神经退行性变
线粒体
氧化应激
生物
神经科学
β淀粉样蛋白
阿尔茨海默病
淀粉样蛋白(真菌学)
淀粉样前体蛋白
细胞生物学
疾病
医学
病理
生物化学
肽
植物
作者
Luis Ángel Monsalvo-Maraver,Marisol Maya-López,Edgar Rangel‐López,Isaac Túnez,Alexey A. Tinkov,Anatoly V. Skalny,Bertha Beatriz Socarrás Ferrer,Michael Aschner,Abel Santamarı́a
出处
期刊:Cns & Neurological Disorders-drug Targets
[Bentham Science]
日期:2023-08-01
卷期号:22 (7): 1039-1056
被引量:1
标识
DOI:10.2174/1871527321666220616094036
摘要
Abstract: Alzheimer’s disease (AD) is considered the most frequent neurodegenerative disorder worldwide, compromising cognitive function in patients, with an average incidence of 1-3% in the open population. Protein aggregation into amyloidogenic plaques and neurofibrillary tangles, as well as neurodegeneration in the hippocampal and cortical areas, represent the neuropathological hallmarks of this disorder. Mechanisms involved in neurodegeneration include protein misfolding, augmented apoptosis, disrupted molecular signaling pathways and axonal transport, oxidative stress, inflammation, and mitochondrial dysfunction, among others. It is precisely through a disrupted energy metabolism that neural cells trigger toxic mechanisms leading to cell death. In this regard, the study of mitochondrial dynamics constitutes a relevant topic to decipher the role of mitochondrial dysfunction in neurological disorders, especially when considering that amyloid-beta peptides can target mitochondria. Specifically, the amyloid beta (Aβ) peptide, known to accumulate in the brain of AD patients, has been shown to disrupt overall mitochondrial metabolism by impairing energy production, mitochondrial redox activity, and calcium homeostasis, thus highlighting its key role in the AD pathogenesis. In this work, we review and discuss recent evidence supporting the concept that mitochondrial dysfunction mediated by amyloid peptides contributes to the development of AD.
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