ArticleFrontiers in neurology2025
Characterization of a humanized mouse model of Charcot-Marie-Tooth type 1A for the discovery of human
Article in Frontiers in neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Peripheral Myelin Protein-22 and Its Prominence in Charcot-Marie-Tooth Disease.Chemical reviews · 2026Review
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Authors and funding
7 authors.
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Abstract
Background and aims: Charcot-Marie-Tooth type 1A (CMT1A) is the most common inherited demyelinating peripheral neuropathy caused by duplication of the peripheral myelin protein 22 ( Methods: Heterozygous (hetero-humanized) and homozygous (homo-humanized) Results: Homo-humanized mice exhibited abnormal mRNA expression of myelin-related genes, slow nerve conduction velocity, reduced compound muscle action potential, demyelinated peripheral nerves, higher levels of plasma neurofilament light chain, muscle weakness and motor/balance disabilities, alterations in electrical impedance myography, and muscle fiber atrophy. In contrast, the hetero-humanized mice did not display any of the previously described impairments. Interpretation: Homo-humanized mice reflect various aspects of CMT1A characteristics in an
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