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Alzheimer's, Dementia & Mental Health
Nuclear Medicine Confirms Beta Amyloid Link to
Alzheimer’s, Plus Brain Dysfunction in Senior Citizens
Researchers report Alzheimer’s detection long
before dementia begins
June 4, 2007 – Researchers have found how to use
new technology to clearly link the accumulation of the toxic brain
protein beta-amyloid to Alzheimer's disease. They also say beta amyloids
are associated with brain dysfunction in even normal senior citizens and
the early pathological changes of Alzheimer's disease can be detected
long before the development of dementia.
The research was presented at the 54th Annual
Meeting of the Society of Nuclear Medicine (SNM), the world's largest
society for molecular imaging and nuclear medicine professionals.
"Our findings show that beta-amyloid is associated
with brain dysfunction - even in apparently normal elderly individuals -
providing further evidence that it is likely related to the fundamental
cause of Alzheimer's disease," said Christopher Rowe, director of the
nuclear medicine department and Centre for PET at Austin Hospital in
Melbourne, Victoria, Australia.
Additionally, in using agent PIB (Pittsburgh
Compound B) and positron emission tomography (PET), researchers
"demonstrated that PIB PET is able to detect the early pathological
changes of Alzheimer's disease long before the development of dementia,"
he indicated.
"Trials of anti-amyloid drugs are underway. If
these prove successful, amyloid imaging will have a vital role in
identifying those in need of treatment to prevent the development of
Alzheimer's dementia," added Rowe.
Alzheimer's disease—a progressive, irreversible
brain disorder—is a formidable opponent with no known cause or cure.
More than 4.5 million Americans are thought to have this disease that
attacks and slowly steals the minds of its victims. Alzheimer's impacts
every nation where life expectancy has increased; estimates indicate
that there are now 18 million people worldwide with the disease.
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About Pittsburgh Compound B (PIB)
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June 4, 2007 – Scientists and researchers at the
University of Pittsburgh discovered a new agent, dubbed “Pittsburgh
Compound B,” which allows researchers to visualize for the first time in
living people the brain plaque suspected of causing the memory-stealing
disease, according to a story in the January 2005 issue of UPMC Health
Journal.
Previously, the presence of plaque could be confirmed only
during autopsy.
Pittsburgh Compound B (PIB) binds to the abnormal
amyloid plaque in the brain. When imaged with a PET scan, PIB shows
researchers actual pathological changes in the brain that could turn out
to be the best and earliest signs of the disease.
It may be possible
that these changes could be detected as many as 10 years before patients
experience serious memory loss.
The groundbreaking discovery by University of
Pittsburgh researchers Chester Mathis, PhD, and
William Klunk, MD, PhD, is being watched with great interest. Along
with Drs. Klunk and Mathis, researchers like
Steven DeKosky, MD, director of the Alzheimer Disease Research
Center at UPMC, are currently collaborating with investigators around
the world to further study PIB and other compounds, as well as potential
new treatments for Alzheimer’s.
>>
Read more of this story, click here.
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One of the hallmarks of the always-fatal disease is
the accumulation of protein amyloid plaques between nerve cells in the
brain. Beta-amyloid is a protein fragment that normally is broken down
and eliminated in a healthy brain. With Alzheimer's, these fragments
form hard, insoluble plaques.
Prior to the development of PIB and use of PET
imaging, the presence of plaque could be confirmed only during autopsy.
"Buildup of beta-amyloid in the brain is thought to
be the underlying cause of Alzheimer's disease. Extensive deposits of
beta-amyloid are found throughout the brains of all patients with
Alzheimer's disease," said Rowe.
Researchers at Austin Health's Centre for PET
studied more than 150 subjects with PIB PET and a detailed battery of
psychometric tests of memory and other brain functions.
PET is a highly specialized, noninvasive imaging
technique that uses short-lived radioactive substances to produce
three-dimensional images of those substances functioning within the
body. "We found that apparently normal elderly subjects with positive
PIB PET scans do have mild—but significant—reduction in memory test
scores, and this is related to the amount of amyloid present," explained
Rowe.
He said that "excess" beta-amyloid is likely
related to the fundamental cause of Alzheimer's disease, probably
preceding cognitive decline by up to 10 years. Besides providing an
accurate diagnosis of early Alzheimer's disease, this research is
helpful in providing the possibility of early diagnosis and intervention
for individuals who are minimally impaired, subject selection for
anti-beta-amyloid clinical trials and monitoring of the effectiveness of
anti-beta-amyloid treatments, said Rowe.
"Additionally, 20 percent of the normal volunteers
in our study whose average age was 72 had a positive scan.
In subjects with mild cognitive impairment (MCI)—a
condition that leads to Alzheimer's dementia in about 60 percent of
cases—we found positive scans in 60 percent of the subjects.
The amount of amyloid present, measured by the PIB
scan, related to the severity of memory impairment in these subjects,"
said Rowe.
"Importantly, we and other researchers using PIB
PET have also observed that by the time dementia has developed—and a
diagnosis of Alzheimer's disease can be made by a clinician—the decline
in cognitive function then continues without a further increase in
amyloid, highlighting the need for early intervention and prevention of
dementia," he added.
"Long-term follow-up of our subjects is underway to
more conclusively show that our asymptomatic individuals and MCI
subjects with positive PIB scans have the early 'preclinical' stages of
Alzheimer's disease," noted Rowe.
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Scientific Paper 193: C.C. Rowe, S. Ng, W. Browne,
U. Ackermann, S. Gong, G. Chan, G. O'Keefe, H. Tochon-Danguy, V.L.
Villemagne, Centre for PET, Austin Hospital, Melbourne, Victoria,
Australia; K. Pike, G. Savage, School of Psychology, Psychiatry and
Psychological Medicine, Monash University, Melbourne, Victoria,
Australia; C.L. Masters, Pathology, University of Melbourne, Melbourne,
Victoria, Australia, "Aâ Burden Correlates With Memory Impairment in
Non-demented Subjects but Plateaus in Established Alzheimer's Disease: A
PIB-PET Cross-Sectional Study," SNM's 54th Annual Meeting, June 2–6,
2007.
About SNM—Advancing Molecular Imaging and Therapy
SNM is holding its 54th Annual Meeting June 2–6 at
the Washington Convention Center in Washington, D.C. Session topics for
the 2007 meeting include brain amyloid imaging, hybrid imaging,
molecular imaging in clinical drug development and evaluation,
functional brain imaging in epilepsy and dementia, imaging
instrumentation, infection imaging, lymphoma and thyroid cancer, cardiac
molecular imaging, general nuclear medicine, critical elements of care
in radiopharmacy and more.
SNM is an international scientific and professional
organization of more than 16,000 members dedicated to promoting the
science, technology and practical applications of molecular and nuclear
imaging to diagnose, manage and treat diseases in women, men and
children. Founded more than 50 years ago, SNM continues to provide
essential resources for health care practitioners and patients; publish
the most prominent peer-reviewed journal in the field (the Journal of
Nuclear Medicine); host the premier annual meeting for medical imaging;
sponsor research grants, fellowships and awards; and train physicians,
technologists, scientists, physicists, chemists and radiopharmacists in
state-of-the-art imaging procedures and advances. SNM members have
introduced—and continue to explore—biological and technological
innovations in medicine that noninvasively investigate the molecular
basis of diseases, benefiting countless generations of patients. SNM is
based in Reston, Va.; additional information can be found online at
http://www.snm.org.
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