TY - JOUR
T1 - A New Hypothesis of the Etiology of Amyotrophic Lateral Sclerosis
T2 - The DNA Hypothesis
AU - Bradley, Walter G.
AU - Krasin, Frank
PY - 1982/11
Y1 - 1982/11
N2 - 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.
AB - 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.
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U2 - 10.1001/archneur.1982.00510230003001
DO - 10.1001/archneur.1982.00510230003001
M3 - Article
C2 - 6181766
AN - SCOPUS:0019935965
VL - 39
SP - 677
EP - 680
JO - Archives of Neurology
JF - Archives of Neurology
SN - 0003-9942
IS - 11
ER -
