The Role of a Pathological Interaction between β-amyloid and Mitochondria in the Occurrence and Development of Alzheimer’s Disease

Acta Naturae

article

Natalya S. Nikolaeva¹  Ekaterina Yu. Yandulova¹  Yulia R. Aleksandrova¹  Andrei S. Starikov¹  Margarita E. Neganova¹ 

[1] Federal State Budgetary Institution of Science Institute of Physiologically Active Compounds of the Russian Academy of Sciences

关键词: Alzheimer’s disease;    beta-amyloid;    mitochondria;    MAM;    mitophagy;   

DOI  :  10.32607/actanaturae.11723

学科分类：生物技术

来源: Moskovskii Gosudarstvennyi Universitet im.M.V.Lomonosova/M.V.Lomonosov Moscow State University

【 摘 要 】

Alzheimer’s disease (AD) is one of the most common neurodegenerative diseases in existence. It is characterized by an impaired cognitive function that is due to a progressive loss of neurons in the brain. Extracellular β-amyloid (Aβ) plaques are the main pathological features of the disease. In addition to abnormal protein aggregation, increased mitochondrial fragmentation, altered expression of the genes involved in mitochondrial biogenesis, disruptions in the ER–mitochondria interaction, and mitophagy are observed. Reactive oxygen species are known to affect Aβ expression and aggregation. In turn, oligomeric and aggregated Aβ cause mitochondrial disorders. In this review, we summarize available knowledge about the pathological effects of Aβ on mitochondria and the potential molecular targets associated with proteinopathy and mitochondrial dysfunction for the pharmacological treatment of Alzheimer’s disease.

【 授权许可】

Unknown