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A New Hypothesis of the Etiology of Amyotrophic Lateral SclerosisThe DNA Hypothesis
Walter G. Bradley, DM, FRCP;
Frank Krasin, PhD
Arch Neurol. 1982;39(11):677-680.
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.
Author Affiliations
From the Departments of Neurology (Dr Bradley) and Therapeutic Radiology (Dr Krasin), Tufts-New England Medical Center, Boston.
Footnotes
Accepted for publication May 13, 1982.
Read in part before the Muscular Dystrophy Scientific Meeting on the Pathogenesis of Motor Neuron Diseases, Scottsdale, Ariz, June 11, 1981.
Reprint requests to Department of Neurology, University of Vermont College of Medicine, Burlington, VT 05401 (Dr Bradley).
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Arch Neurol 1987;44:579-580.
ABSTRACT
Incorrect Priority Claim for the DNA-Damage Hypothesis-Reply
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Arch Neurol 1987;44:581-583.
ABSTRACT
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