AMYLOIDOGENESIS IN ALZHEIMERS-DISEASE - SOME POSSIBLE THERAPEUTIC OPPORTUNITIES

被引：53

作者：

GANDY, S

GREENGARD, P

机构：

[1] The Rockefeller University, b New York, NY 10021

[2] The Rockefeller University, New York, NY 10021

来源：

TRENDS IN PHARMACOLOGICAL SCIENCES | 1992年 / 13卷 / 03期

关键词：

D O I：

10.1016/0165-6147(92)90039-9

中图分类号：

R9 [药学];

学科分类号：

1007 ;

摘要：

Cerebral deposition of fibrils formed from the beta/A4 amyloid protein is an invariable feature of Alzheimer's disease. Evidence suggests that generation of such fibrils may be involved in the etiology of this disease, since mutations in the coding region of the beta/A4 amyloid precursor protein (APP) gene segregate with familial cerebral amyloidoses, including familial Alzheimer's disease. Transgenic models of cerebral amyloidosis have been produced, and some progress has been made in elucidating the cell biology of amyloidogenesis. For example, agents that alter protein phosphorylation are potent modulators of the expression and proteolytic processing of APP. Sam Gandy and Paul Greengard review these recent studies, and discuss those that may provide rational therapeutic opportunities.

引用

页码：108 / 113

页数：6

共 70 条

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