ReviewJournal of anatomy2002
Understanding Schwann cell-neurone interactions: the key to Charcot-Marie-Tooth disease?
Review in Journal of anatomy, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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
8 citing papers in PubMed, 34 citations in OpenAlex.
- Charcot-Marie-Tooth-1A and sciatic nerve crush rat models: insights from proteomics.Neural regeneration research · 2023Article
- Article
- A novel single-point mutation of NEFH and biallelic SACS mutation presenting as intermediate form Charcot-Marie-Tooth: A case report in Vietnam.Surgical neurology international · 2022Article
- Transmembrane protease serine 5: a novel Schwann cell plasma marker for CMT1A.Annals of clinical and translational neurology · 2020Article
- Direct Conversion of Human Fibroblasts into Schwann Cells that Facilitate Regeneration of Injured Peripheral Nerve In Vivo.Stem cells translational medicine · 2017Article
- Morphology of Donor and Recipient Nerves Utilised in Nerve Transfers to Restore Upper Limb Function in Cervical Spinal Cord Injury.Brain sciences · 2016Article
- Regulation of the PMP22 gene through an intronic enhancer.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Charcot-Marie-Tooth disease (CMT) comprises a heterogeneous group of disorders. The most frequent subtype is caused by increased PMP22 gene dosage or missense point mutations affecting the PMP22 gene (CMT type 1A; CMT1A). Animal models in rat and mouse with the corresponding PMP22 alterations are available and mimic many aspects of the human diseases. Detailed examinations of the animal mutants, together with complementary data from patients, point towards altered Schwann cell-neurone interactions as a major underlying mechanism of CMT1A and related hereditary neuropathies. This is evident from the finding that mutated proteins affecting either Schwann cells or neurones have a profound influence on their partner cells. Recently, a number of novel genes causing various forms of CMT have been identified which are expressed either mainly by Schwann cells and/or by the accompanying neurones. These genes can be viewed, in analogy to classic experiments routinely performed in lower vertebrates, as the result of a 'functional screen' revealing crucial players in the interactions between Schwann cells and neurones. Studying how Schwann cell and axon-encoded proteins are functionally interconnected will be an exciting task for the future. It will not only yield insights into the molecular and cellular basis of neuropathies but also provide crucial information about the interplay between Schwann cells and neurones in general.
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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.