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Scientist Make Important Step in Detecting
Alzheimer's Very Early
Neuroimaging Initiative recruiting people 55 to 90 to
participate in study
Dec. 22, 2005 – As with all diseases, if
Alzheimer's can be detected early there is a better chance of delaying
its damage, and a better opportunity to learn more about its
development. Scientist announced yesterday an "important step" in
finding "biomarkers" for AD that will help detect the disease even
before signs of memory loss appear.
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The researchers at Washington University in St.
Louis, MO, and the University of Pittsburgh combined high-tech brain
imaging with measurement of beta-amyloid protein fragments in
cerebrospinal fluid (CSF).
They found that greater amounts of beta-amyloid
containing plaques in the brain were associated with lower levels of a
specific protein fragment, amyloid-beta 1-42, in CSF.
Prior research indicates that amyloid-beta 1-42 is
central to AD development. The fragment is a major component of amyloid
plaques in the brain, which are believed to influence cell-to-cell
communication and are considered a hallmark of the Alzheimer’s brain.
The study, published online yesterday, by the
Annals of Neurology, is the first to examine the relationship between
levels of amyloid plaque deposits in the brain and different forms of
beta-amyloid in CSF in living humans.
It was supported by the National Institute on Aging
(NIA), a component of the National Institutes of Health (NIH) at the
U.S. Department of Health and Human Services, and by the Washington
University General Clinical Research Center, funded by the NIH.
The method studied might one day help to more
accurately diagnose AD, even before the appearance of cognitive
symptoms, and to monitor disease progression. In the near term, the
findings could be useful in a research context, allowing scientists to
track the effects of potential beta-amyloid lowering treatments in
clinical trials.
“We presently don’t have fully validated imaging or
biomarker measures that can help us monitor the development or
progression of Alzheimer’s in living people,” explains Neil Buckholtz,
Ph.D., chief of the Dementias of Aging Branch at the NIA. “This study
represents one step in the progress being made toward identifying
clinically useful biological measures for AD.”
The research was conducted by Anne M. Fagan, Ph.D.,
and colleagues David M. Holtzman, M.D., Mark A. Mintun, M.D., and John
C. Morris, M.D., of the Alzheimer’s Disease Research Center (ADRC) at
Washington University School of Medicine and used a newly developed
imaging tracer for beta-amyloid from investigators at the ADRC at the
University of Pittsburgh. Both ADRCs are funded by the NIA.
The study included 24 people ages 48 to 83 years
who were cognitively normal or had very mild, mild, or moderate
dementia. The researchers used positron emission tomography (PET), a
brain imaging technique, with a tracing substance called Pittsburgh
Compound B (PIB), to determine the amount of plaques in the
participants’ brains.
PIB travels through the bloodstream into the brain
and then binds to beta-amyloid containing plaques in the brain. PIB
makes it possible to see on PET images any areas of the brain with high
concentrations of plaques.
The researchers also analyzed samples of study
participants’ CSF and blood plasma for levels of specific protein
fragments, including two forms of beta-amyloid and the protein tau.
The seven participants whose PET scans showed PIB
binding — and therefore deposits of beta-amyloid containing plaques in
the brain — had the lowest levels of amyloid-beta 1-42 in their CSF.
Those without PIB binding had the highest levels of
CSF amyloid-beta 1-42. No relationship was seen between PIB binding and
the other CSF or blood-plasma biomarkers studied, including plasma
amyloid-beta 1-42. As shown in previous studies of mice, decreases in
CSF beta-amyloid may result from plaques acting as a “sink,” hindering
movement of soluble beta-amyloid between the brain and CSF, the
researchers hypothesize.
Importantly, three of the participants had normal
cognitive evaluations but had high PIB binding and low CSF amyloid-beta
1-42, suggesting the possibility that this combination of methods may be
useful as “antecedent” biomarkers of AD, identifying the presence of AD
amyloid pathology before the development of cognitive impairments.
Alternatively, if these subjects never develop cognitive decline, it is
possible that plaque number is not always a predictor of the disease.
“Although this study involved a very small sample,
the findings suggest that amyloid imaging and CSF beta-amyloid measures
together may have utility as biomarkers of AD before symptoms develop
and as the disease progresses,” says Fagan.
“These measures hold potential for identifying
individuals with AD pathology before cognitive symptoms, improving the
accuracy of clinical diagnosis of AD and facilitating the testing of
future therapies.”
However, she cautions, “It is important to
recognize that this is still a research study and the findings must be
carefully validated before this approach can be considered for clinical
use.”
The search for biomarkers to detect AD and to
monitor disease progression was accelerated recently when the NIA, in
conjunction with more than a dozen other Federal Government and
private-sector organizations, launched the 5-year, $60 million
Alzheimer’s Disease Neuroimaging Initiative.
The initiative is the most comprehensive effort to
date to study and correlate neuroimaging and fluid biomarkers with the
changes associated with mild cognitive impairment and AD. It will
examine whether serial magnetic resonance imaging (MRI), PET, other
biomarkers, and clinical and neuropsychological assessment can be
combined to assess mild cognitive impairment and early AD progression.
The Neuroimaging Initiative has begun recruiting
people ages 55 to 90 to participate in the study. Participants may
be cognitively normal or have MCI or early AD. Further information about
the study and a list of the 58 local study sites in the U.S. and Canada
may be obtained by calling the NIA’s Alzheimer’s Disease Education and
Referral (ADEAR) Center toll free at 1-800-438-4380 or visiting the ADNI
section of the ADEAR website at
www.alzheimers.org/imagine.
Anyone interested in learning more about enrollment in the project may
contact the study site closest to them. Spanish-language capabilities
are available at some of the study sites.
For information on participation in other AD
clinical trials, visit
http://www.clinicaltrials.gov/
(search for Alzheimer’s disease trials) or the ADEAR Center website at
http://www.alzheimers.org, or
call the ADEAR Center toll free at 1-800-438-4380.
The ADEAR Center is sponsored by the NIA to provide
information to the public and health professionals about AD and
age-related cognitive change and may be contacted at the website and
phone number above for a variety of publications and fact sheets, as
well as information on clinical trials.
The National Institutes of Health (NIH) — The
Nation's Medical Research Agency — includes 27 Institutes and Centers
and is a component of the U. S. Department of Health and Human Services.
It is the primary Federal agency for conducting and supporting basic,
clinical, and translational medical research, and it investigates the
causes, treatments, and cures for both common and rare diseases. For
more information about NIH and its programs, visit
http://www.nih.gov.
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