Vitamin B12 neuropathy is not due to failure to methylate myelin basic protein

R. Deacon, P. Purkiss, Ralph Green, M. Lumb, J. Perry, I. Chanarin

Research output: Contribution to journalArticlepeer-review

16 Scopus citations

Abstract

It has been proposed that the biochemical lesion in subacute combined degeneration of the cord due to vitamin B12 deficiency, is impaired methylation of residue 107 (arginine) in myelin basic protein. We have examined myelin basic protein in brains of rats in which vitamin B12 was inactivated by exposure to nitrous oxide for up to 7 days. In addition brains of fruit bats in which vitamin B12 neuropathy had been produced by feeding washed, and hence vitamin B12-free fruit, were examined. There was no difference in the methylation of arginine 107 in myelin basic protein in these animals as compared to healthy control animals. Rats given an inhibitor of transmethylation reactions (cycloleucine) showed the expected fall in methylation of myelin basic protein.

Original languageEnglish (US)
Pages (from-to)113-117
Number of pages5
JournalJournal of the Neurological Sciences
Volume72
Issue number1
DOIs
StatePublished - 1986
Externally publishedYes

Keywords

  • Cobalamin neuropathy
  • Cycloleucine
  • Methylation
  • Nitrous oxide

ASJC Scopus subject areas

  • Aging
  • Clinical Neurology
  • Surgery
  • Neuroscience(all)
  • Developmental Neuroscience
  • Neurology

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