Neurochemistry, Neuropathology, and Heredity in SAMP8: A Mouse Model of Senescence

被引：77

作者：

Tomobe, Koji ^{[2
]}

Nomura, Yasuyuki ^{[1
]}

机构：

[1] Yokohama Coll Pharm, Dept Pharmacotherapeut, Totsuka Ku, Yokohama, Kanagawa 2450066, Japan

[2] Yokohama Coll Pharm, Dept Pathophysiol, Totsuka Ku, Yokohama, Kanagawa 2450066, Japan

来源：

NEUROCHEMICAL RESEARCH | 2009年 / 34卷 / 04期

关键词：

Aging; Alzheimer's disease; Dementia; Genetics; SAM; Spine formation; Mitochondrial dysfunction; Oxidative stress; Estrogen receptor beta; AGE-RELATED-CHANGES; AMYLOID PRECURSOR PROTEIN; ESTROGEN-RECEPTOR-BETA; LONG-TERM POTENTIATION; OXIDATIVE DNA-DAMAGE; RESTRICTION-INDUCED LONGEVITY; ACCELERATED MOUSE; CALORIC RESTRICTION; MITOCHONDRIAL DYSFUNCTION; CREB PHOSPHORYLATION;

D O I：

10.1007/s11064-009-9923-x

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：

The SAMP8 strain spontaneously develops learning and memory deficits with characteristics of aging, and is a good model for studying the mechanism of cognitive dysfunction with age. Oxidative stress occurs systemically in SAMP8 from early on in life and increases with aging. Neuropathological changes such as the deposition of A beta, hyperphosphorylation of tau, impaired development of dendritic spines, and sponge formation, and neurochemical changes were found in the SAMP8 brain. These changes may be partially mediated by oxidative stress. Oxidative damage is a major factor in neurodegenerative disorders and aging. A decline in the respiratory control ratio suggesting mitochondrial dysfunction was found in the brain of SAMP8. The rise in oxidative stress following mitochondrial dysfunction may trigger neuropathological and neurochemical changes, disrupting the development of neural networks in the brain in SAMP8.

引用

页码：660 / 669

页数：10

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