ReviewCurrent neurology and neuroscience reports2001
A molecular basis for hereditary motor and sensory neuropathy disorders.
Review in Current neurology and neuroscience reports, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Myelin Pathology: Involvement of Molecular Chaperones and the Promise of Chaperonotherapy.Brain sciences · 2019Article
- The Gdap1 knockout mouse mechanistically links redox control to Charcot-Marie-Tooth disease.Brain : a journal of neurology · 2014Article
- Rapamycin activates autophagy and improves myelination in explant cultures from neuropathic mice.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Conduction block in PMP22 deficiency.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2010Article
- Pharmacological induction of the heat shock response improves myelination in a neuropathic model.Neurobiology of disease · 2008Article
- Myelin protein zero/P0 phosphorylation and function require an adaptor protein linking it to RACK1 and PKC alpha.The Journal of cell biology · 2007Article
- Mutations in the cytoplasmic domain of P0 reveal a role for PKC-mediated phosphorylation in adhesion and myelination.The Journal of cell biology · 2001Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Charcot-Marie-Tooth disease (CMT), or inherited peripheral neuropathies, is one of the most frequent genetically inherited neurologic disorders, with a prevalence of approximately one in 2500 people. CMT is usually inherited in an autosomal dominant fashion, although X-linked and recessive forms of CMT also exist. Over the past several years, considerable progress has been made toward understanding the genetic causes of many of the most frequent forms of CMT, particularly those caused by mutations in Schwann cell genes inducing the demyelinating forms of CMT, also known as CMT1. Because the genetic cause of these disorders is known, it is now possible to study how mutations in genes encoding myelin proteins cause neuropathy. Identifying these mechanisms will be important both for understanding demyelination and for developing future treatments for CMT.
Indexed as
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.