Amyloid precursor protein secretases as therapeutic targets for traumatic brain injury

被引:202
作者
Loane, David J. [1 ]
Pocivavsek, Ana [1 ]
Moussa, Charbel E-H [1 ]
Thompson, Rachel [1 ]
Matsuoka, Yasuji [2 ]
Faden, Alan I. [1 ]
Rebeck, G. William [1 ]
Burns, Mark P. [1 ]
机构
[1] Georgetown Univ, Med Ctr, Dept Neurosci, Washington, DC 20007 USA
[2] Georgetown Univ, Med Ctr, Dept Neurol, Washington, DC 20007 USA
基金
美国国家卫生研究院;
关键词
LONG-TERM ACCUMULATION; ALZHEIMERS-DISEASE; BETA-SECRETASE; HEAD TRAUMA; PRESENILIN-1; MOUSE; EXPRESSION; DEPOSITION; AXONS; INHIBITORS;
D O I
10.1038/nm.1940
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Amyloid-beta (A beta) peptides, found in Alzheimer's disease brain, accumulate rapidly after traumatic brain injury (TBI) in both humans and animals. Here we show that blocking either beta- or gamma-secretase, enzymes required for production of A beta from amyloid precursor protein (APP), can ameliorate motor and cognitive deficits and reduce cell loss after experimental TBI in mice. Thus, APP secretases are promising targets for treatment of TBI.
引用
收藏
页码:377 / 379
页数:3
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