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The free radical hypothesis in idiopathic parkinsonism: Evidence against it
Author(s) -
Calne Donald B.
Publication year - 1992
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410320615
Subject(s) - parkinsonism , pathogenesis , argument (complex analysis) , disease , mechanism (biology) , parkinson's disease , radical , psychology , degenerative disease , neuroscience , medicine , immunology , chemistry , pathology , philosophy , epistemology , endocrinology , biochemistry
The free radical hypothesis for the pathogenesis of idiopathic parkinsonism (Parkinson's disease) has many similarities to the argument invoking an autoimmune mechanism. In both cases, cellular and molecular machinery that might be involved in neuronal destruction have been demonstrated. In recent years, the free radical hypothesis has become particularly fashionable; several workers have reported observations which, they infer, support the notion that damage by free radicals is a major factor in the underlying disease process. There is, however, no conclusive evidence that free radicals play a prominent role in the causal chain of events that leads to idiopathic parkinsonism; several findings may be construed as evidence against such a contention.