The SAMP8 mouse: a model of Alzheimer disease?

被引：76
|
作者：
Morley, JE [1 ]
机构：
[1] St Louis Univ, Dept Geriatr Med, St Louis, MO 63103 USA
[2] St Louis Vet Affairs Med Ctr, GRECC, St Louis, MO 63104 USA
来源：
BIOGERONTOLOGY | 2002年 / 3卷 / 1-2期
关键词：
ss-amyloid; amyloid precursor protein; antisense; cognition; Delta(9) desaturase;
D O I：
10.1023/A:1015207429786
中图分类号：
R592 [老年病学]; C [社会科学总论];
学科分类号：
03 ; 0303 ; 100203 ;
摘要：
The SAMP8 mice develops early abnormalities in learning and memory, These are related to abnormalities in septo-hippocampal function with a decrease in serotonin leading to an increase in GABA and a decrease in acetylcholine. The cognitive defects in these animals are due to overproduction of beta-amyloid and can be reversed by antibodies to beta-amyloid or specific antisense oligonucleotides. The major defect produced by beta-amyloid in these mice appears to be reduction in Delta(9) desaturase activity leading to altered membrane phospholipid content. The SAMP8 mouse appears to be an excellent model to examine the pathophysiology of early defects seen in Alzheimer disease.
引用
收藏
页码：57 / 60
页数：4
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