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Nevertheless, the molecular mechanisms that regulate \u03b1-synuclein aggregation have not yet been identified fully. TMEM106B is a lysosomal transmembrane protein that has been reported to be associated with brain ageing and neurodegenerative diseases, including Parkinson\u2019s disease.<\/jats:p>\n                  <jats:p>Here we show that TMEM106B is reduced in the brains of patients with Parkinson\u2019s disease. Knockout of Tmem106b increases the formation of \u03b1-synuclein aggregates in primary neurons and mouse brains. TMEM106B deficiency results in impaired lysosomal acidification, lipid metabolism disorders and lipid droplet deposition in neurons. Interestingly, lipid droplets promote \u03b1-synuclein aggregation, resulting in the formation of \u03b1-synuclein fibrils with enhanced seeding activity and neurotoxicity in comparison to \u03b1-synuclein fibrils formed in the absence of lipid droplets. TMEM106B deficiency also leads to retardation of \u03b1-synuclein degradation by reducing the enzymatic activity of the lysosomal protease cathepsin D.<\/jats:p>\n                  <jats:p>Taken together, these results indicate that TMEM106B deficiency contributes to Parkinson\u2019s disease pathogenesis by accelerating \u03b1-synuclein aggregation and halting \u03b1-synuclein degradation.<\/jats:p>","DOI":"10.1093\/brain\/awag065","type":"journal-article","created":{"date-parts":[[2026,2,14]],"date-time":"2026-02-14T12:41:31Z","timestamp":1771072891000},"page":"3150-3165","source":"Crossref","is-referenced-by-count":1,"title":["TMEM106B deficiency exacerbates \u03b1-synuclein aggregation in Parkinson\u2019s disease"],"prefix":"10.1093","volume":"149","author":[{"given":"Lanxia","family":"Meng","sequence":"first","affiliation":[{"name":"Department of Neurology, Renmin Hospital of Wuhan University , Wuhan 430060 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