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dc.rights.licenseAttribution 4.0 International (CC BY 4.0)
dc.creatorWang, Brian Z.
dc.creatorYang, Jane J.
dc.creatorZhang, Hongxia
dc.creatorSmith, Charity A.
dc.creatorJin, Kunlin
dc.identifier.citationWang, B. Z., Yang, J. J., Zhang, H., Smith, C. A., & Jin, K. (2019). AMPK Signaling Regulates the Age-Related Decline of Hippocampal Neurogenesis. Aging and disease, 10(5), 1058-1074.
dc.description.abstractThe global incidence of age-associated neurological diseases is expected to rise with increasingly greying societies. In the aged brain, there is a dramatic decrease in the number of stem cells, which is a main cause for the decrease in brain function. Intrinsic factors, such as cell metabolism, have been studied but its role in neurogenesis is still unknown. Therefore, this study sought to establish whether AMP-activated protein kinase (AMPK) signaling does indeed regulate hippocampal neurogenesis in the aged brain. We found that i) AMPKalpha2 was the predominant catalytic subunit in the subgranular and subventricular zones; ii) AMPK activation was at a significantly higher level in the aged vs. young hippocampus; iii) short term (7 days) treatment with selective AMPK signaling inhibitor Compound C (10 mg/kg/day, i.p.) significantly increased the numbers of newborn (BrdU(+)), Type 2 (MCM2(+)), and Type 3 (DCX(+)) neural stem cells, but not Type 1 (GFAP(+)/Sox2(+)) cells, in the aged hippocampus. Taken together, our results demonstrate that AMPK signaling plays a critical role in the age-related decline of hippocampal neurogenesis.
dc.description.sponsorshipThis work was supported by the National Institute on Aging (grant numbers: R01 AG021980, T32 AG020494), American Heart Association Predocotoral Fellowship (grant number: 15PRE25700416), and Sigma Xi Grantsin-Aid of Research (grant number: G201503151162287).
dc.publisherJKL International
dc.sourceAging and Disease
dc.subjectCompound C
dc.subjectstem cell
dc.titleAMPK Signaling Regulates the Age-Related Decline of Hippocampal Neurogenesis
dc.rights.holder© 2019 Wang BZ et al.
dc.creator.orcid0000-0002-1336-348X (Jin, Kunlin)
dc.creator.orcid0000-0003-1594-6707 (Zhang, Hongxia)

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Attribution 4.0 International (CC BY 4.0)
Except where otherwise noted, this item's license is described as Attribution 4.0 International (CC BY 4.0)