Neuronal C/EBPβ Shortens the Lifespan via Inactivating NAMPT.

Bowei Li, Zhongyun Xie, Mengmeng Wang, Shuke Nie, Zhengjiang Qian, Xin Meng, Xia Liu, Seong Su Kang, Keqiang Ye

Brain Cognition and Brain Disease Institute (BCBDI), Shenzhen Institutes of Advanced Technology (SIAT), Chinese Academy of Sciences, Shenzhen, Guangdong, 518055, China. · pubmed

Paper

Abstract

The brain plays a central role in aging and longevity in diverse model organisms. Morphological and functional alteration in the aging brain elicits age-associated neuronal dysfunctions. However, the primary mechanism deteriorating the brain functions to regulate the aging process remains incompletely understood. Here, it is shown that neuronal CCAAT/enhancer binding protein β (C/EBPβ) escalation during aging dictates the frailty and lifespan via inactivating nicotinamide phosphoribosyltransferase (NAMPT). Upregulated C/EBPβ drives neuronal senescence and neuronal loss, associated with NAMPT fragmentation by active asparagine endopeptidase (AEP), leading to nicotinamide adenine dinucleotide (NAD

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Research summary

The paper claims that neuronal C/EBPβ escalation during aging shortens lifespan by inactivating NAMPT. This research addresses a potential mechanism underlying aging and longevity, focusing on neuronal function and its impact on lifespan, which is central to the study of aging.

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