{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,10]],"date-time":"2026-08-10T15:29:51Z","timestamp":1786375791051,"version":"build-2736575974"},"reference-count":37,"publisher":"American Medical Association (AMA)","issue":"8","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JAMA Neurol"],"published-print":{"date-parts":[[2026,8,1]]},"abstract":"\n Importance<\/jats:title>\n \n TMEM106B<\/jats:italic>\n is a frontotemporal lobar degeneration (FTLD) genetic susceptibility factor, and TMEM106B protein aggregates are a feature of aging and neurodegeneration. Whether TMEM106B protein levels are associated with clinical features is unknown.\n <\/jats:p>\n <\/jats:sec>\n \n Objective<\/jats:title>\n To investigate the clinical associations of cerebrospinal fluid (CSF) TMEM106B in FTLD.<\/jats:p>\n <\/jats:sec>\n \n Design, Setting, and Participants<\/jats:title>\n \n This cross-sectional study was conducted in 2 independent frontotemporal dementia (FTD) cohorts (recruitment from April 2009 through July 2023, with analyses from January 2025 through April 2026), with a 2-year follow up. This multicenter clinical study integrated clinical, genetic, biomarker, and neuroimaging data. Individuals were recruited through the University of California, San Francisco (n\u2009=\u20093733), or ALLFTD (n\u2009=\u20092343). Participants with available CSF were included. A discovery cohort (n\u2009=\u2009271) included participants with sporadic neuropathology-confirmed FTLD; presymptomatic or symptomatic carriers of pathogenic variants in\n C9orf72<\/jats:italic>\n ,\n GRN<\/jats:italic>\n , or\n MAPT<\/jats:italic>\n ; or controls. An independent validation cohort (n\u2009=\u2009383) included participants with clinically diagnosed sporadic FTD, Alzheimer disease (AD), and controls.\n <\/jats:p>\n <\/jats:sec>\n \n Exposures<\/jats:title>\n CSF samples for TMEM106B quantification with aptamer proteomics (SomaScan version 3.0 [discovery cohort] and SomaScan version 4.1 [validation cohort]).<\/jats:p>\n <\/jats:sec>\n \n Main Outcomes and Measures<\/jats:title>\n \n Parametric tests compared the primary outcome, CSF TMEM106B, by disease severity,\n TMEM106B<\/jats:italic>\n rs1990622 genotype, sex, clinical syndrome, pathological diagnosis, and pathogenic variant and determined associations with brain volume.\n <\/jats:p>\n <\/jats:sec>\n \n Results<\/jats:title>\n \n In the discovery (n\u2009=\u2009271; 136 women [51%]; median [IQR] age, 59 [38-80] years) and validation (n\u2009=\u2009383; 183 women [48%]; median [IQR] age, 64 [50-78] years) cohorts, lower CSF TMEM106B was associated with more severe disease (\u03b2, \u22120.15; 95% CI, \u22120.24 to \u22120.04;\n P<\/jats:italic>\n \u2009=\u2009.003), lower frontotemporal brain volumes (\u03b2, 0.42; 95% CI, 0.24-0.61;\n P<\/jats:italic>\n \u2009&amp;lt;\u2009.001), and faster clinical progression (\u03b2, \u22122.21; 95% CI, \u22123.70 to \u22120.72;\n P<\/jats:italic>\n \u2009=\u2009.001). Associations of TMEM106B with clinical disease severity were independent of those with neurofilament light chain. TMEM106B levels were influenced by\n TMEM106B<\/jats:italic>\n rs1990622 genotype, where individuals with the protective G\/G genotype had lower levels than the risk A\/A genotype. CSF TMEM106B levels did not differentiate between FTLD subtypes or between FTLD and AD.\n <\/jats:p>\n <\/jats:sec>\n \n Conclusions and Relevance<\/jats:title>\n \n Per the results of this cross-sectional study, TMEM106B is detectable in CSF and levels reflect disease severity in sporadic and genetic FTLD and AD, but levels are also influenced by the\n TMEM106B<\/jats:italic>\n rs1990622 genotype. CSF TMEM106B could support further studies to understand the mechanisms of disease and develop clinical tools in FTLD and other neurodegenerative diseases.\n <\/jats:p>\n <\/jats:sec>","DOI":"10.1001\/jamaneurol.2026.1927","type":"journal-article","created":{"date-parts":[[2026,6,22]],"date-time":"2026-06-22T15:30:44Z","timestamp":1782142244000},"page":"778","source":"Crossref","is-referenced-by-count":0,"title":["Clinical Associations of Cerebrospinal Fluid TMEM106B in Familial and Sporadic Frontotemporal Dementia"],"prefix":"10.1001","volume":"83","author":[{"given":"Molly","family":"Olzinski","sequence":"first","affiliation":[{"name":"Edward and Pearl Fein Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joshua","family":"Downer","sequence":"additional","affiliation":[{"name":"Edward and Pearl Fein Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yann","family":"Cobigo","sequence":"additional","affiliation":[{"name":"Edward and Pearl Fein Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Binita","family":"Rajbanshi","sequence":"additional","affiliation":[{"name":"Edward and Pearl Fein Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jingyao","family":"Li","sequence":"additional","affiliation":[{"name":"Novartis Institutes for Biomedical Research, Cambridge, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joseph","family":"Loureiro","sequence":"additional","affiliation":[{"name":"Novartis Institutes for Biomedical Research, Cambridge, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kathleen A.","family":"Worringer","sequence":"additional","affiliation":[{"name":"Novartis Institutes for Biomedical Research, Cambridge, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hilary","family":"Heuer","sequence":"additional","affiliation":[{"name":"Edward and Pearl Fein Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter","family":"Ljubenkov","sequence":"additional","affiliation":[{"name":"Edward and Pearl Fein Memory and Aging Center, Department of Neurology, Weill Institute for Neurosciences, University of California, 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