
Disease. Today, Alzheimer advocates from across the country will
deliver this National Program personally to their own Senators and
Representatives.
Today I am here with an urgent request--to ask you to increase
appropriations for Alzheimer research by $200 million this year, and to
$1 billion a year as soon as possible. We applaud you for your support
of our goal, reflected in the language of your Committee Report from
last year and your commitment to Alzheimer's disease research funding
through the years.
There is no time to wait--now is the time for Congress to make this
investment. You have two experts in Alzheimer research here to tell you
about the exciting scientific opportunities that exist today--new
opportunities we must pursue in order to prevent 14 million baby
boomers from getting Alzheimer's disease. I will leave the discussion
of the science to the researchers--my knowledge is in the area of what
it means to live with Alzheimer's disease.
My own personal experience with this horrible disease reflects
those of 19 million Americans who have a family member with Alzheimer's
disease. Our experiences, combined with the knowledge that the
Alzheimer's disease process begins in the brain as many as 20 years
before a person is seriously impaired, have created our sense of
urgency and driven us to this call for action.
It devastated me to watch the disease destroy the beauty and mind
of my mother--a woman who had counseled imminent leaders like the late
Dr. Martin Luther King, and former Atlanta Mayor, Maynard Jackson. My
mother's Alzheimer's disease forced major changes in my personal and
professional life. I don't regret those sacrifices for a moment. My
mother was worth it. But this disease didn't just take a toll on me,
but also robbed my son and daughter of their childhood, took the money
I had saved for their college education, and left an indelible mark on
them that continues to affect their lives.
My children and I are terrified by the prevalence of this disease
in our family. I'm now 16 years younger than my mother when she was
diagnosed with Alzheimer's. My greatest fear is that it has started to
eat away at my brain too, and that my children will be forced to live
this nightmare all over again. Recent studies showing that African-
Americans may be at higher risk of Alzheimer's disease does nothing to
ease my mind.
I am not alone in my fears. Today there are 14 million baby boomers
in the United States who will get Alzheimer's disease, if we don't find
a way to stop it. Think about the implications. For example, it is
difficult to see how you can save Medicare, if 14 million baby boomers
get Alzheimer's disease. Alzheimer's poses a threat to Medicare even
before the baby boomers have all retired. The cost to Medicare of
treating people with Alzheimer's disease is estimated to soar from
$31.9 billion in 2000 to $49.3 billion in 2010, even though Medicare
does not pay for most of the long term care they need.
The survey conducted by Peter D. Hart Research Associates and being
released today by the Alzheimer's Association found that Americans are
also concerned about health care costs. More than eight in ten voters
say that paying for health care costs is the biggest financial
challenge facing the elderly today--far outpacing housing, the cost of
utilities and food. There is no way to preserve Medicare and Medicaid,
and rein in health care costs, if we do not find a way to stop
Alzheimer's disease, and that can only be done through research.
In addition to medical research, there are important programs
before your Committee that are providing immediate help to people who
are living with Alzheimer's disease. We urge you to continue your long-
standing support, and fund further expansion of the Alzheimer matching
grant program to support model programs in all fifty states to reach
underserved communities, particularly minority populations and rural
areas. And we thank you for your support of the Family Caregiver
Support Program.
The Alzheimer's Disease Demonstration Grants to States Program
helps states assure that community services are accessible and
appropriate for the unique needs of people with Alzheimer's and their
families. While these grants are very small--$250,000 to $350,000 per
year for a three-year period--they have had a huge impact by:
--providing services to individuals who were previously left out,
especially minorities and rural populations;
--changing the larger health and long term care systems so that
states to do a better job of serving people with Alzheimer's
disease;
--developing partnerships along with new public and private resources
to continue and expand programs upon conclusion of the
demonstration;
--developing ``best practice'' service delivery models that are being
replicated within and beyond the state; and
--generating an Alzheimer's Disease Resource Room on the
Administration on Aging website that features information on
successful strategies that can be replicated in communities
across the country.
Let me give you a few examples of the innovations your investment
has brought in the states that have received these grants:
--In Maine, dementia teams that are linked to university specialists
now go to the homes of people in isolated rural areas and
regularly consult with their family physicians.
--A mobile dementia day care program now serves small towns in
Georgia that cannot support a full time adult day care center.
--Latino families in South Central Los Angeles now have a
comprehensive Alzheimer community services program, and the
initial seed money from the federal government has been totally
replaced with locally raised funds. This program has now been
replicated in the African American and Asian American
communities.
--Oregon has trained all of the case managers in its long term care
system to understand the special needs of people with dementia
and, as a result, the entire system is more responsive to those
needs.
--A current grant in Rhode Island is focused on developing a model of
consumer directed respite care provided by and for minority
elders. It is also creating a model of workforce development,
including Certified Nursing Assistant (CNA) training and the
establishment of career ladders for CNA's.
In each case, the state has partnered with local Alzheimer's
Association chapters to apply for and implement the grant. We urge you
to appropriate $25 million to allow these innovations to go forward in
every state. As states and health care systems redefine their services
to meet the needs of a growing aging population, this program will help
assure that people with Alzheimer's disease do not fall through the
cracks.
Alzheimer's disease is an epidemic, and we simply cannot wait to do
something about it. The Alzheimer's Association continues its own
investment in Alzheimer research--nearly $120 million to date. We will
do everything we can to bring as much private money as we can into the
search for the answers. But we all know it will take your support, and
the resources of the NIH to harness and stop this disease.
To allow researchers to capitalize on new knowledge gained through
past investments in research and reach answers in time to make a
difference, Congress must provide an additional $200 million this year
for a government-wide assault on Alzheimer's disease. We are asking you
to join us in this effort. Time is running out for our children and
grandchildren, and for 14 million baby boomers who may be living with a
sentence of Alzheimer's disease. Please, for all of us, act now. Thank
you.
Senator Harkin. Thank you, Ms. Reid. Great testimony. Thank
you for your leadership.
Next we will turn to Dr. Marilyn Albert, Professor in
Psychiatry and Neurology at Harvard Medical School and Director
of Gerontology Research Unit at the Massachusetts General
Hospital. Dr. Albert also serves as Chair of the Alzheimer's
Association's Medical and Scientific Advisory Committee. She
received her Ph.D. in psychology from McGill University.
Welcome, Dr. Albert.
STATEMENT OF MARILYN ALBERT, Ph.D., CHAIR, MEDICAL AND
SCIENTIFIC ADVISORY COMMITTEE, ALZHEIMER'S
ASSOCIATION
Dr. Albert. Thank you very much, Senator Harkin, Senator
Specter. It is a great honor to speak to you this morning in my
position as Chair of the Medical and Scientific Advisory
Committee of the Alzheimer's Association.
I wanted to begin by commending you for your past and very
strong support of research funding for the NIH and for
Alzheimer's Association in particular. My research colleagues
around the country are certain that it is that strong support
that has enabled us to learn so much about Alzheimer's disease
so quickly over the last 20 years. We believe it is this
progress that has put us on the brink of finding truly
effective treatments for the disease in the coming years.
In my written statement that I submitted for the record, I
identified five major research areas where we believe an
infusion of money would be greatly helpful. But in the brief
time allotted to me, what I would like to do is talk to you
about the research area that I know the best, the one that I
work in, which is longitudinal clinical research for the early
diagnosis of Alzheimer's disease.
As you may know, recent studies have demonstrated that the
pathology of Alzheimer's disease begins many years before
clinical dementia can be diagnosed. Most of my colleagues
believe that when we get effective treatments for the disease
it is highly unlikely that they are going to be benign, and yet
it is going to be critically important to intervene before
substantial damage has been done to the brain.
