ArticleActa neuropathologica communications2023
Lack of a protective effect of the Tmem106b "protective SNP" in the Grn knockout mouse model for frontotemporal lobar degeneration.
Article in Acta neuropathologica communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Granulin loss and TMEM106B risk converge on lysosomal C-terminal fragment pathology in frontotemporal dementia.bioRxiv : the preprint server for biology · 2026Article
- The role of endolysosomal progranulin and TMEM106B in neurodegenerative diseases.Molecular neurodegeneration · 2025Review
- Treatment-resistant depression: role of genetic factors in the perspective of clinical stratification and treatment personalisation.Molecular psychiatry · 2025Review
- Two novel variants in GRN: the relevance of CNV analysis and genetic screening in FTLD patients with a negative family history.Journal of neurology · 2024Article
- TMEM106B coding variant is protective and deletion detrimental in a mouse model of tauopathy.Acta neuropathologica · 2024Article
- A 3'UTR Insertion Is a Candidate Causal Variant at theNeurology. Genetics · 2024Article
- Assessing the impact of novel risk loci on Alzheimer's and Parkinson's diseases in a Chinese Han cohort.Frontiers in neurology · 2024Article
- A 3'UTR Insertion Is a Candidate Causal Variant at themedRxiv : the preprint server for health sciences · 2023Article
- TMEM106B aggregation in neurodegenerative diseases: linking genetics to function.Molecular neurodegeneration · 2023Review
- The TMEM106B T186S coding variant increases neurite arborization and synaptic density in primary hippocampal neurons.Frontiers in neuroscience · 2023Article
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genetic variants in TMEM106B are a common risk factor for frontotemporal lobar degeneration and the most important modifier of disease risk in patients with progranulin (GRN) mutations (FTLD-GRN). TMEM106B is encoding a lysosomal transmembrane protein of unknown molecular function. How it mediates its disease-modifying function remains enigmatic. Several TMEM106B single nucleotide polymorphisms (SNPs) are significantly associated with disease risk in FTLD-GRN carriers, of which all except one are within intronic sequences of TMEM106B. Of note, the non-coding SNPs are in high linkage disequilibrium with the coding SNP rs3173615 located in exon six of TMEM106B, resulting in a threonine to serine change at amino acid 185 in the minor allele, which is protective in FTLD-GRN carriers. To investigate the functional consequences of this variant in vivo, we generated and characterized a knockin mouse model harboring the Tmem106b
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