Key result
Targeting cellular senescence with senolytic therapy emerges as a promising strategy for post-stroke secondary neurodegeneration.
Cellular senescence may be a key driver of secondary neurodegeneration following TBI and stroke, presenting a potential therapeutic target for senolytic therapies.
Traumatic brain injury (TBI) and stroke pose major health challenges, impacting millions of individuals globally. Once considered solely acute events, these neurological conditions are now recognized as enduring pathological processes with long-term consequences, including an increased susceptibility to neurodegeneration. However, effective strategies to counteract their devastating consequences are still lacking. Cellular senescence, marked by irreversible cell-cycle arrest, is emerging as a crucial factor in various neurodegenerative diseases. Recent research further reveals that cellular senescence may be a potential driver for secondary neurodegeneration following brain injury. Herein, we synthesize emerging evidence that TBI and stroke drive the accumulation of senescent cells in the brain. The rationale for targeting senescent cells as a therapeutic approach to combat neurodegeneration following TBI/stroke is outlined. From a translational perspective, we emphasize current knowledge and future directions of senolytic therapy for these neurological conditions.
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Huang et al. (2024) conducted a review in Traumatic brain injury and stroke. Senolytic therapy was evaluated. Cellular senescence is a potential driver for secondary neurodegeneration following traumatic brain injury and stroke, highlighting senolytic therapy as a promising therapeutic approach.
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