Neuroinflammaging and the Immune Landscape: The Role of Autophagy and Senescence in Aging Brain

  • Rajesh Tamatta
  • , Varsha Pai
  • , Charu Jaiswal
  • , Ishika Singh
  • , Abhishek Kumar Singh*
  • *Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

15 Citations (Scopus)

Abstract

Neuroinflammation is closely linked to aging, which damages the structure and function of the brain. It is caused by the intricate interactions of immune cells in the aged brain, such as the dysregulated glial cells and the dysfunctional astrocytes. Aging-associated chronic low inflammation, referred to as neuroinflammaging, shows an upregulated proinflammatory response. Autophagy and senescence play crucial roles as moderators of aging and neuroinflammatory responses. The dysregulated neuroimmune system, dystrophic glial cells, and release of proinflammatory factors alter blood-brain barrier, causing a neuroinflammatory landscape. Chronic inflammation combined with deteriorating neurons exacerbate neurological disorders and decline in cognitive function. This review highlights the neuroinflammaging and mechanism associated with immune cells interplay with central nervous system and aging, cellular senescence, and autophagy regulation in the brain's immune system under neuroinflammatory conditions. Moreover, the roles of microglia and peripheral immune cells in the neuroinflammatory process in the aging brain have also been discussed. Determining treatment targets and comprehending mechanisms that influence immune cells in the aged brain is necessary to decrease neuroinflammation.

Original languageEnglish
Article number52
JournalBiogerontology
Volume26
Issue number2
DOIs
Publication statusPublished - 04-2025

All Science Journal Classification (ASJC) codes

  • Ageing
  • Gerontology
  • Geriatrics and Gerontology

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