TY - JOUR
T1 - ALZHEIMER'S DISEASE, PARKINSON'S DISEASE, AND MOTONEURONE DISEASE
T2 - ABIOTROPIC INTERACTION BETWEEN AGEING AND ENVIRONMENT?
AU - Calne, D. B.
AU - Mcgeer, E.
AU - Eisen, A.
AU - Spencer, P.
N1 - Funding Information:
D. B. C., A. E., and E. McG. by the MRC of Canada; P. S. by NIH grant NS 19611 and the Muscular Dystrophy Association of America.
Funding Information:
We thank Dr R. C. Agrawal, Prof K. Ahmad, Dr D. Cohn, Dr M. Das, Dr A. Haque, Dr A. Hirano, Dr S. Huddar, Prof N. Islam, Dr A. Kaul, Dr A. Korcyn, Dr A. M. Md. Hossain, Prof M. A. Mannan, Dr G. D. Mohammad, Dr P. Nunn, and Dr S. P. Singh for their assistance and discussion, Mr R. Robertson and Mrs L. Galietti for technical help, and Mrs V. Palmer for videotaping subjects. We also thank the following institutions for their cooperation-Industrial Toxicology Research Centre, Lucknow, and Occupational Health Centre, Kanpur, India, Institution of Food Sciences, Dhaka, Bangladesh, Postgraduate Medical Research Institute, Dhaka, Bangladesh, Rewa Medical College, Rewa, India, Swedish Free Church Aid Lathyrism Project, Dhaka and Rajshahi, Bangladesh. The work was supported by NIH grant NS 19611 and by grants from the Amyotrophic Lateral Sclerosis Society of America, Ford Foundation, Dhaka, Muscular Dystrophy Foundation, New York, Third World Medical Research Foundation, Inc, New York, Deutsche Forschungsgemeinschaft, FRG, and Fondation pour la Recherche Medicale, France. Correspondence should be addressed to P. S. Neurotoxicology, Albert Einstein College of Medicine, Avenue, Bronx, New York 10461, USA.
Funding Information:
We thank Dr H. Teravainen and Miss J. Calne for helpful discussion. D. B. C. is supported by the Dystonia Medical Research Foundation;
PY - 1986/11/8
Y1 - 1986/11/8
N2 - The hypothesis is that Alzheimer's disease, Parkinson's disease (PD), and motoneurone disease are due to environmental damage to specific regions of the central nervous system and that the damage remains subclinical for several decades but makes those affected especially prone to the consequences of age-related neuronal attrition. This proposal is based on the association between environmental factors and certain neurodegenerative diseases (eg, methylphenyltetrahydropyridine and parkinsonism, poliovirus infection and post-poliomyelitis syndrome, chickling pea ingestion and lathyrism, an unidentified environmental factor and amyotrophic lateral sclerosis-PD complex of Guam, and trauma and pugilist's encephalopathy) and on the long latent period between exposure to environmental factor and the appearance of symptoms in some of these disorders. The practical implications of this hypothesis are that (1) epidemiological attention should be focussed on the environment in early rather than late life, (2) prevention may be a realistic goal if the cause of subclinical damage can be identified, (3) a search should be undertaken for causal mechanisms linking subclinical neuronal damage due to an environmental factor and the normal ageing process, and (4) better understanding of the regional selective vulnerability of the nervous system to the ageing process might allow a rational approach to treatment.
AB - The hypothesis is that Alzheimer's disease, Parkinson's disease (PD), and motoneurone disease are due to environmental damage to specific regions of the central nervous system and that the damage remains subclinical for several decades but makes those affected especially prone to the consequences of age-related neuronal attrition. This proposal is based on the association between environmental factors and certain neurodegenerative diseases (eg, methylphenyltetrahydropyridine and parkinsonism, poliovirus infection and post-poliomyelitis syndrome, chickling pea ingestion and lathyrism, an unidentified environmental factor and amyotrophic lateral sclerosis-PD complex of Guam, and trauma and pugilist's encephalopathy) and on the long latent period between exposure to environmental factor and the appearance of symptoms in some of these disorders. The practical implications of this hypothesis are that (1) epidemiological attention should be focussed on the environment in early rather than late life, (2) prevention may be a realistic goal if the cause of subclinical damage can be identified, (3) a search should be undertaken for causal mechanisms linking subclinical neuronal damage due to an environmental factor and the normal ageing process, and (4) better understanding of the regional selective vulnerability of the nervous system to the ageing process might allow a rational approach to treatment.
UR - http://www.scopus.com/inward/record.url?scp=0022994157&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0022994157&partnerID=8YFLogxK
U2 - 10.1016/S0140-6736(86)90469-1
DO - 10.1016/S0140-6736(86)90469-1
M3 - Article
C2 - 2877227
AN - SCOPUS:0022994157
SN - 0140-6736
VL - 328
SP - 1067
EP - 1070
JO - The Lancet
JF - The Lancet
IS - 8515
ER -