Electronic Resource
Palo Alto, Calif.
:
Annual Reviews
Annual Review of Genomics and Human Genetics
3 (2002), S. 67-99
ISSN:
1527-8204
Source:
Annual Reviews Electronic Back Volume Collection 1932-2001ff
Topics:
Biology
Notes:
Abstract A remarkable rise in life expectancy during the past century has made Alzheimer's disease (AD) the most common form of progressive cognitive failure in humans. Compositional analyses of the classical brain lesions, the senile (amyloid) plaques and neurofibrillary tangles, preceded and has guided the search for genetic alterations. Four genes have been unequivocally implicated in inherited forms of AD, and mutations or polymorphisms in these genes cause excessive cerebral accumulation of the amyloid ss-protein and subsequent neuronal and glial pathology in brain regions important for memory and cognition. This understanding of the genotype-to-phenotype conversions of familial AD has led to the development of pharmacological strategies to lower amyloid ss-protein levels as a way of treating or preventing all forms of the disease.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1146/annurev.genom.3.022502.103022
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