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We hypothesize that age\u2010dependent impairment of the NAD\n                      <jats:sup>+<\/jats:sup>\n                      \u2013mitophagy axis contributes to brain aging and neurodegeneration.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>METHODS<\/jats:title>\n                    <jats:p>\n                      We analyzed transcriptomic data from 12 human brain regions across 77 integrated public datasets spanning major neurodegenerative diseases and controls to assess NAD\n                      <jats:sup>+<\/jats:sup>\n                      \u2013mitophagy axis alterations, focusing on Alzheimer's disease (AD). Key targets were validated in\n                      <jats:italic>Caenorhabditis elegans<\/jats:italic>\n                      , a human Tau cell model, and induced pluripotent stem cell (iPSC)\u2010derived cortical neurons.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>RESULTS<\/jats:title>\n                    <jats:p>\n                      The NAD\n                      <jats:sup>+<\/jats:sup>\n                      \u2013mitophagy axis is more severely dysregulated in neurodegeneration than in brain aging. Integrating computational and experimental approaches, we identified five AD\u2010protective genes (\n                      <jats:italic>ULK1<\/jats:italic>\n                      ,\n                      <jats:italic>OPA1<\/jats:italic>\n                      ,\n                      <jats:italic>LAMP2<\/jats:italic>\n                      ,\n                      <jats:italic>MFN1<\/jats:italic>\n                      , and\n                      <jats:italic>ATP6V0E1<\/jats:italic>\n                      ) linked to synaptic resilience and\/or reduced Tau pathology.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>DISCUSSION<\/jats:title>\n                    <jats:p>\n                      Our study combines artificial intelligence\u2010driven and experimental approaches to identify novel targets for neurodegeneration, revealing disruption of the NAD\n                      <jats:sup>+<\/jats:sup>\n                      \u2013mitophagy axis as a central player in brain aging and AD.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/alz.71680","type":"journal-article","created":{"date-parts":[[2026,8,21]],"date-time":"2026-08-21T11:01:16Z","timestamp":1787310076000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["A combined artificial intelligence\u2013wet lab approach identifies a pivotal role of the NAD\n                    <sup>+<\/sup>\n                    \u2013mitophagy axis on aging and neurodegeneration"],"prefix":"10.1002","volume":"22","author":[{"given":"Sofie","family":"Lautrup","sequence":"first","affiliation":[{"name":"Department of Clinical Molecular Biology University of Oslo and Akershus University Hospital  L\u00f8renskog Norway"},{"name":"The Norwegian Centre on Healthy Ageing (NO\u2010Age) and the Norwegian National anti\u2010Alzheimer's Disease (NO\u2010AD) Networks  Oslo Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shu\u2010qin","family":"Cao","sequence":"additional","affiliation":[{"name":"Department of Clinical Molecular Biology University of Oslo and Akershus University Hospital  L\u00f8renskog Norway"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xi","family":"Long","sequence":"additional","affiliation":[{"name":"Hong Kong Science and Technology Park Insilico Medicine Hong Kong Ltd.  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