Microglial Nrf2 Functions as a Cell-Autonomous Regulator of Neuroinflammation and Trained Immunity in the Aging Brain.

Hallel C Paraiso, Jui-Hung Jimmy Yen, Barbara A Scofield, Ping-Chang Kuo, Fen-Lei Chang, I-Chen Ivorine Yu

Department of Anatomy, Cell Biology, and Physiology, Indiana University School of Medicine, Fort Wayne, Indiana, USA.Department of Anatomy, Cell Biology, and Physiology, Indiana University School of Medicine, Fort Wayne, Indiana, USA. · pubmed

Paper

Abstract

Aging is the primary risk factor for Alzheimer's disease (AD) and related dementias, with chronic neuroinflammation contributing to disease progression. Microglia, the brain's resident immune cells, undergo age-associated changes that disrupt neuroimmune homeostasis and exacerbate neuroinflammation. The transcription factor Nuclear Factor Erythroid 2-Related Factor 2 (Nrf2), a master regulator of cellular stress responses, has an undefined role in microglial aging. We demonstrate that Nrf2 mRNA expression and protein decline in aged microglia, coinciding with increased neuroinflammation and antigen presentation. Global Nrf2-deficient (Nrf2

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Research summary

The paper claims that Nrf2 functions as a cell-autonomous regulator of neuroinflammation in aging microglia. This research is relevant as it explores the role of a specific transcription factor in the aging process and its potential implications for neuroinflammation, which is a significant factor in age-related diseases like Alzheimer's.

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