So the kind of work that I do has been involved in trying
to identify people before the disease symptoms become full-
blown, when intervention would be of the greatest benefit. The
work of my research colleagues and of several other groups
around the country has been using cognitive testing, neuro-
imaging, genetics to try to identify individuals who have
memory problems that are relatively mild and be able to predict
when those symptoms are going to progress and which of those
individuals are going to go on to meet criteria for Alzheimer's
disease in subsequent years.
Now, when I started this phase of my work 10 years ago, it
seemed sort of incredible in retrospect, but I thought that we
would have clear answers within 5 years. It turns out, on the
basis of our research, that people progress with varying rates,
people with mild memory difficulty. Some progress quite quickly
and do develop Alzheimer's disease within a very short period
of time. Some progress very slowly and seem to be going in the
direction of developing the disease, but do not within even a
decade. Some who appear to be at high risk actually remain
stable, and we have a great deal of difficulty then predicting
what is going to happen to people over time.
So that, although we have made a great deal of progress, it
has been much harder than we ever anticipated, it has required
much more time, many more subjects, and of course that
translates into many more dollars.
We believe that we are on the right track. We have
anticipation that pharmaceutical companies will be close to
adopting some of the methods that we have used to help screen
drugs that might be effective for the disease and study
patients to determine whether or not the drugs that they have
developed actually slow down the progress of the disease. But
it is really going to take considerably more effort to get the
answers that we are seeking.
This one research effort I think illustrates how much more
complicated and expensive long-term clinical research is on a
day to day basis and why it is so important for us to have
additional research dollars for this problem as well as the
many others that Dr. Hodes just described.
PREPARED STATEMENT
Like my other colleagues in the Alzheimer's Association, I
want to emphasize how important it is for us to have additional
funding for research in this area. As Orien just said to you,
it is not an exaggeration to say that if we do not find
effective treatments for Alzheimer's disease there is no health
care system in the world that will be able to support the
problem that we will face.
Thank you.
[The statement follows:]
Prepared Statement of Marilyn Albert
Mr. Chairman and members of the Subcommittee: Thank you for
inviting me to participate in this very important hearing on
Alzheimer's disease--the epidemic of the 21st century. Others on this
panel are here to describe the human side of Alzheimer's and its
enormous cost--to individuals, to families, to our health care system
and our national economy. The case for the war against Alzheimer's is
clear. My task, as a scientist, is to convince you we can win this
war--if we are willing to put the resources into the fight.
The possibility of ending Alzheimer's disease as we know it has
never been more real. We have reached this historic point because of
your unflagging support of funding for the National Institutes of
Health as a whole, and for Alzheimer's disease research in particular.
We are now poised to yield enormous return on that prior investment.
When I started my own research on Alzheimer's disease 22 years ago,
there were a relative handful of scientists working in the field. NIH
was investing about $12 million in Alzheimer research. We were just
beginning to understand the basic mechanisms of the disease. Only a
handful of papers on Alzheimer's disease found their way to
publication. Caregivers struggling with the disease were starting to
find each other and forming the local support groups that would soon
become the Alzheimer's Association.
How the world has changed! This July, the Alzheimer's Association
will convene the 8th International Conference on Alzheimer's Disease
and Related Disorders in Stockholm. More than 4,000 scientists working
on Alzheimer's disease will gather to report new findings on the
biology, epidemiology, genetics, environmental risk factors, diagnosis,
treatment, and prevention of Alzheimer's disease. This year alone, more
than 3,000 peer-reviewed papers on Alzheimer's research will appear in
leading American and international journals.
We have come this far, this fast, because of the systematic care
with which the National Institute on Aging has nurtured and developed
the field of Alzheimer research, creating a scientific infrastructure
that has made possible not only the rapid accumulation of knowledge,
but an unprecedented sharing of data among laboratories and the
translation of basic science to clinical studies.
All of this work is directed toward two objectives:
First, to delay and prevent the onset of disease in the tens of
millions of people who are now at risk. We now understand that the
process that leads to Alzheimer's may start in a person's brain many
years before he or she becomes clinically impaired. That gives us a
window of time to prevent the devastation of Alzheimer's in millions of
today's babyboomers--if we can find effective and affordable
therapeutic interventions, and if we can identify those individuals who
are at risk so that we can intervene early enough to make a difference.
The second and equally important goal is to treat and delay the
progress of Alzheimer's in those for whom we cannot prevent disease.
Both of these goals are within reach. But Alzheimer's disease has
turned out to be much more complicated than we originally thought. That
is why we need a $1 billion investment from NIH, to pursue
simultaneously the immediate opportunities in 5 essential and
interrelated areas of research.
First, we must continue basic biomedical research to find the last
pieces of the complex puzzle of Alzheimer's disease, to complete our
understanding of how and why brain cells shrink and die. We are
constantly learning more about the two major characteristic of
Alzheimer's--the amyloid plaques and neurofibulary tangles--and how
they interact. We know how plaques are formed and deposited in the
brain and how they act as toxins. Now, scientists are working
aggressively to block their formation. We are assembling the same type
of information about the formation of tangles. And evidence is mounting
that inflammation and oxidative stress may play an important role in
the disease. Neuroscience, and the study of Alzheimer's disease
particularly, is one of the most exciting and promising areas of basic
science today. We will continue to attract the best minds to the field
as long as we maintain our investment here.
Second, we must conduct large scale clinical trials to test
potential therapies to slow or halt onset and progression of disease
and to prevent or delay disability. Basic research is identifying
multiple targets for such therapies, and observational studies have
suggested that drugs already used widely by middle-aged and older
people may have a protective effect. The only way to figure out how to
turn all of this discovery into safe and effective treatment is to do
large-scale, controlled clinical trials of each of these interventions
that holds promise.
These trials--especially prevention trials--are very expensive. We
have to recruit large numbers of people who do not yet have Alzheimer's
disease and follow them long enough to see whether the compound has the
desired effect. And we have to test for variability by race and
ethnicity. At the urging of Congress and under the leadership of the
National Institute on Aging, NIH is investing in a number of these
trials already, at costs as high as $25 million for a single trial. But
if we are going to take advantage of the window of time we have before
large numbers of babyboomers succumb to the disease, there must be a
steady infusion of funds for additional trials to validate initial
results and to explore new potential therapies as rapidly as science
identifies their potential.
Third, we have to do the longitudinal clinical studies that will
tell us who is really at risk of getting Alzheimer's disease and to
find the surrogate markers that will make it possible to identify
people before the disease is apparent. We are not just doing science
for science's sake. We have a moral obligation to make sure that the
people who can benefit from what we learn get the treatment they need,
and that they get it early enough to make a difference.
This is the kind of work I do. For the past 10 years, my research
team has been following people with mild memory difficulty to try to
see if we can predict which ones will get worse and which one's won't
and what factors influence progression. We started with a relatively
small group of subjects, but as we learned more about how complicated
the disease is and how slowly it progresses, and as other research has
brought us new tools and new questions, our research has grown. We have
increased the number of people we are following. We are looking at
people who are normal as well as those with memory difficulties. And we
are now able to take the enormous scientific progress that has been
made by others and apply it in our clinical studies. When we started,
we were excited that we could use CAT scans to ``see'' the brain. Now,
we are using three types of structural imaging that give us
extraordinary ability to measure changes in the brain over time. We are
applying increased knowledge of genetics to look at its influence on
cognitive performance and imaging measures in our subjects. We have
also been able to confirm the findings of other researchers by looking
at the impact of anti-inflammatories in our population.
