TMEM106B coding variant is protective and deletion detrimental in a mouse model of tauopathy
Author:
Funder
National Institutes of Health
Alzheimer's Association
Publisher
Springer Science and Business Media LLC
Link
https://link.springer.com/content/pdf/10.1007/s00401-024-02701-5.pdf
Reference55 articles.
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3. Briggs DI, Defensor E, Memar Ardestani P, Yi B, Halpain M, Seabrook G et al (2017) Role of endoplasmic reticulum stress in learning and memory Impairment and Alzheimer’s disease-Like neuropathology in the PS19 and APP(Swe) mouse models of tauopathy and amyloidosis. ENeuro. https://doi.org/10.1523/ENEURO.0025-17.2017
4. Brody AH, Nies SH, Guan F, Smith LM, Mukherjee B, Salazar SA et al (2022) Alzheimer risk gene product Pyk2 suppresses tau phosphorylation and phenotypic effects of tauopathy. Mol Neurodegener 17:32. https://doi.org/10.1186/s13024-022-00526-y
5. Cabron AS, Borgmeyer U, Richter J, Peisker H, Gutbrod K, Dormann P et al (2023) Lack of a protective effect of the Tmem106b “protective SNP” in the Grn knockout mouse model for frontotemporal lobar degeneration. Acta Neuropathol Commun 11:21. https://doi.org/10.1186/s40478-023-01510-3
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1. Cleaved TMEM106B forms amyloid aggregates in central and peripheral nervous systems;Acta Neuropathologica Communications;2024-06-17
2. TMEM106B C-terminal fragments aggregate and drive neurodegenerative proteinopathy;2024-06-11
3. Physiological and pathological functions of TMEM106B in neurodegenerative diseases;Cellular and Molecular Life Sciences;2024-05-06
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