Cellular senescence as a key contributor to secondary neurodegeneration in traumatic brain injury and stroke

 I'm sure your competent? doctor has been all over this subject for years! NO? So, you don't have a functioning stroke doctor, do you?

Senescence (7 posts to March 2015)

Senolytics (5 posts to March 2015)

senolytic drugs (1 post to July 2021)

Cellular senescence as a key contributor to secondary neurodegeneration in traumatic brain injury and stroke

Zhihai Huang1,2

, Peisheng Xu 3

, David C. Hess1 and Quanguang Zhang

*Correspondence:

Quanguang Zhang

qzhang@augusta.edu

1 Department of Neurology, Medical College of Georgia, Augusta

University, 1120 15th Street, Augusta, GA 30912, USA

2 Department of Pharmacology, Toxicology and Neuroscience, Louisiana

State University Health Sciences Center, 1501 Kings Highway, Shreveport,

LA 71103, USA

3 Department of Drug Discovery and Biomedical Sciences, College

of Pharmacy, University of South Carolina, 715 Sumter, Columbia, SC

29208, USA

Abstract

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.