
Journal of Neurochemistry, Journal Year: 2025, Volume and Issue: 169(3)
Published: March 1, 2025
Glial cell senescence, characterized by the irreversible arrest of division and a pro-inflammatory secretory phenotype, has emerged as critical player in pathogenesis Alzheimer's disease (ad). While much attention been devoted to role neurons ad, growing evidence suggests that glial cells, including astrocytes, microglia, oligodendrocytes, contribute significantly progression through senescence. In this review, we explore molecular mechanisms underlying senescence focusing on cellular signaling pathways, DNA damage response accumulation senescence-associated phenotypes (SASP). We also examine how senescent cells exacerbate neuroinflammation, disrupt synaptic function, promote neuronal death ad. Moreover, discuss emerging therapeutic strategies aimed at targeting mitigate neurodegenerative processes By providing comprehensive overview current research disease, review highlights its potential novel target fight against
Language: Английский