细胞内
体内
细胞生物学
淀粉样蛋白(真菌学)
细胞外
转基因
阿尔茨海默病
生物
转基因小鼠
P3肽
神经科学
疾病
化学
淀粉样前体蛋白
生物化学
医学
病理
遗传学
基因
植物
作者
Lina Ji,Xi Zhao,Wei Lü,Qing Zhang,Hua Zhang
标识
DOI:10.2174/1567205013666160322142226
摘要
Accumulation of intraneuronal amyloid-β peptide (Aβ) appears to be an early event in Alzheimer's disease (AD), suggesting its important role in the neurodegenerative process of AD. It is indicated that intracellular Aβ originates from a portion of Aβ, which is not secreted and consequently remains intracellular, or alternatively from the secreted Aβ, which is internalized into intracellular Aβ pool. A number of cell and transgenic animal models are established to study the pathological role of intracellular Aβ, and to screen for drugs against Aβ aggregation and associated toxicity. Aβ aggregates, particularly oligomers, may lead to synaptic dysfunction and neuronal loss. Screened from high-throughput methods, a number of cellpermeable agents reduce the aggregation of intracellular Aβ and antagonize its cytotoxicity by inhibiting the formation of Aβ oligomers in vivo. The multi-functional roles of Aβ in alternate pathways and associated clinical implications for AD treatment are also discussed. Keywords: Alzheimer’s disease, aggregation, animal models, cell models, intracellular Aβ, oligomers, neurotoxicity, synaptic dysfunction.
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