Epidemiology of Parkinson’s disease-interplaying genes and environmental factors

  • K. Kondo
Part of the Key Topics in Brain Research book series (KEYTOPICS)


Epidemiology is one of the methods for solving a complex interplay of genes and environmental factors in Parkinson’s disease (PD).

A multifactorial inheritance has been proposed. Low concordance in twins refuted the role of genes in PD, but the small sample size did not allow a final conclusion. This author pooled twin and sib data from various sources and obtained 65% as the heritability of PD.

Risk factors are of importance in resolving the interplay. Well-accepted factors are age, smoking, preclinical personality profiles, and affection of the relatives with PD. We evaluated 271 questions in 166 cases along with two each of controls. PD-prone lifestyles were: 1) non-Japanese diet; 2) less smoking 3) less drinking; 4) fewer hobbies and if any, indoor hobbies requiring no partner; 5) interested only in business, narrow surroundings, etc.; 6) more habitual constipation, less circulatory disease; 7) less physical exercise; and 8) preclinical personality.

PD is probably a consequence of a long-standing age-dependent process modified by the interaction of a genetic predisposition and cumulated effects of numerous neurotoxins exposed for decades of time.


Motor Neuron Disease None None Dizygotic Twin Xeroderma Pigmentosum Circulatory Disease 
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  1. Barbeau A, Cloutier T, Roy M, Plasse L, Paris S, Poirier J (1985) Ecogenetics of Parkinson’s disease; 4-hydroxylation of debrisoquine. Lancet ii: 1213–1216Google Scholar
  2. Calne DB, Langston JW, Martin WR, Sloessl AJ, Ruth TJ, Adam MJ, Pate BD, Schulzer M (1985) Positron emission tomography after MPTP; observation relating to the cause of Parkinson’s disease. Nature 317: 246–248PubMedCrossRefGoogle Scholar
  3. Falconer DS (1965) The inheritance of liability to certain diseases estimated from the incidence among relatives. Ann Hum Genet 29: 51–76CrossRefGoogle Scholar
  4. Grima B, Lamouroux A, Boni C, Julien J-F, Javoy-Agid F, Mallet J (1987) A single human gene coding multiple tyrosine hydroxylases with different predicted functional characteristics. Nature 326: 707–711PubMedCrossRefGoogle Scholar
  5. Kondo K (1986) Epidemiological evaluation of risk factors in Parkinson’s disease. In: Yahr MD, Bergmann KJ (eds) Parkinson’s disease. Raven Press, New York, pp 289–293Google Scholar
  6. Kondo K (1989) Interplay of the environment and genes in Parkinson’s disease. Adv Neurol Sci (Jpn) 33: 759–765Google Scholar
  7. Kondo K, Yamashita (1990) A case-control study of Alzheimer’s disease in Japan; association with inactive phychosocial behaviors. In: Hasegawa K, Homma A (eds) Psychogeriatrics: biomedical and social advances. Excerpta Medica, Amsterdam, pp 49–53Google Scholar
  8. Kondo K, Kurland LT, Schull WJ (1973) Parkinson’s disease, genetic analysis and evidence of a multifactorial etiology. Mayo Clin Proc 48: 465–475PubMedGoogle Scholar
  9. Kondo I, Kanazawa I (1991) Association of Xba I allele (Xba I 44 kb) of the human cytochrome P-450 dbl (CYP2D6) gene in Japanese patients with idiopathic Parkinson’s disease (this volume)Google Scholar
  10. Li SC, Schoenberg BS, Wang C, Cheng X, Rui D, Bolis CL, Schoenberg DG (1985) A prevalence survey of Parkinson’s disease and other movement disorders in the People’s Republic of China. Arch Neurol 42: 655–657Google Scholar
  11. Myrianthopoulos NC, Waldrop IN, Vincent BL (1966) A repeated study of hereditary predisposition in drug-induced parkinsonism. In: Barbeau A, Brunette JB(eds) Progress in neurogenetics. Excerpta Medica, Amsterdam, pp 486–491Google Scholar
  12. Niwa T, Yoshizumi H, Tatematsu A, Matsuura S, Nagatsu T (1989) Presence of tetrahydroisoquinoline, a parkinsonism-related componend in foods. J Chromatogr 493: 347–352PubMedCrossRefGoogle Scholar
  13. Ottman R (1990) An epidemiologic approach to gene-environment interaction. Gen Epidemiol 7: 177–185CrossRefGoogle Scholar
  14. Riederer P, Wuketich S (1976) Time course of nigrostriatal degeneration in Parkinson’s disease. J Neural Transm 38: 277–301PubMedCrossRefGoogle Scholar
  15. Schoenberg BS, Anderson DW, Haerer AF (1985) Prevalence of Parkinson’s disease in the biracial population of Copiah Country, Mississippi. Neurology 35: 841–845PubMedGoogle Scholar
  16. Smith C (1970) Heritability of liability and concordance in monozygotic twins. Ann Hum Genet 34: 85 - 91.PubMedCrossRefGoogle Scholar
  17. Ward CD, Duvoisin RC, Ince SE, Nutt JD, Eldridge R, Calne DB (1983) Parkinson’s disease in 65 pairs of twins and in a set of quadruplets. Neurology 33: 815–824PubMedGoogle Scholar
  18. Yoshida M, Ogawa M, Nagatsu T (1991) Can tetrahydroisoquinoline (TiQ) or N- methyl-TiQ produce parkinsonism? (this volume)Google Scholar

Copyright information

© Springer-Verlag/Wien 1991

Authors and Affiliations

  • K. Kondo
    • 1
  1. 1.Department of Public HealthHokkaido University, School of MedicineKitaku, SapporoJapan 060

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