Age-related defects in lifespan and learning ability in SAMP8 mice

被引：117

作者：

Nomura, Y ^{[1
]}

Okuma, Y ^{[1
]}

机构：

[1] Hokkaido Univ, Grad Sch Pharmaceut Sci, Dept Pharmacol, Sapporo, Hokkaido 0600812, Japan

来源：

NEUROBIOLOGY OF AGING | 1999年 / 20卷 / 02期

关键词：

SAMP8; mice; animal model of dementia; neurochemical parameters; drug action;

D O I：

10.1016/S0197-4580(99)00006-8

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：

Pertinent animal models of age-related learning deficiencies are required to elucidate the mechanism of age-related learning deficiencies and to develop novel therapeutic drugs for age-related diseases such as learning defects. Among many strains of accelerated senescence prone, senescence-accelerated mouse (SAM), SAMP8 mice have age-related defects in learning and cognitive abilities. We review recent findings on alterations in SAMP8 brain in neurochemical parameters related to neurotransmission and synaptic plasticity compared to those in SAMR1 brain as the control. In addition, we report the preventive effects of drugs on learning deficiencices in SAMP8 and discuss the usefulness of SAMP8 as an animal model of age-related learning deficiencies. (C) 1999 Elsevier Science Inc. All rights reserved.

引用

页码：111 / 115

页数：5

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