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SARM1 is the central executioner of pathological axon degeneration. Here, we demonstrate functional and mechanistic links among these three pro-degenerative processes. In a neuroinflammatory model of glaucoma, TNF-\u03b1 induces SARM1-dependent axon degeneration, oligodendrocyte loss, and subsequent retinal ganglion cell death. TNF-\u03b1 also triggers SARM1-dependent axon degeneration in sensory neurons via a noncanonical necroptotic signaling mechanism. MLKL is the final executioner of canonical necroptosis; however, in axonal necroptosis, MLKL does not directly trigger degeneration. Instead, MLKL induces loss of the axon survival factors NMNAT2 and STMN2 to activate SARM1 NADase activity, which leads to calcium influx and axon degeneration. Hence, these findings define a specialized form of axonal necroptosis. The demonstration that neuroinflammatory signals and necroptosis can act locally in the axon to stimulate SARM1-dependent axon degeneration identifies a therapeutically targetable mechanism by which neuroinflammation can stimulate axon loss in neurodegenerative disease.<\/jats:p>","DOI":"10.1083\/jcb.201912047","type":"journal-article","created":{"date-parts":[[2020,4,28]],"date-time":"2020-04-28T02:21:51Z","timestamp":1588040511000},"update-policy":"https:\/\/doi.org\/10.1083\/jcb.crossmarkpolicy","source":"Crossref","is-referenced-by-count":140,"title":["SARM1 acts downstream of neuroinflammatory and necroptotic signaling to induce axon degeneration"],"prefix":"10.1083","volume":"219","author":[{"given":"Kwang Woo","family":"Ko","sequence":"first","affiliation":[{"name":"Department of Developmental Biology, Washington University School of Medicine, St. Louis, MO 1"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5477-7689","authenticated-orcid":true,"given":"Jeffrey","family":"Milbrandt","sequence":"additional","affiliation":[{"name":"Department of Genetics, Washington University School of Medicine, St. Louis, MO 2"},{"name":"Needleman Center for Neurometabolism and Axonal Therapeutics, Washington University School of Medicine, St. Louis, MO 3"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7262-0968","authenticated-orcid":true,"given":"Aaron","family":"DiAntonio","sequence":"additional","affiliation":[{"name":"Department of Developmental Biology, Washington University School of Medicine, St. Louis, MO 1"},{"name":"Needleman Center for Neurometabolism and Axonal Therapeutics, Washington University School of Medicine, St. Louis, MO 3"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"291","published-online":{"date-parts":[[2020,7,1]]},"reference":[{"key":"2023072811425456600_bib1","doi-asserted-by":"publisher","first-page":"152","DOI":"10.1016\/j.preteyeres.2011.11.002","article-title":"The molecular basis of retinal ganglion cell death in glaucoma","volume":"31","author":"Almasieh","year":"2012","journal-title":"Prog. 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