ArticleJournal of the peripheral nervous system : JPNS2022
SARM1 knockout does not rescue neuromuscular phenotypes in a Charcot-Marie-Tooth disease Type 1A mouse model.
Article in Journal of the peripheral nervous system : JPNS, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Junctions in Jeopardy: the neuromuscular junction is a selective pathological target in Charcot-Marie-Tooth disease.Mammalian genome : official journal of the International Mammalian Genome Society · 2026Review
- Article
- SARM1 Inhibition in Three Mouse Models of Charcot-Marie-Tooth Disease.Journal of the peripheral nervous system : JPNS · 2025Article
- Characterization of a humanized mouse model of Charcot-Marie-Tooth type 1A for the discovery of humanFrontiers in neurology · 2025Article
- hESC- and hiPSC-derived Schwann cells are molecularly comparable and functionally equivalent.iScience · 2024Article
- Axolemmal nanoruptures arising from paranodal membrane injury induce secondary axon degeneration in murine Guillain-Barré syndrome.Journal of the peripheral nervous system : JPNS · 2023Article
- Application Research of Tooth Arrangement Based on Rotation Matrix Calculation and Resistance Detection in Oral.Computational intelligence and neuroscience · 2022Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Charcot-Marie-Tooth disease Type 1A (CMT1A) is caused by duplication of the PMP22 gene and is the most common inherited peripheral neuropathy. Although CMT1A is a dysmyelinating peripheral neuropathy, secondary axon degeneration has been suggested to drive functional deficits in patients. Given that SARM1 knockout is a potent inhibitor of the programmed axon degeneration pathway, we asked whether SARM1 knockout rescues neuromuscular phenotypes in CMT1A model (C3-PMP) mice. CMT1A mice were bred with SARM1 knockout mice to generate CMT1A/SARM1
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Registered trials
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