Linked Life Data

9467003

Source:http://linkedlifedata.com/resource/pubmed/id/9467003

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pubmed-article:9467003pubmed:abstractTextCharcot-Marie-Tooth disease type 1A is most commonly caused by a duplication of a 1.5 Mb region of chromosome 17 which includes the peripheral myelin protein 22 gene (PMP22). Over-expression of this gene leads to a hypomyelinating/demyelinating neuropathy and to severely reduced nerve conduction velocity. Previous mouse and rat models have had relatively high levels of expression of the mouse or human PMP22 gene leading to severe demyelination. Here we describe five lines of transgenic mice carrying increasing copies of the human PMP22 gene (one to seven) and expressing increasing levels of the transgene. From histological and electrophysiological observations there appears to be a threshold below which expression of PMP22 has virtually no effect; below a ratio of human/mouse mRNA expression of approximately 0.8, little effect is observed. Between a ratio of 0.8 and 1.5, histological and nerve conduction velocity abnormalities are observed, but there are no behavioural signs of neuropathy. An expression ratio >1.5 leads to a severe neuropathy. A second observation concerns the histology of the different lines; the level of expression does not affect the type of demyelination, but influences the severity of involvement.lld:pubmed
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pubmed-article:9467003pubmed:dateRevised2009-9-29lld:pubmed
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pubmed-article:9467003pubmed:articleTitleCorrelation between varying levels of PMP22 expression and the degree of demyelination and reduction in nerve conduction velocity in transgenic mice.lld:pubmed
pubmed-article:9467003pubmed:affiliationImperial College School of Medicine at St Mary's, London W2 1PG, UK. c.huxley@ic.ac.uklld:pubmed
pubmed-article:9467003pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:9467003pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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