All of this takes money. Our own research--this one clinical study,
for example--now costs $2.5 million a year. And it requires a sustained
commitment of funds for a decade or more. Without a continued
substantial increase in funding from Congress, NIA will be forced to
make impossible choices between multi-year funding for these large
scale clinical studies and funding for new investigator-initiated basic
science. If we are going to find the answers to Alzheimer's in time to
make a difference, there must be enough money in the system to do both.
Fourth, we need to track down the linkages between vascular disease
and Alzheimer's. This is an increasingly promising avenue of research
with enormous potential payoff. Evidence from a number of longitudinal
studies here and abroad suggests there is a direct relationship between
vascular disease and Alzheimer's. Vascular abnormalities in the brain,
on top of the lesions of Alzheimer's disease, appear to make cognitive
impairment worse. Vascular risk factors like high cholesterol and high
blood pressure may be significant risk factors for Alzheimer's disease
as well. And there is now some accumulating evidence that statins--
cholesterol-lowering drugs--may have a protective effect.
Many of the long-term population-based studies of heart disease,
like the Framingham Study and the Nurses Health Study, now have cohorts
that have aged. These studies have accumulated a lifetime of data on
their subjects, which we can examine now to study the risks for
cognitive decline.
The public health implications of this avenue of research are
enormous, particularly for racial and ethnic groups disproportionately
affected by vascular disease. We already know a lot about primary and
secondary prevention of vascular disease. Now, we may have a route to
prevention of Alzheimer's as well, for a significant number of people
at risk. It will take increased resources at the National Heart, Blood,
and Lung Institute as well as the NIA to pursue this research as
rapidly as possible.
Fifth, we must find more effective ways to treat Alzheimer's
disease. No matter how quick and successful we are in finding a way to
prevent Alzheimer's disease, millions of Americans like Mr. and Mrs.
Gratz will still be living with a diagnosis of Alzheimer's for the
foreseeable future. Congress must continue to invest resources in the
search for more effective and affordable treatments to improve the
quality of life and delay the disabling impact of the disease. This
requires investment in:
--drug discovery for direct treatment of Alzheimer's and for the
management and treatment of the behavioral symptoms that make
care so difficult and costly;
--health services research and demonstrations to find effective ways
to manage comorbid medical conditions in people with
Alzheimer's who cannot self-manage those conditions and to
prevent avoidable illness, injury, and hospitalization;
--social and behavioral research to improve the quality of care and
the quality of life for persons with Alzheimer's and their
caregivers in every setting.
The Alzheimer demonstration grant program, which other witnesses
have discussed, is a critical piece of this research agenda. I join in
urging the subcommittee to increase funding of that highly successful
program to $25 million to allow all 50 states to participate.
In conclusion, I want to acknowledge the enormous task this
subcommittee faces in balancing the competing demands in this most
important part of the federal budget, which touches so directly on the
health and well-being of every American family. Finding room in that
budget for the investment needed to keep 14 million Americans from
getting Alzheimer's disease is one of the most important things this
subcommittee can do for our long term economic and social security.
Thank you.
Senator Harkin. Thank you very much, Dr. Albert.
Next we turn to Carol and Gene Gratz, who are from New
Hampton, Iowa, a small town that I have been to many, many
times in the northeastern part of the State. Gene was diagnosed
with Alzheimer's last June. Carol and Gene have been married
for 12 years. They are here with their 11-year-old son, Kris.
Again, I want to thank you both for taking all the time and
the trouble to travel here and to give us some personal insight
as to what has happened to you just in the last year or so
since Gene was diagnosed. So Carol, we will recognize you if
you would like to kick it off.
STATEMENT OF CAROL GRATZ, NEW HAMPTON, IA, EAST CENTRAL
IOWA CHAPTER, ALZHEIMER'S ASSOCIATION
Ms. Gratz. Mr. Chairman and members of the subcommittee:
Thank you very much for giving me the opportunity to testify
this morning. I am truly honored to be here representing my
home State of Iowa and our East Central Iowa Chapter of the
Alzheimer's Association. My name is Carol Gratz and I am here
today with my husband Gene and our 11-year-old son, Kristopher,
who is sitting right behind me.
We have traveled here to Washington from New Hampton, Iowa,
a rural community of approximately 3800 people, to ask you to
please do everything to increase funding for the Alzheimer's
research so a cure or prevention can be found as soon as
possible. Our plea for increased research funding is extremely
personal. Ten months ago Gene, at age 57, was diagnosed with
Alzheimer's disease.
The symptoms of Gene's disease actually started appearing 4
years ago. Gene at 53 began having problems with his short-term
memory and was having great difficulty in dialing a phone or
reading a newspaper. Naturally, our first instinct was to see
an eye doctor. However, the eye doctor could find no medical
explanation for Gene's vision problems.
Over 2 years, he continued to have problems with his vision
and his memory, but rarely complained, so I was not fully aware
of the extent of Gene's problems. By this time he was having
trouble driving and also decided he could no longer endure a 2-
hour daily commute to his job as a forklift driver. He found a
new job as a produce manager closer to our home and he worked
there for about a year. The produce manager's job involved
substantial amounts of paperwork, which he had great difficulty
doing because of his vision problems.
In January 2000, Gene changed jobs a second time and wound
up with a position on an assembly line at a local manufacturing
plant. The assembly line work involved repetitive tasks and did
not require reading or writing, so Gene did well at his job.
However, in April 2001, with a slowdown in the assembly
line, it forced him to switch jobs in the plant, and he had to
begin to read blueprints, which he had trouble doing as his
vision was very poor. His supervisor asked him to visit a
doctor for a checkup.
By this time I knew that Gene's vision problems and short-
term memory problems were not normal and began researching his
symptoms on the Internet. My search took me to the Alzheimer's
Association web site. I contacted our local chapter and the
people at the East Central Iowa Chapter were extremely helpful,
and sent us many information packets as well as a list of
doctors in our community.
After seeing a general practitioner and multiple visits to
various specialists, we were referred to the University of Iowa
hospital for additional testing. Finally, in June of 2001 we
got the terrible news that Gene had Alzheimer's disease. We
were also told that he had a rare form of the disease that
attacked his eyesight as well as his memory.
As you might imagine, in the past year it has been very
difficult for our family in many ways. Gene can no longer work,
drive a car, or read a newspaper. He has also had to give up
his favorite hobby of woodworking because his doctor has told
him it is not safe to use power tools.
Gene is on one of the newer Alzheimer's medicines, which
helps maintain his moods and his functions. His doctor
evaluates him every 6 months, but we are putting a lot of miles
on our car as we must travel 2\1/2\ hours to Iowa City for
every appointment. There are no doctors in our local community
specializing in Alzheimer's.
I have had to switch jobs, dealing with unsympathetic
employers who would not grant my repeated requests for time off
to take Gene to multiple appointments in Iowa City. I was lucky
enough to find a job closer to home at a manufacturing plant.
My employer is very accommodating and sympathetic and I
currently work the third shift from 8:30 p.m. to 6:30 a.m.,
which allows me to be home with Gene during the day and help my
son with his homework after school and also fix dinner for my
guys before going off to work.
While the disease has been very difficult on Gene and me,
it has been especially difficult for our son, Kris. He is 11
years old and seeing his father struggle to do many things that
other dads do is very tough.
Gene and I learned a great deal about Alzheimer's. I know
the scientists are studying the genetic aspects and that is why
we have chosen to advocate for increased research funding, in
hopes that a cure or a prevention can be found soon to save our
son from this dreadful disease.
