DEPOSITS OF AMYLOID-BETA PROTEIN IN THE CENTRAL-NERVOUS-SYSTEM OF TRANSGENIC MICE

被引：116

作者：

WIRAK, DO ^{[1
]}

BAYNEY, R ^{[1
]}

RAMABHADRAN, TV ^{[1
]}

FRACASSO, RP ^{[1
]}

HART, JT ^{[1
]}

HAUER, PE ^{[1
]}

HSIAU, P ^{[1
]}

PEKAR, SK ^{[1
]}

SCANGOS, GA ^{[1
]}

TRAPP, BD ^{[1
]}

UNTERBECK, AJ ^{[1
]}

机构：

[1] JOHNS HOPKINS UNIV,SCH MED,DEPT NEUROL,BALTIMORE,MD 21205

来源：

SCIENCE | 1991年 / 253卷 / 5017期

关键词：

D O I：

10.1126/science.1857970

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Alzheimer's disease is characterized by widespread deposition of amyloid in the central nervous system. The 4-kilodalton amyloid beta-protein is derived from a larger amyloid precursor protein and forms amyloid deposits in the brain by an unknown pathological mechanism. Except for aged nonhuman primates, there is no animal model for Alzheimer's disease. Transgenic mice expressing amyloid beta-protein in the brain could provide such a model. To investigate this possibility, the 4-kilodalton human amyloid beta-protein was expressed under the control of the promoter of the human amyloid precursor protein in two lines of transgenic mice. Amyloid beta-protein accumulated in the dendrites of some but not all hippocampal neurons in 1-year-old transgenic mice. Aggregates of the amyloid beta-protein formed amyloid-like fibrils that are similar in appearance to those in the brains of patients with Alzheimer's disease.

引用

页码：323 / 325

页数：3

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