CHANNEL FORMATION IN PLANAR LIPID BILAYERS BY A NEUROTOXIC FRAGMENT OF THE BETA-AMYLOID PEPTIDE

被引:108
|
作者
MIRZABEKOV, T
LIN, MC
YUAN, WL
MARSHALL, PJ
CARMAN, M
TOMASELLI, K
LIEBERBURG, I
KAGAN, BL
机构
[1] UNIV CALIF LOS ANGELES,INST NEUROPSYCHIAT,DEPT PSYCHIAT & BEHAV SCI,LOS ANGELES,CA 90024
[2] UNIV CALIF LOS ANGELES,BRAIN RES INST,LOS ANGELES,CA 90024
[3] ATHENA NEUROSCI INC,S SAN FRANCISCO,CA 94080
[4] W LOS ANGELES VET AFFAIRS MED CTR,LOS ANGELES,CA 90073
关键词
D O I
10.1006/bbrc.1994.2047
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
Alzheimer's disease (AD) pathology is characterized by plaques, tangles, and neuronal cell loss. The main constituent of plaques is beta-amyloid peptide (A beta), a 39-42 residue peptide which has been linked to disruption of calcium homeostasis and neurotoxicity in vitro. We demonstrate that a neurotoxic fragment of A beta, A beta (25-35) spontaneously inserted into planar lipid membranes to form weakly selective, voltage dependent, ion-permeable channels. We suggest that channel formation may be involved in the pathogenesis of AD and that A beta (25-35) may be the active channel forming segment. (C) 1994 Academic Press, Inc
引用
收藏
页码:1142 / 1148
页数:7
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