We also want to let people know that Alzheimer's is not
just for seniors, it is for younger people, too.
I would like to thank you very much for giving me the
opportunity to be here today and I commend you for everything
you have done to help the Alzheimer's research and funding.
Thank you very much.
I would like to introduce my husband, Gene, to say a few
words.
Senator Harkin. Thank you, Carol.
Gene.
STATEMENT OF GENE GRATZ, NEW HAMPTON, IA, EAST CENTRAL
IOWA CHAPTER, ALZHEIMER'S ASSOCIATION
Mr. Gratz. Senators Harkin and Specter, I am very, very
happy and really feel privileged to be here. My eyesight, like
Carol says, is not real good. I had to make kind of a scribbly-
scratch notepad. She did a pad for me on a tape recorder, but
it is kind of hard to listen to that too and still talk to
everybody.
But the worst thing, I guess, in this whole deal: I lost my
oldest boy, 18 years old, in a car accident, and now I am going
to lose my son, Kris, to Alzheimer's, and I am the one that has
got it. He is going to be without a father eventually.
Hopefully it is not going to be soon. The doctors tell me it is
going to be a long time down the road.
But we need the funding. We need that extra funding to get
this thing killed and get it dead. That is the only reason I
came here.
The paperwork that I was given, I really cannot remember
most of it. But I can tell you that I raise a few small
animals, about all I can do anymore. I have got a new Dodge
pickup sitting in the garage that I cannot drive. And my son
wants to drive already, but good old Marty, our sheriff in
town, he says I cannot teach him out in the field. But Kris
wants to know how.
PREPARED STATEMENT
But anyway, it makes life miserable. I was extremely
independent all my life. I ran major businesses. And to have it
happen to me like this--it came from my father and my
grandfather. We have got to stop it in this generation, have
got to stop it. I do not care what it costs. We have got to get
the funding in some way, shape, or form to get this disease
killed.
Thank you very much, gentlemen. I wish I could be of more
assistance, but I did my best I could do. Thank you.
[The combined statement follows:]
Prepared Statement of Carol and Gene Gratz
Mr. Chairman and members of the Subcommittee: Thank you very much
for giving me the opportunity to testify this morning. I am truly
honored to be here, representing my home state of Iowa and the East
Central Iowa Chapter of the Alzheimer's Association.
My name is Carol Gratz and I am here today with my husband, Gene
and our 11-year old son Kris, who is sitting right behind me. We have
traveled to Washington from New Hampton, Iowa, a rural community of
approximately 3,800 people, to ask you to please do everything you can
to increase funding for Alzheimer research so that a cure or prevention
can be found as soon as possible. Our plea for increased research
funding is extremely personal because 10 months ago, at the age of 57,
Gene was diagnosed with Alzheimer's disease.
The symptoms of Gene's disease actually started appearing about 5
years ago. When Gene was 53, he began having some problems with his
short-term memory and his vision. He complained of not being able to
see very well and was having great difficulty dialing the telephone and
reading the newspaper. Gene went to the eye doctor, who did not find
any explanation for the vision problems.
Since the eye doctor could find no explanation for Gene's vision
problems we did not pursue the issue. Gene continued to experience
difficulties with his vision and memory for another two years but he
rarely complained, so I was not fully aware of the extent of his
problems. He was also having trouble driving and decided that he could
no longer endure the daily two-hour commute to his job as a forklift
operator at a John Deere warehouse. He found a new job as a produce
manager at a small grocery store much closer to our home, and we
thought that would solve all of his problems. Gene lasted about a year
at his new job but the amount of paperwork he was required to do
combined with the frequent inventory reports caused him a lot of stress
due to his continuing vision problems.
In January 2000, Gene left the small grocery store and took a job
on the assembly line at a plant that manufactures horse trailers and
trailers for NASCAR races. Since the assembly line work involved
repetitive tasks and did not require reading or writing, Gene was able
to handle the job. Gene was doing well until April 2001 when a slowdown
in assembly line work forced him to switch jobs in the plant. In his
new assignment, Gene was required to read blueprints, which was
impossible for him to do with his poor vision. Gene told his supervisor
that he was having trouble reading the blueprints and his supervisor
suggested that he visit a doctor for a check-up.
By this time, I knew that Gene's vision and short-term memory
problems were not normal and with my daughter's help, began researching
his symptoms on the Internet. Our search led us to the Alzheimer's
Association website and we contacted our local chapter. The people at
the East Central Iowa chapter were extremely helpful and sent us an
information packet as well as a list of doctors in our community. We
went to a general practitioner, a neurologist and a neuropsychologist.
We were also referred to the University of Iowa hospitals for
additional testing. Finally, in June 2001, we got the terrible news
that Gene had Alzheimer's disease. We were also told that Gene had a
very rare form of the disease that was attacking his eyesight as well
as his memory.
As you might imagine, this past year has been very difficult for
our family in many ways. Gene can no longer work, drive a car or read
the newspaper. He has also had to give up his favorite hobby of
woodworking because his doctor told him that it is not safe to use
power tools anymore.
Gene is on one of the newer Alzheimer's drugs which is helping to
maintain his functioning and mood swings. His doctors evaluate him
every six months but we are putting a lot of miles on our car because
we must travel two and a half hours to Iowa City for every appointment.
There are no doctors in our rural community who specialize in treating
Alzheimer's.
I have had to switch jobs and deal with an unsympathetic employer
who would not grant my repeated requests for time off to take Gene to
his multiple appointments in Iowa City. I was lucky enough to find
another job, closer to home, at an employee-owned manufacturing plant.
My new employer has been very accommodating and sympathetic. I
currently work the third shift, from 8:30 p.m. until 6:30 a.m., which
allows me to be home with Gene during the day, help Kris with his
homework after school and fix dinner for ``my guys'' before going off
to work. This schedule also gives me piece of mind since Gene and Kris
are generally sleeping during the hours that I am at work and I don't
have to worry about their safety.
While this disease has been hard on both Gene and me it has been
especially difficult for our son Kris. He is only 11 years old and
seeing his father struggle to do many of the things that other dads do
is very tough. With assistance from the Alzheimer's Association, we
found a counselor who has been working with Kris to help him cope with
the changes we've experienced due to Gene's diagnosis.
Gene and I have learned a great deal about Alzheimer's and we know
that scientists are actively studying the genetic aspects of the
disease. We worry that Kris is at risk and we've chosen to advocate for
increased research funding in the hope that a cure or prevention will
be found and our son will be spared from this dreaded disease. We have
also decided to speak out about Alzheimer's to let everyone know that
it is not just older people who suffer from the disease. Younger people
get it too and the impact of Alzheimer's is especially painful when it
strikes early. Alzheimer's has taken so much from our family. It has
robbed Gene of his career and hobbies and has threatened our financial
future. But worst of all, it has stolen Gene's second chance at being a
father. Gene's son from his first marriage was killed in a tragic car
accident a few years before we met so we were thrilled when we learned
that I was pregnant with Kris and that Gene would get another chance at
fatherhood.
In closing, I want to thank you again Senators Harkin and Specter
for giving me the opportunity to share how Alzheimer's disease has
impacted my family. I commend you for all that you have done to
increase research funding and raise awareness about Alzheimer's and am
grateful for your leadership in the U.S. Senate. As you will hear from
the others who are speaking today, scientists are on the verge of
finding ways to prevent and treat Alzheimer's disease and the actions
we take today may save future generations--including my son--from this
devastating illness. Thank you.
