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New Biochemical Markers in Alzheimer Disease
Arch Neurol. 2001;58:354-356.
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| Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings. |
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THE RECENTLY completed "Decade of the Brain" witnessed fundamental advances
in many areas of basic and clinical neurosciences, but few fields experienced
greater progress than those dealing with Alzheimer disease (AD). Mutations
in the amyloid precursor protein (APP), presenilin 1 (PS1) , and presenilin 2 (PS2) genes that result
in autosomal dominant familial AD were identified in the early part of the
decade.1 These discoveries made possible the
development of transgenic animals,2 which provide
the best available experimental models to study AD neuropathology and therapeutics.
More recently, the enzymes involved in processing APP, ß-secretase, and
probably  -secretase (which may turn out to be PS1), have been identified,
and specific inhibitors of these proteases have been developed and are nearing
or undergoing clinical trials. Furthermore, much has been learned about inflammatory
reactions in brain tissue during the course of AD,3
and both epidemiologic and animal model–based experimental . . . [Full Text of this Article]
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ABSTRACT
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