β-Hydroxybutyrate alleviates brain aging through the MTA1 pathway in D-galactose injured mice.
Abstract
Aging is an inevitable law of the process of life during which many physiological functions change. Brain aging is an important mechanism in the occurrence and development of degenerative diseases of the central nervous system. β-Hydroxybutyrate (BHBA) is a water-soluble, endogenous small-molecule ketone that can cross the blood-brain barrier and induce neuroprotective effects. This study aimed to investigate the effects of BHBA on D-galactose (D-gal) induced aging in mice and its underlying mechanisms using in vitro and in vivo experiments. These results indicated that D-gal-induced senescence, oxidative stress, and inflammatory responses were inhibited by BHBA, and autophagy was promoted by BHBA. Mechanistically, we explored the role of metastasis-associated antigen-1 (MTA1) in D-gal-induced damaged in HT22 cells using small interfering RNA (siRNA). The results demonstrated that the expression of MTA1 was significantly increased by BHBA, which attenuated D-gal-induced aging, oxidative stress, and inflammatory responses, and promoted autophagy through the upregulation of MTA1. In conclusion, MTA1 may be a novel target for treating aging caused by neurological damage. BHBA improves brain aging by activating the MTA1 pathway.
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Research summary
The paper investigates the effects of β-Hydroxybutyrate on brain aging and its mechanisms, specifically focusing on the MTA1 pathway, which is relevant to understanding and potentially mitigating aspects of aging. However, while it presents interesting findings, the study primarily addresses a specific mechanism rather than providing a broad solution to the root causes of aging. Thus, it contributes solid research but has limited impact on the overall field of longevity research.
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