Senator Harkin. Thank you both very much.
You said you want to be of more help. What you are doing is
of immense help. We must put a human face on this. Senators,
Congressmen, researchers have to know the human toll that this
is taking. These are not just statistics. They are real people
with real families, working hard, getting hit like this.
The fact that you, Carol--just think about that, everybody.
She works from 8:30 p.m. to 6:30 a.m. every night so she can be
home to get Kris off to school, get him home from school, take
care of Gene during the day. That is the kind of toll it takes
on families. You are a brave woman, and you are a brave man.
Mr. Gratz. She is, she is a fantastic woman, and I thank
God I married her.
Senator Harkin. You are lucky to have her for a wife, I
will tell you that. She is great.
Mr. Gratz. I have got a piece of gold sitting next to me
and I know that.
Senator Harkin. So thank you very much for sharing your
story with us.
Mr. Gratz. Thank you very much.
Senator Harkin. Now we turn to David Hyde Pierce. I did not
know that was his real name. I always thought it was Niles
Crane. So we all know Niles from Frasier. He has won three Emmy
Awards, a Golden Globe Award; obviously, someone that is known
nationally.
He is also a national board member of the Alzheimer's
Association and an extraordinarily committed advocate in the
effort to cure Alzheimer's. Mr. Pierce testified before the
subcommittee last year and, Niles, we certainly welcome you
back again.
STATEMENT OF DAVID HYDE PIERCE, ACTOR
Mr. Pierce. Thank you, Dr. Harkin. I appreciate that.
Senator Harkin. The floor is yours. Thanks.
Mr. Pierce. I am very pleased to be back here. Thank you
for inviting me back to testify.
My grandfather, my father, and, I recently found out, one
of my dad's sisters all suffered from Alzheimer's and dementia.
In my written testimony I say that over the years my fears of
Alzheimer's have increased, but I have to tell you, sitting
here today, listening to the breakthroughs in research and the
leadership that people like Orien provide and the incredible
bravery of Gene and Carol and their son, Kris, my fears have
evaporated and they are replaced by hope and determination.
We are so close to catastrophe and we are so close to a
cure. That is why I am here urging you, in spite of the
enormous challenges you face today, to maintain your commitment
to medical research for Alzheimer's and as soon as possible to
increase funding to a billion dollars a year.
Today the Alzheimer's Association is releasing a national
survey by Peter D. Hart Research Associates regarding
Americans' feelings about Alzheimer's disease. The survey
confirms what I have seen every day, that Americans of every
age are terrified by the threat of Alzheimer's disease and that
they overwhelmingly support the shared efforts of this
committee and the Alzheimer's Association to increase funding.
I am going to give you just some of the results. Ninety-
five percent of Americans believe that Alzheimer's disease is a
serious concern for this country. Senators Harkin and Specter,
you have led this Congress in the effort to double funding for
the NIH. The survey shows that Americans support the work. In
fact, in this election year these voters say medical research
is one of the most important areas for Federal spending,
ranking second only to education and ranking above military
spending.
Three-quarters of Americans specifically support the
proposal to increase funding to $1 billion a year. Here is the
amazing thing: 77 percent of people 65 and older support that,
which you would expect, but 75 percent of Americans 18 to 34
also support this increase in funding.
Mr. Chairman, members of the committee, we understand that
the world has changed since we were all here last year, and we
understand that because of that there are many competing
priorities before this subcommittee. But one of the lessons
that we have learned over the last months is that when
Americans are faced with a real threat and a terrible enemy, we
stand together and we marshall our resources to fight.
For 14 million Americans, Alzheimer's disease is that
threat. Alzheimer's disease is that enemy. The case for
increasing funding to a billion dollars is overwhelming and the
support for increasing funding is overwhelming.
PREPARED STATEMENT
You by convening this hearing demonstrate your own concerns
about this looming crisis and your dedication to preventing it.
I want to thank you on behalf of the Alzheimer's Association,
on behalf of all the families dealing with this disease, on
behalf of everyone in this room, and certainly today in honor
of our dear friend Maureen Reagan, for whom this was her
greatest goal.
Thank you very much.
[The statement follows:]
Prepared Statement of David Hyde Pierce
Mr. Chairman and Members of the Subcommittee, thank you for
inviting me back to testify before your Subcommittee. As you know, I am
a National Board member of the Alzheimer's Association. You have heard
my personal story before. Both my grandfather and my father died of
Alzheimer's disease.
With each year that passes, my fear grows--my fear that the disease
process that destroyed their memories, and ultimately their lives, has
begun developing in my own brain. My fear grows not just for myself,
but also for my generation--the 14 million baby boomers who will get
Alzheimer's disease if we don't find a way to beat this dreadful
disease.
At the same time, my hope grows. Today I testify with more
enthusiasm, more confidence that scientists are on the verge of a
breakthrough. My hope is joined with a sense of urgency. In the quest
to find a breakthrough for Alzheimer's disease, this nation is in a
race against time.
In the midst of the enormous challenges you face, I urge you to
maintain your commitment to medical research funding for Alzheimer's
disease, and increase funding to $1 billion a year as soon as possible.
In this race against time, we can't afford to slip.
Today, the Alzheimer's Association is releasing a national survey
by Peter D. Hart Research Associates regarding Americans' concerns
about Alzheimer's disease. I ask that the survey analysis be submitted
for the record. This survey confirms what I see every day--that
Americans of every age are terrified by the threat of Alzheimer's
disease, and that they overwhelmingly support the shared efforts of
this Subcommittee and the Alzheimer's Association to increase funding
for Alzheimer research to $1 billion annually. I would like to share
just a few of the findings from the survey.
Ninety-five percent of Americans believe that Alzheimer's disease
is a serious problem facing our nation. Perhaps they know as well as we
in this room do--our window of time is very short. Perhaps they know
that this disease can strike anyone, even a President of the United
States.
Senator Harkin and Senator Specter, you have led this Congress in
the effort to double funding for NIH. Our survey shows that Americans
support your work. In fact, in this election year, voters say medical
research is one of the most important areas for federal spending,
ranking second only to education spending, and placing ahead of
spending on the military.
More importantly, however, to those of us who sit before you
today--three fourths of Americans agree with the proposal that Congress
should increase funding for Alzheimer research to $1 billion per year.
There is a broad coalition of voters who unite behind this proposal,
with large majorities of both young (75 percent of 18-34 year olds) and
old (77 percent 65 years old and older) agreeing that funding for
Alzheimer research should be increased.
Half of us in the room already have the time bomb of Alzheimer's
disease ticking away in our brains, each and every day. Congress must
find a way to defuse this bomb, before it destroys our brains and
ultimately our entire selves.
The American people have every right to be afraid of this horrible
disease. By the middle of the century, 14 million of today's baby
boomers will have Alzheimer's disease. For most of them, the process
that will destroy their memories, their lives, and their savings has
already begun.
Mr. Chairman. We know there are many competing priorities before
this Subcommittee, and we understand the fiscal constraints you face as
you balance those priorities. But as we look to the future of the 14
million baby boomers and indeed, the future of each and every American,
the case for $1 billion investment in Alzheimer research is
overwhelming. This hearing demonstrates your own concern about the
looming crisis and your commitment to averting it. On behalf of
everyone in the Alzheimer's Association, for every family dealing with
Alzheimer's disease, and for all of us sitting here before you, thank
you.
Senator Harkin. Thank you very much.
Dr. Hodes, do you want to come back up. We have got an
extra chair there. Just join David there.
