Molecular Mechanisms of Cellular Senescence in Neurodegenerative Diseases |
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Affiliation: | 1. Department of Anatomy, Konkuk University, Seoul 05029, Republic of Korea;2. IBST, Konkuk University, Seoul 05029, Republic of Korea;3. Department of Biomedical Sciences, Neuroscience Research Institute, Convergence Research Center for Dementia, Seoul National University College of Medicine, Seoul, Republic of Korea;4. Neuramedy, Co., Ltd., Seoul, Republic of Korea |
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Abstract: | Neurodegenerative diseases, such as Alzheimer’s and Parkinson’s, are characterized by several pathological features, including selective neuronal loss, aggregation of specific proteins, and chronic inflammation. Aging is the most critical risk factor of these disorders. However, the mechanism by which aging contributes to the pathogenesis of neurodegenerative diseases is not clearly understood. Cellular senescence is a cell state or fate in response to stimuli. It is typically associated with a series of changes in cellular phenotypes such as abnormal cellular metabolism and proteostasis, reactive oxygen species (ROS) production, and increased secretion of certain molecules via senescence-associated secretory phenotype (SASP). In this review, we discuss how cellular senescence contributes to brain aging and neurodegenerative diseases, and the relationship between protein aggregation and cellular senescence. Finally, we discuss the potential of senescence modifiers and senolytics in the treatment of neurodegenerative diseases. |
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Keywords: | cellular senescence neurodegenerative diseases protein aggregation senolytic therapy senescence-associated secretory phenotype |
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