ArticleActa neuropathologica communications2022
TMEM106B deficiency impairs cerebellar myelination and synaptic integrity with Purkinje cell loss.
Article in Acta neuropathologica communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 30 citations in OpenAlex.
- TRIM2 E3 ligase substrate discovery reveals zinc-mediated regulation of TMEM106B in the endolysosomal pathway.EMBO reports · 2026Article
- Microglial phagocytosis in Alzheimer disease.Nature reviews. Neurology · 2026Review
- Genetic association analyses of cognitive performance across multi-ancestry older adults: Application of Tobit models.Journal of Alzheimer's disease : JAD · 2025Article
- SARS-CoV-2 spike triggers TLR7-dependent endolysosome dysfunction and senescence in human astrocytes.Journal of neuroinflammation · 2025Article
- The role of endolysosomal progranulin and TMEM106B in neurodegenerative diseases.Molecular neurodegeneration · 2025Review
- Increased TMEM106B levels lead to lysosomal dysfunction which affects synaptic signaling and neuronal health.Molecular neurodegeneration · 2025Article
- TMEM106B deficiency leads to alterations in lipid metabolism and obesity in the TDP-43Communications biology · 2025Article
- TMEM106B Knockdown Exhibits a Neuroprotective Effect in Parkinson's Disease via Decreasing Inflammation and Iron Deposition.Molecular neurobiology · 2025Article
- Loss of TMEM106B exacerbates Tau pathology and neurodegeneration in PS19 mice.Acta neuropathologica · 2024Article
- TMEM106B coding variant is protective and deletion detrimental in a mouse model of tauopathy.Acta neuropathologica · 2024Article
- TMEM106B reduction does not rescue GRN deficiency in iPSC-derived human microglia and mouse models.iScience · 2023Article
- Loss of TMEM106B exacerbates Tau pathology and neurodegeneration in PS19 mice.bioRxiv : the preprint server for biology · 2023Article
- TMEM106B aggregation in neurodegenerative diseases: linking genetics to function.Molecular neurodegeneration · 2023Review
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- AAV-iScience · 2023Article
- Article
- TMEM106B regulates microglial proliferation and survival in response to demyelination.Science advances · 2023Article
- Lack of a protective effect of the Tmem106b "protective SNP" in the Grn knockout mouse model for frontotemporal lobar degeneration.Acta neuropathologica communications · 2023Article
- The TMEM106B T186S coding variant increases neurite arborization and synaptic density in primary hippocampal neurons.Frontiers in neuroscience · 2023Article
- Multi-omic profiling reveals the ataxia protein sacsin is required for integrin trafficking and synaptic organization.Cell reports · 2022Article
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8 authors at 3 institutions in 1 country.
Funding
Abstract
TMEM106B, a type II lysosomal transmembrane protein, has recently been associated with brain aging, hypomyelinating leukodystrophy, frontotemporal lobar degeneration (FTLD) and several other brain disorders. TMEM106B is critical for proper lysosomal function and TMEM106B deficiency leads to myelination defects, FTLD related pathology, and motor coordination deficits in mice. However, the physiological and pathological functions of TMEM106B in the brain are still not well understood. In this study, we investigate the role of TMEM106B in the cerebellum, dysfunction of which has been associated with FTLD and other brain disorders. We found that TMEM106B is ubiquitously expressed in neurons in the cerebellum, with the highest levels in the Purkinje neurons. Aged TMEM106B-deficient mice show significant loss of Purkinje neurons specifically in the anterior lobe of the cerebellum. Increased microglia and astrocyte activation, as well as an accumulation of ubiquitinated proteins, p62 and TDP-43 were also detected in the cerebellum of aged TMEM106B deficient mice. In the young mice, myelination defects and a significant loss of synapses between Purkinje and deep cerebellar nuclei neurons were observed. Interestingly, TMEM106B deficiency causes distinct lysosomal phenotypes in different types of neurons and glia in the cerebellum and frontal cortex. In humans, TMEM106B rs1990622 risk allele (T/T) is associated with increased Purkinje neuron loss. Taken together, our studies support that TMEM106B regulates lysosomal function in a cell-type-specific manner and TMEM106B is critical for maintaining synaptic integrity and neural functions in the cerebellum.
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