I again know he has to leave soon, but I would yield to
Senator Specter for any comments or questions.
Senator Specter. Thank you very much, Mr. Chairman.
I want to thank especially Mr. and Mrs. Gratz for coming in
and providing some real insights for not only this
subcommittee, but really for all America, on the kinds of
difficulties which you have had to face. You are very brave and
I thank you for coming in.
I would like to ask Ms. Reid and Mr. Pierce, with the
family backgrounds that you have and with the obvious
additional risks which you face, Orien, what do you think about
the intensive work being done by NIH to try to prevent the
onset of Alzheimer's?
Ms. Reid. I think NIH has been doing an outstanding job and
I am looking forward. You know, we can invest at the
Association, we already have invested almost $120 million into
research. But we know that the real resources come from NIH.
They are the ones who are going to be able to really jump-start
the effort and continue at the pace that they are continuing at
to find a cure for this disease.
I am absolutely desperate for us to find a way to prevent
this disease.
Senator Specter. Mr. Pierce, how do you look to your
future?
Mr. Pierce. Well, I tell you, what I have noticed, I have
worked for the Association for a few years and I have used this
quote of 14 million in the year 2050 so often I have forgotten
that that 14 million is not going to happen in the year 2050.
It is happening now. I have friends who are beginning to suffer
from this. I look to my brother and my sisters and other
members of my family and I just wonder when.
So I applaud the NIH for its efforts, but I am really
impassioned about doubling our research while there is time.
Senator Specter. Dr. Albert, in your capacity as a
psychiatrist would you care to offer an opinion as to the
desirability of having people at random take a test to find out
what their gene consistency is, the so-called genome, with a
view to seeing if there is some latent problem that a person
may have which could be acted upon in a preventive way? Or does
it open up Pandora's box for too many worries that you cannot
really effectively deal with?
Dr. Albert. As you probably know, there are four genes that
have been identified that are associated with risk for
Alzheimer's disease, and three of them are fortunately
extremely rare. They only affect people who are primarily young
and they occur in families where in every generation multiple
individuals have the disease. These genes are dominant genes,
which means if you carry the mutation you will definitely get
the disease.
For those individuals, genetic testing along with genetic
counseling is often available. It is not discouraged if people
understand the consequence of finding the answer and if the
genetic counselors feel as if it is appropriate to do the
testing.
The other gene that we know about is a gene that increases
risk for Alzheimer's disease late in life. All of us carry some
form of that gene and all that it does in its particular risk
form is to increase the likelihood that you will get it across
your lifetime. That is called the APOE gene and it is the APOE4
form of the gene that increases risk.
There are multiple organizations, health care organizations
throughout the country, that have met and determined that this
sort of genetic testing is not to be recommended because it
does not tell you within a short period of time what is going
to happen to you. In fact, in my own research we have looked at
that gene and we have tried to see whether or not it tells us,
if you have trouble with your memory, whether or not you will
get Alzheimer's disease in 4 or 5 years. It is of no
informative value. It does not help at all.
But in general, people feel that knowing that you have a
slightly increased risk by having genetic testing is not to be
recommended.
Senator Specter. Thank you very much, Dr. Albert, and thank
you all. Senator Harkin has urged me to urge you to get behind
us on this nuclear transplant issue. You ladies and gentlemen
come from all over the country. Our staff can tell you which
Senators need to hear from you. If you are from Tennessee,
illustratively, and you write to your Senators, Dr. Frist for
example, that could be very, very influential. He is the one
physician in the Senate, and he is not alone in needing
counvincing.
We have a very, very tough battle and your lives, the lives
of your loved ones, and the lives of millions of Americans may
need to turn on the availability of nuclear transplants. To
criminalize that kind of medical research and tie the hands of
scientists, will drive many scientists out of the United States
to other countries, will severely impact medical research, and
severely impact the ability of medical research to find a cure
for Alzheimer's.
Thank you very much, Mr. Chairman.
Senator Harkin. Thank you, Senator Specter.
I just wanted to echo what Senator Specter just said. There
is so much confusion out there on this issue. I do not know of
anyone that I have really met, I do not know of anyone on this
committee or in the Senate, that is in favor of human cloning.
We are all opposed to human cloning. That is not somatic cell
nuclear transplantation.
So a number of us have bills in to criminalize, actually
criminalize, and put severe civil penalties on anyone who would
transplant that to a uterus for the purpose of human life. But
to cut off the research for nuclear transplantation and the
great promise that it holds to me is just really
unconscionable, to try to cut that off when so many people are
suffering and this holds such great promise for so many people.
So we are going to have a big debate here in the Senate in
May on this issue, probably before the Memorial Day break. But
I think it is going to be an extremely, extremely close vote.
So we really need your help.
Dr. Hodes, you talked about a study in which scientists
used an immunization strategy to reverse the formation of the
amyloid plaques in mice. I have followed this quite closely and
we really got excited about it because it looked like it might
be a possibility for the development of vaccine for
Alzheimer's.
But then I was surprised when I picked up the paper and
read that the vaccine was permanently shelved after 15 patients
who were taking it developed meningitis. Can you inform us or
enlighten us a little bit about this? What happened? Are we
still looking at a possible vaccine? Just what has happened to
that, because it looked like it was so promising.
Dr. Hodes. Yes, I can relate to you in a limited extent at
least what occurred. I say limited extent because this was a
study that was carried out by a pharmaceutical company, Elan.
NIH was not involved in its support and so I do not have the
level of information that I might otherwise have.
But precisely as you described, on the basis of animal
experimentation, humans were immunized with an amyloid peptide
that was designed to treat the buildup of that protein
abnormally in the brains of individuals with Alzheimer's
disease. In the first phase of the study, a number of
individuals were treated with one immunization to see if any
side effects would appear. In that initial study there were
none.
The study then moved on to a second stage, in which
individuals were immunized multiple times, which was the
process that appeared to be effective in the mouse and animal
models. It was a number of individuals after the second
immunization who developed symptoms consistent with
inflammation of the brain and spinal cord and led to the
cessation of the study.
In answer to your question about what this means for the
future, I think it is important to understand that, although
this is enormously disappointing, that it is not entirely
unexpected nor unusual that the first attempt at a new approach
to treatment is met with the discovery of side effects.
The National Institutes of Health continues to support
basic research looking at alternative strategies that use
immune therapy targeted towards finding something that will be
therapeutic without the unacceptable side effects that occur.
So the very impressive initial scientific discoveries remain
reason for hope. There is continued experimentation to try to
find nontoxic variants of an immunization approach to
Alzheimer's disease, all this at the same time that we examine
the alternatives, other approaches, as many as we can find in
opportunities provided by basic research at multiple levels.
Senator Harkin. So there is under your Institute some
ongoing basic research into immunological approaches, for
example?
Dr. Hodes. Yes, precisely so. In an initiative that was
encouraged by the White House 2 years ago and was funded last
year, there is specifically funding of a large cohort of
investigators who are looking at different aspects of immune
approaches to Alzheimer's disease in animal model systems.
Senator Harkin. These initial studies by Elan--they went
through all the safety tests, so it was pretty shocking that it
turned out like that. Again, you are right, this was not an NIH
thing. This was through a private drug company.
But can you assure me that there are researchers that are
being funded by NIH that are looking at what happened and
perhaps sort of, in my own nonscientific way of saying it,
backing down from that and starting over again with that type
of research on a vaccine?
