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Alzheimer's, Dementia & Mental Health
New Imaging Method Identifies People-At-Risk for
Alzheimer's Disease
More effective in showing patients with Alzheimer’s
or mild cognitive impairment from normal subjects
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Brain PET scans from a healthy volunteer (top), a
subject with mild cognitive impairment (middle) and a subject with
Alzheimer's disease (bottom). Red and yellow areas show the new chemical
marker FDDNP binding to abnormal brain proteins or "plaques and
tangles." |
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December 21, 2006 - UCLA researchers used
innovative brain scan technology to show that the abnormal brain protein
deposits that define Alzheimer’s disease can be detected in mild
cognitive impairment – a condition that increases the risk for
developing Alzheimer’s disease and affects 15 to 20 million Americans.
The study will be published in the Dec. 21 New England Journal of
Medicine.
Scientists are in the early stages of identifying
biomarkers in the blood and spinal fluid to help with Alzheimer’s
diagnosis, but this new study is the first to report a real time “window
into the brain” that identifies both of the major abnormal deposits of
the disease in living people who may not develop Alzheimer’s for years
to come.
The researchers used positron emission tomography
(PET) imaging with a small molecule invented at UCLA that binds to the
abnormal proteins – amyloid plaques and tangles – that may cause the
disease. Previously only an autopsy could determine these deposits and
confirm a definitive diagnosis.
Study results found that the new method was able to
track disease progression over a two-year period and was more effective
in differentiating patients with Alzheimer’s disease and mild cognitive
impairment from normal study subjects when compared to conventional
imaging techniques. Researchers are working with Siemens Medical to
begin a clinical trial using this new molecular marker in order to
obtain Food and Drug Administration (FDA) approval so that it will be
available in the future for use by physicians with their patients.
“The study suggests that we may now have a new
diagnostic tool for detecting pre-Alzheimer’s conditions to help us
identify those at risk, perhaps years before symptoms become obvious,”
said Dr. Gary Small, Parlow-Solomon Professor on Aging, lead study
author and a professor with the Semel Institute for Neuroscience and
Human Behavior at UCLA. “This imaging technology may also allow us to
test novel drug therapies and manage disease progression over time,
possibly protecting the brain before damage occurs.”
The study included 83 volunteers aged 49 to 84.
Based on cognitive testing, 25 patients had Alzheimer’s disease, 28 had
mild cognitive impairment and 30 were normal controls.
Researchers performed PET brain scans after
intravenously injecting the volunteers with the new chemical marker
called FDDNP, the molecule that binds to the plaque and tangle deposits
found in Alzheimer’s disease.
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Scientists found distinct differences among people
with normal brain aging, patients with Alzheimer’s disease and people
with mild cognitive impairment.
The PET imaging showed that the more advanced the
disease the higher the FDDNP concentration in areas where the abnormal
protein deposits typically accumulate – in the temporal, parietal and
frontal brain regions. Patients with Alzheimer’s disease showed the most
FDDNP binding, indicating a higher level of plaques and tangles than
other subjects.
“We could see the definitive patterns starting
early in patients with mild cognitive impairment and advancing in those
with Alzheimer’s disease,” said Dr. Jorge Barrio, study author and
professor of medical and molecular pharmacology, David Geffen School of
Medicine at UCLA.
All subjects also received a PET brain scan using a
more conventional chemical marker called FDG, which measures the
metabolic function of cells and has previously been used in aiding
diagnosis for Alzheimer’s disease. However, FDG cannot identify the
abnormal brain protein deposits that may cause the disease.
In addition, 72 subjects received magnetic
resonance imaging (MRI) scans which show brain structure and size.
Scientists found that FDDNP-PET differentiated
between study subject groups better than did the FDG-PET combination or
MRI.
“FDDNP yielded excellent diagnostic accuracy and
precisely predicted disease progression and brain pathology
accumulation,” said Barrio. “FDDNP-PET also delivers the promise of new
drug monitoring in human subjects for a more rapid introduction of
therapeutic candidates to control or slow progression of the disease.”
Researchers performed follow-up scans two years
later on 12 research subjects using FDDNP-PET. Patients who grew worse –
declining from normal cognitive function to mild cognitive impairment or
from mild cognitive impairment to Alzheimer’s disease – showed an
increase of FDDNP binding between five and 11 percent compared with
their previous brain scans, suggesting an increase in plaques and
tangles.
A brain autopsy completed on a follow-up
Alzheimer’s patient who died 14 months later showed high plaque and
tangle concentrations in areas that had previously demonstrated high
FDDNP binding values on the PET scan.
“This is the first time this pattern of plaque and
tangle accumulation has been tracked in living humans over time in a
longitudinal study,” said Small.
Editor's Notes:
The study was funded by National Institutes of
Health; the Department of Energy; General Clinical Research Centers
Program; the Rotary CART Fund; the Fran and Ray Stark Foundation Fund
for Alzheimer's Disease Research; the Ahmanson Foundation; the Larry L.
Hillblom Foundation; the Lovelace Foundation; the Judith Olenick Elgart
Fund for Research on Brain Aging; the John D. French Foundation for
Alzheimer’s Research; and the Tamkin Foundation. Department of Energy
funds supported FDDNP synthesis, which was performed at the UCLA
Cyclotron Laboratory under Nagichettiar Satyamurthy’s direction. No
company provided support of any kind for this study.
Other UCLA authors include Vladimir Kepe, Ph.D.;
Linda M. Erocoli, Ph.D.; Prabha Siddarth, Ph.D.; Susan Y. Bookheimer,
Ph.D.; Karen J. Miller, Ph.D.; Dr. Helen Lavretsky; Alison C. Burggren,
Ph.D.; Greg M.Cole, Ph.D.; Dr. Harry V. Vinters; Paul M. Thompson,
Ph.D.; S.C. Huang, Ph.D.; N.Satyamurthy, Ph.D.; Michael E. Phelps,
Ph.D.; and Jorge R. Barrio, Ph.D.
UCLA owns a U.S. patent that uses the approach
outlined in the study that has been licensed to Siemens. Small, Huang,
Cole, Satyamurthy and Barrio are among the inventors, have received
royalties, and will receive royalties on future sales. Small reports
having served as a consultant and/or having received lecture fees from
Abbott, Brainstorming Co., Dakim, Eisai, Forest, Memory Fitness
Institute, Myriad Genetics, Novartis, Ortho-McNeil, Pfizer, Radica and
Siemens. Small also reports having received stock options from Dakim and
having received a grant from GlaxoSmithKline. Kepe reports consulting
fees from Siemens; Lavretsky reports having received lecture fees from
Eisai, Janssen and Pfizer and receiving a grant from Forest. Ercoli
reports having received lecture fees from the Memory Fitness Institute.
Huang reports having received lecture fees from GlaxoSmithKline.
Satyamurthy reports having served as a consultant for PETNet
Pharmaceuticals and Siemens. Dr. Barrio reports having served as a
consultant and having received lecture fees from Nihon Medi-Physics Co,
Bristol-Meyer Squibb, PETNet Pharmaceuticals, and Siemens.
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