Fate-mapping and functional dissection reveal perilous influence of type I interferon signaling in mouse brain aging.

ABSTRACT:

Background

Aging significantly elevates the risk of developing neurodegenerative diseases. Neuroinflammation is a universal hallmark of neurodegeneration as well as normal brain aging. Which branches of age-related neuroinflammation, and how they precondition the brain toward pathological progression, remain ill-understood. The presence of elevated type I interferon (IFN-I) has been documented in the aged brain, but its role in promoting degenerative processes, such as the loss of neurons in vulnerable regions, has not been studied in depth.

Methods

To comprehend the scope of IFN-I activity in the aging brain, we surveyed IFN-I-responsive reporter mice at multiple ages. We also examined 5- and 24-month-old mice harboring selective ablation of Ifnar1 in microglia to observe t

SUBMITTER: Roy ER 

PROVIDER: S-EPMC11184889 | biostudies-literature | 2024 Jun

REPOSITORIES: biostudies-literature