The SAMP8 Mouse: A Model to Develop Therapeutic Interventions for Alzheimer's Disease

被引：3
|
作者：
Morley, John E. [1 ,2 ]
Farr, Susan A. [2 ]
Kumar, Vijaya B. [2 ]
Armbrecht, Harvey J. [2 ,3 ]
机构：
[1] St Louis Univ, Sch Med, Div Geriatr Med, St Louis, MO 63104 USA
[2] St Louis VA Med Ctr, GRECC, St Louis, MO USA
[3] St Louis Univ, Dept Biochem & Mol Biol, St Louis, MO 63104 USA
来源：
CURRENT PHARMACEUTICAL DESIGN | 2012年 / 18卷 / 08期
关键词：
Antisense; amyloid-beta; SAMP8; oxidative damage; Alzheimer's; antisense; blood brain barrier; testosterone; SENESCENCE-ACCELERATED MOUSE; BLOOD-BRAIN-BARRIER; AGE-RELATED-CHANGES; AMYLOID PRECURSOR PROTEIN; ALPHA-LIPOIC ACID; A-BETA-REGION; GENE-EXPRESSION; CEREBRAL-CORTEX; ANIMAL-MODEL; MICE SAMP8;
D O I：
暂无
中图分类号：
R9 [药学];
学科分类号：
1007 ;
摘要：
The senescence accelerate mouse P8 (SAMP8) is an excellent model of early learning and memory problems. A number of studies have shown that it has cholinergic deficits, oxidative damage, alterations in membrane lipids and circadian rhythm disturbances. The brains of the SAMP8 overproduce amyloid precursor protein (APP), amyloid-beta protein and have an increased physphorylation of tau. An antisense to APP has been developed that reverses the cognitive deficits and oxidative damage. This antisense represents a potential treatment for Alzheimer's disease.
引用
收藏
页码：1123 / 1130
页数：8
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