Cellular senescence, neuroinflammation, and microRNAs: Possible interactions driving aging and neurodegeneration in the hippocampal neurogenic niche

IF 2.7 Q3 CLINICAL NEUROLOGY
O. Polzer , E. Kinloch , C.P. Fitzsimons
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Abstract

Cellular senescence influences normal physiology and ageing-related diseases, including neurodegeneration. Senescent cells accumulate with age in the brain, secreting pro-inflammatory factors that promote neuroinflammation, which has been linked to disorders like Alzheimer’s and Parkinson’s. Neurons and other brain cells such as microglia, astrocytes, and neural stem/progenitor cells (NSPCs), exhibit senescence in aged brains. NSPCs, essential for neurogenesis, may enter senescence due to inflammatory signals and other factors and microRNAs may regulate this process. Here we discuss senescence mechanisms, neuroinflammation, and potential therapeutic targets, proposing that modulating senescence by microRNA-mediated pathways could help combat neurodegenerative diseases.
细胞衰老、神经炎症和microrna:海马神经源性生态位中驱动衰老和神经变性的可能相互作用
细胞衰老影响正常生理和衰老相关疾病,包括神经变性。随着年龄的增长,衰老细胞在大脑中积累,分泌促炎因子,促进神经炎症,这与阿尔茨海默氏症和帕金森症等疾病有关。神经元和其他脑细胞,如小胶质细胞、星形胶质细胞和神经干/祖细胞(NSPCs),在衰老的大脑中表现出衰老。NSPCs作为神经发生所必需的细胞,可能会受到炎症信号等因素的影响而进入衰老,而microrna可能调控这一过程。在这里,我们讨论了衰老机制,神经炎症和潜在的治疗靶点,提出通过微rna介导的途径调节衰老可以帮助对抗神经退行性疾病。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Aging brain
Aging brain Neuroscience (General), Geriatrics and Gerontology
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