title: The behavioral, pathological and therapeutic features of the senescence-accelerated mouse prone 8 strain as an Alzheimer's disease animal model.
abstract: Alzheimer's disease (AD) is a widespread and devastating progressive neurodegenerative disease. Disease-modifying treatments remain beyond reach, and the etiology of the disease is uncertain. Animal model are essential for identifying disease mechanisms and developing effective therapeutic strategies. Research on AD is currently being carried out in rodent models. The most common transgenic mouse model mimics familial AD, which accounts for a small percentage of cases. The senescence-accelerated mouse prone 8 (SAMP8) strain is a spontaneous animal model of accelerated aging. Many studies indicate that SAMP8 mice harbor the behavioral and histopathological signatures of AD, namely AD-like cognitive and behavioral alterations, neuropathological phenotypes (neuron and dendrite spine loss, spongiosis, gliosis and cholinergic deficits in the forebrain), β-amyloid deposits resembling senile plaques, and aberrant hyperphosphorylation of Tau-like neurofibrillary tangles. SAMP8 mice are useful in the development of novel therapies, and many pharmacological agents and approaches are effective in SAMP8 mice. SAMP8 mice are considered a robust model for exploring the etiopathogenesis of sporadic AD and a plausible experimental model for developing preventative and therapeutic treatments for late-onset/age-related AD, which accounts for the vast majority of cases.
authors.affiliation: Beijing Institute of Pharmacology and Toxicology, Beijing 100850, China.
authors.forename: Xiao-rui
authors.initials: XR
authors.lastname: Cheng
authors.affiliation: Beijing Institute of Pharmacology and Toxicology, Beijing 100850, China. Electronic address: zhouwx@bmi.ac.cn.
authors.forename: Wen-xia
authors.initials: WX
authors.lastname: Zhou
authors.affiliation: Beijing Institute of Pharmacology and Toxicology, Beijing 100850, China. Electronic address: zhangyx@bmi.ac.cn.
authors.forename: Yong-xiang
authors.initials: YX
authors.lastname: Zhang
mesh_terms: D000367:Age Factors; D000375:Aging / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000523:psychology; D000544:Alzheimer Disease / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology / Q000523:psychology / Q000628:therapy; D016229:Amyloid beta-Peptides / Q000378:metabolism; D000818:Animals; D001522:Behavior, Animal; D001921:Brain / Q000378:metabolism / Q000473:pathology* / Q000503:physiopathology; D016922:Cellular Senescence / Q000235:genetics; D003071:Cognition; D004195:Disease Models, Animal; D020022:Genetic Predisposition to Disease; D018782:Maze Learning; D008568:Memory; D051379:Mice; D008817:Mice, Mutant Strains; D009410:Nerve Degeneration; D010641:Phenotype; D010766:Phosphorylation; D058225:Plaque, Amyloid; D011379:Prognosis; D016875:tau Proteins / Q000378:metabolism
chemical_list: D016229:Amyloid beta-Peptides; D016875:tau Proteins
keywords: Alzheimer's disease; Cognition; Learning and memory; Senescence-accelerated mouse prone 8 strain; Tau hyperphosphorylation; β-Amyloid deposit