{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,22]],"date-time":"2026-01-22T23:36:19Z","timestamp":1769124979911,"version":"3.49.0"},"reference-count":57,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2020,11,16]],"date-time":"2020-11-16T00:00:00Z","timestamp":1605484800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"}],"funder":[{"name":"N.I.A."},{"name":"N.I.N.D.S."},{"DOI":"10.13039\/100008590","name":"Falk Medical Research Trust","doi-asserted-by":"crossref","id":[{"id":"10.13039\/100008590","id-type":"DOI","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2021,1,16]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>TMEM106B is a transmembrane protein localized to the endo-lysosomal compartment. Genome-wide association studies have identified TMEM106B as a risk modifier of Alzheimer\u2019s disease and frontotemporal lobar degeneration, especially with progranulin haploinsufficiency. We recently demonstrated that TMEM106B loss rescues progranulin null mouse phenotypes including lysosomal enzyme dysregulation, neurodegeneration and behavioural alterations. However, the reason whether TMEM106B is involved in other neurodegenerative lysosomal diseases is unknown. Here, we evaluate the potential role of TMEM106B in modifying the progression of lysosomal storage disorders using progranulin-independent models of Gaucher disease and neuronal ceroid lipofuscinosis. To study Gaucher disease, we employ a pharmacological approach using the inhibitor conduritol B epoxide in wild-type and hypomorphic Tmem106b\u2212\/\u2212 mice. TMEM106B depletion ameliorates neuronal degeneration and some behavioural abnormalities in the pharmacological model of Gaucher disease, similar to its effect on certain progranulin null phenotypes. In order to examine the role of TMEM106B in neuronal ceroid lipofuscinosis, we crossbred Tmem106b\u2212\/\u2212 mice with Ppt1\u2212\/\u2212, a genetic model of the disease. In contrast to its conduritol B epoxide-rescuing effect, TMEM106B loss exacerbates Purkinje cell degeneration and motor deficits in Ppt1\u2212\/\u2212 mice. Mechanistically, TMEM106B is known to interact with subunits of the vacuolar ATPase and influence lysosomal acidification. In the pharmacological Gaucher disease model, the acidified lysosomal compartment is enhanced and TMEM106B loss rescues in vivo phenotypes. In contrast, gene-edited neuronal loss of Ppt1 causes a reduction in vacuolar ATPase levels and impairment of the acidified lysosomal compartment, and TMEM106B deletion exacerbates the mouse Ppt1\u2212\/\u2212 phenotype. Our findings indicate that TMEM106B differentially modulates the progression of the lysosomal storage disorders Gaucher disease and neuronal ceroid lipofuscinosis. The effect of TMEM106B in neurodegeneration varies depending on vacuolar ATPase state and modulation of lysosomal pH. These data suggest TMEM106B as a target for correcting lysosomal pH alterations, and in particular for therapeutic intervention in Gaucher disease and neuronal ceroid lipofuscinosis.<\/jats:p>","DOI":"10.1093\/braincomms\/fcaa200","type":"journal-article","created":{"date-parts":[[2020,11,16]],"date-time":"2020-11-16T13:51:10Z","timestamp":1605534670000},"source":"Crossref","is-referenced-by-count":12,"title":["Fronto-temporal dementia risk gene <i>TMEM106B<\/i> has opposing effects in different lysosomal storage disorders"],"prefix":"10.1093","volume":"3","author":[{"given":"Azucena","family":"Perez-Canamas","sequence":"first","affiliation":[{"name":"Cellular Neuroscience, Neurodegeneration and Repair Program, Yale University School of Medicine, New Haven, CT, USA"},{"name":"Department of Neurology, Yale University School of Medicine, New Haven, CT, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hideyuki","family":"Takahashi","sequence":"additional","affiliation":[{"name":"Cellular Neuroscience, Neurodegeneration and Repair Program, Yale University School of Medicine, New Haven, CT, USA"},{"name":"Department of Neurology, Yale University School of Medicine, New Haven, CT, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Jane A","family":"Lindborg","sequence":"additional","affiliation":[{"name":"Cellular Neuroscience, Neurodegeneration and Repair Program, Yale University School of Medicine, New Haven, CT, USA"},{"name":"Department of Neurology, Yale University School of Medicine, New Haven, CT, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-8188-3092","authenticated-orcid":false,"given":"Stephen M","family":"Strittmatter","sequence":"additional","affiliation":[{"name":"Cellular Neuroscience, Neurodegeneration and Repair Program, Yale University School of Medicine, New Haven, CT, USA"},{"name":"Department of Neurology, Yale University School of Medicine, New Haven, CT, USA"},{"name":"Department of Neuroscience, Yale University School of Medicine, New Haven, CT, USA"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"286","published-online":{"date-parts":[[2020,11,16]]},"reference":[{"key":"2021032417083297700_fcaa200-B1","doi-asserted-by":"crossref","first-page":"218","DOI":"10.1186\/s40478-019-0872-6","article-title":"Impaired \u03b2-glucocerebrosidase activity and processing in frontotemporal dementia due to progranulin mutations","volume":"7","author":"Arrant","year":"2019","journal-title":"Acta Neuropathol Commun"},{"key":"2021032417083297700_fcaa200-B2","doi-asserted-by":"crossref","first-page":"14612","DOI":"10.1038\/ncomms14612","article-title":"Misrouting of v-ATPase subunit V0a1 dysregulates lysosomal acidification in a neurodegenerative lysosomal storage disease model","volume":"8","author":"Bagh","year":"2017","journal-title":"Nat Commun"},{"key":"2021032417083297700_fcaa200-B3","doi-asserted-by":"crossref","first-page":"36","DOI":"10.1186\/2051-5960-1-36","article-title":"Expression of TMEM106B, the frontotemporal lobar degeneration-associated protein, in normal and diseased human brain","volume":"1","author":"Busch","year":"2013","journal-title":"Acta Neuropathol Commun"},{"key":"2021032417083297700_fcaa200-B4","first-page":"2681","article-title":"Increased expression of the frontotemporal dementia risk factor TMEM106B causes C9orf72-dependent alterations in lysosomes","volume":"25","author":"Busch","year":"2016","journal-title":"Hum Mol Genet"},{"key":"2021032417083297700_fcaa200-B5","doi-asserted-by":"crossref","first-page":"1245","DOI":"10.1016\/j.yexcr.2012.03.005","article-title":"Lysosomal pathways to cell death and their therapeutic applications","volume":"318","author":"\u010cesen","year":"2012","journal-title":"Exp Cell 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