Kosyreva Anna Mikhailovna, Sentyabreva Alexandra Vladislavovna, Tsvetkov Ivan Sergeevich, Makarova Olga Vasilievna
Avtsyn Science Research Institute of Human Morphology of FSBI "Petrovsky National Research Centre of Surgery", 117418 Moscow, Russia.
Brain Sci. 2022 Sep 13;12(9):1237. doi: 10.3390/brainsci12091237.
Alzheimer's disease is one of the most common age-related neurodegenerative disorders. The main theory of Alzheimer's disease progress is the amyloid-β cascade hypothesis. However, the initial mechanisms of insoluble forms of amyloid-β formation and hyperphosphorylated tau protein in neurons remain unclear. One of the factors, which might play a key role in senile plaques and tau fibrils generation due to Alzheimer's disease, is inflammaging, i.e., systemic chronic low-grade age-related inflammation. The activation of the proinflammatory cell phenotype is observed during aging, which might be one of the pivotal mechanisms for the development of chronic inflammatory diseases, e.g., atherosclerosis, metabolic syndrome, type 2 diabetes mellitus, and Alzheimer's disease. This review discusses the role of the inflammatory processes in developing neurodegeneration, activated during physiological aging and due to various diseases such as atherosclerosis, obesity, type 2 diabetes mellitus, and depressive disorders.
阿尔茨海默病是最常见的与年龄相关的神经退行性疾病之一。阿尔茨海默病进展的主要理论是淀粉样β级联假说。然而,神经元中不溶性淀粉样β形成和过度磷酸化tau蛋白的初始机制仍不清楚。炎症衰老,即全身性慢性低度与年龄相关的炎症,可能是因阿尔茨海默病在老年斑和tau原纤维生成中起关键作用的因素之一。在衰老过程中观察到促炎细胞表型的激活,这可能是慢性炎症性疾病(如动脉粥样硬化、代谢综合征、2型糖尿病和阿尔茨海默病)发展的关键机制之一。本综述讨论了炎症过程在神经退行性变发展中的作用,这种神经退行性变在生理衰老过程中以及由于各种疾病(如动脉粥样硬化、肥胖、2型糖尿病和抑郁症)而被激活。