Senolytic treatment diminishes microglia and decreases severity of experimental autoimmune encephalomyelitis.

Sienna S Drake, Aliyah Zaman, Christine Gianfelice, Elizabeth M-L Hua, Kali Heale, Elia Afanasiev, Wendy Klement, Jo Anne Stratton, Alexandre Prat, Stephanie Zandee, Alyson E Fournier

Montréal Neurological Institute, McGill University, Montréal, Québec, Canada. · pubmed

Paper

Abstract

The role of senescence in disease contexts is complex, however there is considerable evidence that depletion of senescent cells improves outcomes in a variety of contexts particularly related to aging, cognition, and neurodegeneration. Much research has shown previously that inflammation can promote cellular senescence. Microglia are a central nervous system innate immune cell that undergo senescence with aging and during neurodegeneration. The contribution of senescent microglia to multiple sclerosis, an inflammatory neurodegenerative disease, is not clear, but microglia are strongly implicated in chronic active lesion pathology, tissue injury, and disease progression. Drugs that could specifically eliminate dysregulated microglia in multiple sclerosis are therefore of great interest to the field.

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Research summary

The paper addresses the role of senescent microglia in the context of multiple sclerosis, an age-related neurodegenerative disease. While it explores the potential for senolytic treatment to improve outcomes by targeting senescent cells, the focus remains on treating symptoms of a specific disease rather than addressing the root causes of aging itself. Therefore, while it contributes to the understanding of cellular senescence in neurodegeneration, its impact on the broader field of longevity research is limited.

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