Parkinson's, Alzheimer's, and motor neurone diseaseBMJ 1996; 312 doi: https://doi.org/10.1136/bmj.312.7033.724 (Published 23 March 1996) Cite this as: BMJ 1996;312:724
- Yoav Ben-Shlomo,
- Alexander Steven Whitehead,
- George Davey Smith
- Lecturer in clinical epidemiology Department of Epidemiology and Public Health, University College London, London WC1E 6BT
- Professor of medical genetics Department of Genetics, Trinity College, Dublin 2, Ireland
- Professor of clinical epidemiology Department of Social Medicine, University of Bristol, Bristol BS8 2PR
Clinical and pathological overlap may suggest common genetic and environmental factors
The label “neurodegenerative” is often used as an umbrella term for the distinct pathological conditions of Parkinson's, Alzheimer's, and motor neurone disease. However, there has been speculation that all three conditions represent different phenotypic expressions of a common aetiology.1 Calne and colleagues have argued that these diseases are examples of selective, premature decay of functionally related populations of neurones due to interactions between the environment and the aging process.2 Their two component hypothesis postulates that environmental insults, such as infection or neurotoxins, partially deplete selected neuronal populations, and that age related degeneration results in further neuronal loss beyond a threshold necessary for clinical disease. This model argues that age related cell death is a common contributory factor for all three diseases, although there may be specific environmental factors for each condition.
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