Abstract
A working hypothesis of the aetiology of Parkinson’s disease has been postulated (Calne and Langston, 1983). It was proposed that some environmental factor causes selective damage to the nigrostriatal dopaminergic system. When this insult is followed by the gradual age related decline in the population of dopaminergic cells, eventually the system decompensates and clinical parkinsonsism becomes manifest perhaps many years after the initial damage had occurred. This theory recieves support from recent studies of the amyotrophic lateral sclerosis-parkinsonism-dementia complex of Guam and of parkinsonism induced by l-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). The combination of selective environmental damage followed by age related attrition may also be important in the aetiology of Alzheimer’s disease and amyotrophic lateral sclerosis (ALS).
Access this chapter
Tax calculation will be finalised at checkout
Purchases are for personal use only
Preview
Unable to display preview. Download preview PDF.
References
Ambani L, Van Woert M H, Murphy S (1975) Brain peroxidase and catalase in Parkinson disease. Arch Neurol 32: 114–118
Barbeau A (1984) Etiology of Parkinson’s disease: a research strategy. Can J Neurol Sci 11: 24–28
Beale M F, Kowall N W, Ellison D W, Mazurek M F, Swartz K J, Martin J B (1986) Replication of the neurochemical characteristics of Huntington’s disease by quinolinic acid. Nature 321: 168–171
Berheimer H, Birkmayer W, Hornykiewicz O, Jellinger K, Scitelberger F (1973) Brain dopamine and the syndromes of Parkinson and Huntington. J Neurol Sci 20: 415–455
Calne D B, Teravainen H (1979) Parkinsonism: Its relation to aging and its treatment. Interdisciplinary Topics in Gerontology 15: 179
Calne D B, Langston J W (1983) Aetology of Parkinson’s disease. Lancet ii: 1457–1459
Calne D B, Langston J W, Martin W R W, Stoessl A J, Ruth T J, Adam M J, Pate B D, Schulzer M (1985) Positron emission tomography after MPTP: observations relating to the cause of Parkinson’s disease. Nature 317: 246–248
Carlsson A, Winblad B (1976) Influence of age and time interval between death and autopsy on dopamine and 3-methoxytyramine levels in human basal ganglia. J Neural Transm 38: 271–276
Dalakas M C (1986) How relevant are recent studies of ALS and post-polio muscular atrophy patients regarding PET scanning, polio antigen/antibody, and AIDS virus. Muscle and Nerve 9. Suppl 5S: 108
Duvoisin R C (1984) Is Parkinon’s disease acquired or inherited? Can J Neurol Sci 11 (supp): 151–155
Ehringer H, Hörnykiewicz O (1960) Verteilung von noradrenalin und dopamin im Gehirn des Menschen und ihr Verhalten bei Erkrankungen des extrapyramidalen Systems. Wien Klin Wochenchir 72: 1236–1239
Firnau G, Garnett E S, Sourkes T L, Missala K (1975) [18F] Fluoro- Dopa: a unique gamma emmitting substrate for dopa decarboxylase. Experentia 31: 1254–1255
Garnett E S, Firnau G, Nahmias C, Chirakal R (1983) Striatal dopamine metabolism in living monkeys examined by positron emission tomography. Brain Research 180: 169–171
Garnett E S, Nahmias C, Firnau G (1984) Central dopaminergic pathways in living monkeys examined by positron emission tomography. Can J Neurol Sci 11: 174–179
Garruto R M, Gajdusek C, Chen K M (1980) Amyotrophic lateral sclerosis among Chamorro migrants. Ann Neurol 8: 612–619
Garruto R M, Yanagihara R, Gajdusek D C (1985) Disappearance of high incidence amyotrophic lateral sclerosis and parkinsonism dementia on Guam. Neurology 35: 193–198