Dr. Hodes. Certainly attempts to try to----
Senator Harkin. Let me say this. We are trying to find out,
why did it not cause the inflammation in mice? It passed the
safety studies, then, as you mentioned, after multiple
vaccinations resulted in problems. Well, there is something in
there that needs to be looked at. I was just wondering, is NIH
funding any research in the area to find out what might have
gone wrong there?
Dr. Hodes. The NIH is funding research looking at
approaches in animal models to determine which of them might be
more or less prone to the kind of complication that you
mention. Actual studies on the patients who underwent these
clinical trials and who suffered the side effects is being
carried out by Elan and those precise studies on those patients
are not a part of NIH-supported research.
But certainly the efforts to understand what in immune
therapy is likely to cause those side effects and how it can be
avoided is most certainly a part of the ongoing research
supported by NIH.
Dr. Albert. Senator Harkin, if I might just add one brief
word. As Dr. Hodes mentioned, we do not know all the details of
what went on because it was done by the pharmaceutical company.
But the initial safety studies were done with a very small
number of people. I think it was no more than about 30 people
that were in those studies. In the larger trial there were over
300, and that is when you increase the possibility of having
side effects. So I think that is the primary reason why the
side effects were not identified early on; and as Dr. Hodes
said, because they gave multiple injections and it was only
after two or more that people developed side effects.
But there are many reasons to be optimistic, because the
particular strategy that they used included a large portion of
this protein that we know to be important for Alzheimer's
disease. Some people feel, for example, that if they used a
smaller part of the protein it might be just as efficacious and
not harmful.
Senator Harkin. So you think it still holds some promise?
Dr. Albert. Absolutely.
Senator Harkin. And we should continue the research and
development into that.
Dr. Albert, one other aspect of this that is intriguing to
me is this idea of use it or lose it, using your brain. Someone
told me you are working on a book about that right now.
Dr. Albert. That is correct. It is very nice of you to ask.
Senator Harkin. Well, let us talk about this book.
Dr. Albert. It is called ``Keep Your Brain Young.''
Senator Harkin. When can we expect it out?
Dr. Albert. It is actually out right now.
Senator Harkin. Oh, it is?
Dr. Albert. Yes, within the last few weeks.
Senator Harkin. Oh my goodness. Well, I will have to get a
copy of that. What are you advocating?
Dr. Albert. In fact, research has shown over the last
decade or so that it is important to be both physically and
mentally active. It makes sense to us that being mentally
active might be helpful to the brain, form more connections,
but recent research has demonstrated that physical activity
seems to work and interact with mental activity to be
beneficial for the brain.
Basic animal research suggests that that might be because
the brain releases certain kinds of protective factors that
help it respond to injury. There is very recent exciting
research that being physically active in a so-called enriched
environment helps with neurogenesis, the generation of new
nerve cells, particularly in the part of the brain that has to
do with memory.
So there are several avenues that people can take just in
their daily lives to maximize function.
Senator Harkin. In your book are you specific to saying do
certain things? Are there certain types of things?
Dr. Albert. The book is based on scientific evidence and so
we outline a number of things that are available. As Dr. Hodes
mentioned, there are a number of prevention trials that are
ongoing looking at the effects of vitamin E, ibuprofen,
statins, estrogen. We talk about those as well. We talk about
the importance of stress and data on the fact that high levels
of stress hormones in the brain are bad for it.
Senator Harkin. Let me ask another question to anyone here.
Again, there is a lot of talk, I do not know if studies have
been done, or at least preliminary types of things, to indicate
that certain types of vitamins, folic acid, maybe some of the B
vitamins, gingko biloba, others--in fact, before my older
brother passed away a couple of years ago he had been having
some problems with memory, and his doctor actually prescribed
gingko biloba to him to take, which I found interesting. This
would be 3, almost 4 years ago now.
What can you tell us about that? Antioxidants, things like
that, these are things I read about, but is there any basis for
that at all, Dr. Hodes?
Dr. Hodes. I think for each of the agents you have
mentioned--and we can discuss them in more detail--the answer
is yes, there is something to it. Yes, there is a basis for
considering the possibility they will be effective, but for
none of them is there as yet definitive incontrovertible
evidence of effectiveness.
Those are precisely the situations where we think it
important to conduct rigorous clinical trials as expeditiously
as possible. So that currently for vitamin E, for other
antioxidants, for folate, for B12, for gingko biloba, among
other agents, there are prevention trials that are currently in
progress. These are randomized trials in which the individuals
taking the drugs or supplements, the physicians who are taking
care of them, do not know the identity of the drug.
Then over a period of years observations will determine
whether those individuals who did or did not take a particular
agent are more or less likely to develop Alzheimer's disease.
These studies most definitely have the ability to determine
whether there is a significant effect of these agents or not.
We have every reason to hope that one or more of them will be
effective. But at the same time we convey this optimism, it is
important to convey to the public that none of them is yet
proven and none of them can be recommended in the absence of
further scientific evidence.
Senator Harkin. Any other observations on that at all?
Ms. Reid. No, except to tell you that I take them all.
Senator Harkin. Well, I would guess on that side they
cannot harm you.
Dr. Hodes. I guess responsibly it is important to qualify
that last statement, that they cannot harm you. Certainly if
these agents were absolutely without risk it would be hard to
deny the logic that says why not try them. But in fact, even
for the most benign of them, agents such as vitamin E, it has
been shown that at some of the dosage levels that people are
taking that they can interact with other drugs and can
predispose to problems. So that one does have to be quite
cautious.
Senator Harkin. Well, you are right in terms of interaction
with other drugs and stuff. That is why we always say you
should make sure that your health care provider knows all you
are taking and stuff like that, and do the research and do your
own reading on it yourself, and take matters into your own
hands.
But I am not certain, Dr. Hodes, that I would agree fully
with you on that. Certainly anything taken in excess can hurt
you. An aspirin, if you take a bottle, will kill you. People
die every year. We have hundreds of deaths in this country from
aspirin. But to take things like, I do not take gingko, but
vitamin E or folic acid, the B drugs, I think taken in dosages
that have been at least recommended by various studies over the
years, I cannot see how that would ever harm anybody.
Obviously, if you overdosed or something like that on
anything----
Dr. Hodes. I think I agree very much with what you said. It
is important to distinguish between recommendations that are
well-founded on experience or doses of vitamins, including
folate or the B vitamins--quite right, there are
recommendations for daily intake that are consistent with
health and have minimal side effects.
But for some of the agents being recommended, being used by
some for treatment or prevention of Alzheimer's, the evidence
is simply not clearcut, and it is in those cases where the risk
of overdosing, if you will, exists, because what constitutes a
safe or dangerous dose is not as well determined as it is for
some of these other agents.
Senator Harkin. One of the reasons I have been pushing for
years for that National Center on Complementary and Alternative
Medicine to do more research in that area, because the RDA's
that we have today were established--help me out here--60 years
ago, something like that?
Dr. Hodes. Many are quite old, correct.
Senator Harkin. I think they are 60 or 70, something like
that. The recommended daily allowances were set up as the
minimums, as I understand it, to prevent things like vitamin C
deficiencies. They were set up as the bare minimums that you
need.
Other medical researchers over the years have said, well,
that may be fine, but in some of these cases actually boosting
those levels up will help your immunological system.
So I am not certain that just taking RDA's or recommended
daily allowances is effective at all in some of these cases. I
know I will bet you there are millions of people out there
leading healthful lives that take much more than the
recommended daily allowances of a lot of different vitamins,
like E and A and everything else. But again, we need more
research in that area.
Dr. Hodes. That is certainly an area I think where we agree
entirely on that last statement. We in studies such as the
gingko biloba trial are working closely with Steve Strauss and
the National Center for Complementary and Alternative Medicine
to assure that the best kind of science is applied with an open
mind to the efficacy and safety of agents such as this.
