ReviewFrontiers in cellular neuroscience2026
Cellular senescence in brain aging and neurodegeneration: from molecular mechanisms to translational opportunities.
Review in Frontiers in cellular neuroscience, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Aging remains the predominant risk factor for Alzheimer's disease (AD) and other neurodegenerative disorders, yet the mechanisms linking systemic aging to brain dysfunction remain incompletely understood. Cellular senescence, a state of stable cell-cycle arrest coupled with metabolic and secretory reprogramming, has emerged as a pivotal and context-dependent driver of brain aging. Accumulation of senescent glial cells (astrocytes, microglia, and oligodendrocyte progenitors) and emerging evidence of "neurescence" in post-mitotic neurons contribute to neuroinflammation, impaired proteostasis, and synaptic dysfunction. This review synthesizes molecular, cellular, and translational findings that reframe senescence as an active process shaping brain vulnerability. We discuss SASP-mediated neurotoxicity, crosstalk among senescent glial subtypes, and context-specific pathways (NF-κB, p38 MAPK, mTOR, cGAS-STING) as therapeutic targets. Senomorphic and senolytic strategies, alongside emerging systemic interventions such as therapeutic plasma exchange with albumin replacement, are evaluated for their potential to mitigate senescence burden and restore homeostasis. Integrating evidence from fluid, imaging, and multi-omic biomarkers, we highlight how senescence can now be monitored
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