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23 September 2004
A remarkable rise in life expectancy during the past century
has made Alzheimer's disease (AD) the most common form of
progressive intellectual failure in humans. Patients with
AD lose their most human qualities - reasoning, abstraction,
language and memory. Analyses of the classical brain lesions
that Alois Alzheimer described, the senile (amyloid) plaques,
and the neurofibrillary tangles, preceded and has guided
the search for genetic alterations that could underlie AD.
Four genes have been unequivocally implicated to date in
inherited forms of AD, and mutations or natural variations
in these genes cause excessive accumulation of the amyloid ß-protein and subsequent neuronal degeneration in
brain regions important for memory and cognition. This understanding
of the genotype-to-phenotype conversions of familial AD,
coupled with cell culture and animal models of the process,
has led to the development of specific pharmacological strategies
to lower amyloid ß-protein levels as a way of treating
or preventing all forms of the disease. While hard work
lies ahead, the movement of basic research on AD to the
clinic represents a triumph of reductionist biology applied
to the most complex of all biological systems, the human
cerebral cortex. In addition to leading to new opportunities
for treatment, research on the Alzheimer's Disease is also
providing new insights into one of the great mysteries of
nature: how the functions of our brains constitute our selves.
Keynote Speaker
- Dennis J. Selkoe, M.D., Vincent and Stella Coates Professor of Neurologic Diseases, Harvard Medical School, and Director, Center for Neurologic Diseases, Brigham and Women's Hospital
Respondent
Coverage:
 Listen to Dr. Selkoe
Listen to Dr. Hogue
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