{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Lee J"],"funding":["National Research Foundation of Korea (NRF)","NCATS NIH HHS","NIDDK NIH HHS","NIA NIH HHS","U.S. Department of Health &amp; Human Services | NIH | National Institute on Aging","NCI NIH HHS","NINDS NIH HHS","U.S. Department of Health & Human Services | NIH | National Institute on Aging (U.S. National Institute on Aging)","U.S. Department of Health & Human Services | National Institutes of Health (NIH)","National Research Foundation of Korea","U.S. Department of Health &amp; Human Services | National Institutes of Health"],"pagination":["2070-2085"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12532575"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["5(10)"],"pubmed_abstract":["Nicotinamide adenine dinucleotide (NAD<sup>+</sup>) is a critical metabolic co-enzyme implicated in brain aging, and augmenting NAD<sup>+</sup> levels in the aging brain is an attractive therapeutic strategy for neurodegeneration. However, the molecular mechanisms of brain NAD<sup>+</sup> regulation are incompletely understood. In cardiac tissue, the circadian nuclear receptor REV-ERBα has been shown to regulate NAD<sup>+</sup> via control of the NAD<sup>+</sup>-producing enzyme NAMPT. Here we show that REV-ERBα controls brain NAD<sup>+</sup> levels through a distinct pathway involving NFIL3-dependent suppression of the NAD<sup>+</sup>-consuming enzyme CD38, particularly in astrocytes. REV-ERBα deletion does not affect NAMPT expression in the brain and has an opposite effect on NAD<sup>+</"],"journal":["Nature aging"],"pubmed_title":["REV-ERBα regulates brain NAD&lt;sup&gt;+&lt;/sup&gt; levels and tauopathy via an NFIL3-CD38 axis."],"pmcid":["PMC12532575"],"funding_grant_id":["RF1AG061776","RF1 AG062077","R01AG063743","RF1 AG062171","UL1 TR002345","P01 NS084974","RF1AG062077","P30 DK020579","R35NS097273","RF1AG062171","R35 NS097273","R01 DK045586","P30 CA091842","P01NS084974-01","R01DK45586","R21 AG089851","R01 AG063743","RS-2019-NR040055","RF1 AG061776"],"pubmed_authors":["Voorhees JR","Kang R","Burris TP","Lee J","Woodie LN","Park S","Lazar MA","Lananna BV","Musiek ES","Gan L","Goo YA","Zhao G","Saliu IO","Son M","Dimitry JM","Quillin EI"],"additional_accession":[]},"is_claimable":false,"name":"REV-ERBα regulates brain NAD&lt;sup&gt;+&lt;/sup&gt; levels and tauopathy via an NFIL3-CD38 axis.","description":"Nicotinamide adenine dinucleotide (NAD<sup>+</sup>) is a critical metabolic co-enzyme implicated in brain aging, and augmenting NAD<sup>+</sup> levels in the aging brain is an attractive therapeutic strategy for neurodegeneration. However, the molecular mechanisms of brain NAD<sup>+</sup> regulation are incompletely understood. In cardiac tissue, the circadian nuclear receptor REV-ERBα has been shown to regulate NAD<sup>+</sup> via control of the NAD<sup>+</sup>-producing enzyme NAMPT. Here we show that REV-ERBα controls brain NAD<sup>+</sup> levels through a distinct pathway involving NFIL3-dependent suppression of the NAD<sup>+</sup>-consuming enzyme CD38, particularly in astrocytes. REV-ERBα deletion does not affect NAMPT expression in the brain and has an opposite effect on NAD<sup>+</","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Oct","modification":"2026-06-04T14:31:55.589Z","creation":"2026-05-10T03:11:05.403Z"},"accession":"S-EPMC12532575","cross_references":{"pubmed":["40890338"],"doi":["10.1038/s43587-025-00950-x"]}}