Senator Harkin. I might just say, for the benefit of
everyone here, that there is really pretty extensive research
going on through that National Center on gingko biloba. I
assume you work together with them on that, Dr. Hodes. Do you?
Dr. Hodes. We do. That study is being carried out
collaboratively with that center.
Senator Harkin. Very good.
Mr. Pierce, you may have told us last year, but remind us:
How old were your father and grandfather when they were
diagnosed?
Mr. Pierce. We noticed the symptoms in my grandfather in
his mid-eighties. Well, actually in his case the diagnosis was
done on autopsy after he passed away, which was in his early
nineties. My dad was in his late seventies, early eighties. I
actually do not know about his sister, but they were of a
contemporary age, so I imagine it was the same.
Senator Harkin. Is it not true you really cannot diagnose
still today Alzheimer's until you do an autopsy? Is that not
right, Dr. Hodes?
Dr. Hodes. That is true, that is the definitive test. But
the ability to diagnose during life has improved greatly with
more extensive testing of biology function imaging, so that in
the hands of people well versed the accuracy of that diagnosis
can be in the range of 90 percent or more.
Senator Harkin. Getting to the funding level, you mentioned
how many people would be affected in the future and you are
right, that baby boom generation is here now. They are alive
right now.
We have all this talk about what we are going to do to save
the Medicare system because of the onset of the baby boom
generation and people living longer. A lot of people are
scratching their heads on how to fund it.
I saw a figure about a year ago that said that if we could
just delay the onset of Alzheimer's by 5 years, we would have
no problem in Medicare funding. That would decrease the cost of
Medicare so much that we would have no problems. Think what it
would do if we could actually find a cure of Alzheimer's. Then
we really could provide prescription drugs for everyone under
Medicare and things like that.
Eighteen clinical trials, is that what you said, Dr. Hodes?
Dr. Hodes. Correct.
Senator Harkin. Can you give us some idea of some that you
think really are looking good?
Dr. Hodes. We do not have information from them as they are
in progress. The way that these studies are done, because they
are masked or blinded so that individuals do not know what they
are taking, leads to the consequence that in general we do not
know the outcome until a study is over. Now, it is monitored
carefully and confidentially, so that if we should find an
overwhelming positive result or evidence of toxicity, a
negative effect, early, the study would be stopped. But this is
the unusual circumstance. So in general we will not know the
outcome until the studies are terminated and the data analyzed.
Senator Harkin. I am just going to ask a question of
everyone in the audience. How many people here in this audience
today take multi-vitamins on a daily basis and supplement that
with maybe other doses of vitamin E or the B vitamins or
vitamin C or other things like that? I am just curious as to
how many people do that here. How many people here take that on
a daily basis?
[A show of hands.]
Look around, Dr. Hodes. I'd better raise my hand, too,
because I do also.
I think there is a great sense among people that somehow we
know what our bodies are telling us, that we need this, and we
better get the researchers going on this. That is not in your
bailiwick. That is in that other center, NCCAM. That is why I
am trying to push them.
I will close up. Again, talking about the caregiver portion
of this, we cannot lose sight of the fact that as we proceed in
the funding for research that we have to be very cognizant of
support for caregives. The toll that this takes on families is
incredible. The Gratzes, it just tears our hearts out.
I have been blessed in my own family. We have not really
had Alzheimer's in my own family, but we do have very dear and
close friends with this disease. Joann Hutchins, who I have
known all my adult life, is now in a nursing home and does not
recognize her husband. Watching this as a close personal
friend, it is just mind-boggling what this does to families.
My elementary school teacher lived across the street from
me until about 5 years ago. Mary King was wonderful. She
actually got me started in school. She was the first one who
ever read a book to me. All of a sudden, she got hit with
Alzheimer's. It came on really suddenly, like within a year,
and she could not take care of herself, and now she is in a
nursing home. So you see, we just have to make sure we do not
forget about that aspect of it, the caregivers.
To the Gratz family, you are extremely courageous. All I
can say is, Kris, you chose well when you chose these parents,
I can tell you that. They are very brave parents. We need them
to keep telling their story. I know it is tough, but people
have to understand the human dimensions of this. These are not
just statistics on pieces of paper. These are our friends, our
relatives, our loved ones, our family members.
I have found around here that many times the most powerful
way to get to someone here is just to give them that human
story. That is what we need you to do while you are here today
and tomorrow, I do not want to say lobbying, I want to say
educating the Members of Congress. But do not take no for an
answer. Get in to see these people, because obviously we do
what we can here, but we need support--I mean we here on this
committee--we need the support of our fellow Senators.
I will say right here now to all of my friends who are
here, I love you dearly and this is a cause of mine that I took
up a long time ago. I might just say again--I should have said
this when Senator Specter was here. I said when I was chairman
we doubled Alzheimer's funding, when he was chairman he has
doubled it. Well, now it is my turn again, and I intend to do
it again.
But we need the support of our fellow Senators to do this.
I cannot do it by myself and Senator Specter cannot do it by
himself. The two of us working together can do a lot, but we
cannot do everything. We do need a lot of help here and we need
help in the House of Representatives, too. That is why it is so
important what you are doing here.
I just cannot tell each of you how important it is for you
to get to these offices and to talk to people and bring them
the human dimensions of what we are talking about. And yes,
tell them about Medicare, tell them about the impact on the
money. They need to understand that, too.
We will continue to do our job here to support Dr. Hodes
and the National Institute and to support all of NIH here. It
is not just in Dr. Hodes' Institute. There is research that
affects this in just about every Institute, I think, going
throughout the whole spectrum of the Institutes at NIH. Dr.
Hodes has the lead agency, but there are a lot of others that
are out there.
So again, I just want to thank you all for being here.
Orien, thank you very much for your great leadership. You
are a wonderful spokesperson. You get the point across. You
have a great persona. We need people like you to get those
points across. So God bless you and thank you so much.
David, thank you again also. People look to people like
you. You are a well-known person in this country and people
like you. Again, your persona comes across as someone that
people like and they trust. Your words, your leadership, can be
very powerful in moving us here and getting the American people
to understand the dimensions of this. So I congratulate you. I
thank you for the leadership.
To Dr. Albert and to Carol and Gene again, please continue
to tell your story and please continue to get the word out on
what we can do. Hopefully, we are going to have some
breakthroughs here. You are a young man and hopefully pretty
soon we are going to have some breakthroughs here that will
help you out. That is my fervent hope, my wish, and now we have
just got to get the money behind it.
Mr. Gratz. I really appreciate you guys letting us be here.
I guess one thing we have to do with Alzheimer's, when times
are bad you have got to laugh at it a little bit. It makes the
day go better. Sometimes you have got to act a little crazy,
but that is okay, too, because it makes your day go better.
The folks in New Hampton, I want to get them out of their
houses instead of hibernating anymore. I mean, I walk around, I
was kind of pushed aside for quite a while until they finally
realized that I was the sort that was not going to go away.
Senator Harkin. Good for you.
Mr. Gratz. And I will be there until the Lord says it is
time for me to leave.
Senator Harkin. Just remember, you are not alone. You have
got everybody here. You are not alone and we are with you.
CONCLUSION OF HEARING
Thank you all very much for being here, that concludes our
hearing.
[Whereupon, at 10:29 a.m., Tuesday, April 30, the hearing
was concluded, and the subcommittee was recessed, to reconvene
subject to the call of the Chair.]
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