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Physiological Reviews, Vol. 81, No. 2, April 2001, pp. 741-766
Copyright ©2001 by the American Physiological Society
Department of Neurology and Program in Neuroscience, Harvard Medical School, and Center for Neurologic Diseases, Brigham and Women's Hospital, Boston, Massachusetts
Selkoe, Dennis J.
Alzheimer's Disease: Genes, Proteins, and Therapy. Physiol. Rev. 81: 741-766, 2001.
Rapid progress in
deciphering the biological mechanism of Alzheimer's disease (AD) has
arisen from the application of molecular and cell biology to this
complex disorder of the limbic and association cortices. In turn, new
insights into fundamental aspects of protein biology have resulted from
research on the disease. This beneficial interplay between basic and
applied cell biology is well illustrated by advances in understanding
the genotype-to-phenotype relationships of familial Alzheimer's
disease. All four genes definitively linked to inherited forms of the
disease to date have been shown to increase the production and/or
deposition of amyloid 
-protein in the brain. In particular, evidence
that the presenilin proteins, mutations in which cause the most
aggressive form of inherited AD, lead to altered intramembranous
cleavage of the -amyloid precursor protein by the protease called
-secretase has spurred progress toward novel therapeutics. The
finding that presenilin itself may be the long-sought
-secretase, coupled with the recent identification of -secretase,
has provided discrete biochemical targets for drug screening and
development. Alternate and novel strategies for inhibiting the early
mechanism of the disease are also emerging. The progress reviewed here,
coupled with better ability to diagnose the disease early, bode well
for the successful development of therapeutic and preventative drugs
for this major public health problem.
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