A New Hypothesis of the Etiology of Amyotrophic Lateral Sclerosis: The DNA Hypothesis

Walter G. Bradley, Frank Krasin

Research output: Contribution to journalArticle

69 Scopus citations

Abstract

Evidence is accumulating that a number of previously unexplained human diseases may arise from a deficiency of DNA repair enzymes. Studies on the motoneurons of patients with amyotrophic lateral sclerosis (ALS), and those of an animal model of motoneuronal degeneration, the wobbler mouse, indicate the presence of major abnormalities of RNA metabolism. We advance the hypothesis that the primary abnormality in ALS is the accumulation of abnormal DNA, which is unable to undertake normal transcription, in motoneurons. This abnormal DNA may arise from a deficiency of an isozyme of one of the DNA repair enzymes.

Original languageEnglish (US)
Pages (from-to)677-680
Number of pages4
JournalArchives of neurology
Volume39
Issue number11
DOIs
StatePublished - Nov 1982
Externally publishedYes

ASJC Scopus subject areas

  • Arts and Humanities (miscellaneous)
  • Clinical Neurology

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