Hornikiewicz O (1986) Dopamine deficiency and dopamine substition in Parkinson’s disease. In: Winslow W, Markstein R (eds) The neurobiology of dopamine systems. University Press, Manchester, p319–330
Leenders K L, Poewe W H, Palmer A J, Brenton D P, Frackowiak R S J (1986) Inhibition of L-[18F]fluorodopa uptake into human brain by amino acids demonstrated by positron emission tomography. Ann Neurol 20: 258–262
Mann D M A, Yates PO (1982) Pathogenesis of Parkinson’s disease. Arch Neurol 39: 545–549
Martin W R W, Beckman J H, Calne D B, Adam M J, Harrop R, Rogers J G, Ruth T J, Sayre C I, Pate B D (1984) Cerebral glucose metabolism in Parkinson’s disease. Can J Neurol Sci 11: 169–173
Martin W R W, Stoessl J, Adam M J, Ammann W, Bergstrom M, Harrop R, Laihinen A, Rogers J G, Ruth T J, Sayre C I, Pate D B, Calne D B (1986) Positron emission tomography in Parkinson’s disease: glucose and dopa metabolism. In: Yahr M, Bergmann K (eds) Advances in neurology volume 45, Parkinson’s disease. Raven Press, New York, (in press)
Mawdsley C, Ferguson F R (1963) Neurological disease in boxers. Lancet ii: 795–801
McGeer P L, McGeer E G, Suzuki J (1977) Aging and extrapyramidal function. Arch Neurol 34: 33–35
McGeer P L, McGeer E G, Suzuki J, Dolman C E, Nagai T (1984) Aging, Alzheimern disease and the cholinergic system of the basal forebrain. Neurology 34: 741–745
Mena I, Cotzias C (1975) Protein uptake and treatment of Parkinson’s disease with levodopa. N Engl J Med 292: 181–184
Newman R P, LeWitt P A, Jaffe M, Calne D B, Larsen T A (1985) Motor function in the normal aging population: treatment with levodopa. Neurology 35: 571–573
Nutt J G, Woodward W R, Hämmerstad J P, Carter J H, Anderson J L (1984) The “on-off” phenomenon in Parkinson’s disease: relations to levodopa absorption and transport. N Engl J Med 310: 483–487
Perry T L, Yong U W, Clavier R M, (1985) Partial protection from the dopaminergic neurotoxin in N-methy1-4-phenyl-1,2,3,6- tetrahydropyridine by four different anti- oxidants in the mouse. Neurosci Lett 60: 109–114
Spencer P, Nunn P, Hugon J, Ludolph A, Ross S, RRoy D, Schaumburg H, Soiefer A’(1986) Primate motor neuron disorders induced by chemically related excitatory neurotoxins isolated from Guamanian cycad and Indian chickling pea. Muscle and Nerve 9. Suppl 5S: 108
Tomlinson B E, Irving D (1977) The numbers of limb motor neurons in the human lumbrosacral cord throughout life. J Neurol Sci 34: 213–219
Ward C D, Duvoisin R C, Ince S E, Nutt J D, Eldridge R, Calne D B (1983) Parkinson’s disease in 65 pairs of twins and in a set of quadruplets. Neurology 33: 815–824
Wooten G F, Collins R C (1981) Metabolic effects of unilateral lesions of the subtantia nigra. J Neurosci 1: 285–291
Author information
Authors and Affiliations
Editor information
Editors and Affiliations
Rights and permissions
Copyright information
© 1987 Springer-Verlag Berlin Heidelberg
About this paper
Cite this paper
Peppard, R.F., Calne, D.B. (1987). New Perspectives in Parkinson’s Disease. In: Govoni, S., Battaini, F. (eds) Modification of Cell to Cell Signals During Normal and Pathological Aging. NATO ASI Series, vol 9. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-72729-0_18
Download citation
DOI: https://doi.org/10.1007/978-3-642-72729-0_18
Publisher Name: Springer, Berlin, Heidelberg
Print ISBN: 978-3-642-72731-3
Online ISBN: 978-3-642-72729-0
eBook Packages: Springer Book Archive