Parkinson's disease in 65 pairs of twins and in a set of quadruplets

Ward, C D; Duvoisin, Roger C.; Ince, Susan; Nutt, J.; Eldridge, Roswell; Calne, Donald B.

doi:10.1212/wnl.33.7.815

Cited by 332 publications

(93 citation statements)

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“…Similarly, concordances were low in all zygosity groups when the definition of affected was expanded to include twins with parkinsonian symptoms or use of anti-parkinson medication. Thus, these results were similar to the early twin studies in PD [113][114][115][116]. The NAS-NRC study reported higher concordance rates both in monozygotic and dizygotic twins, a finding that may partially be explained by higher prevalence of PD (867 per 100,000 men in the NAS-NRC study [119], versus 547 per 100,000 men in the Swedish study [68]).…”

Section: Mortalitysupporting

confidence: 85%

Epidemiology and etiology of Parkinson’s disease: a review of the evidence

et al. 2011

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Section: Mortalitysupporting

confidence: 85%

Epidemiology and etiology of Parkinson’s disease: a review of the evidence

et al. 2011

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“…The aggregated MZ\DZ concordance ratio of 1.2 : 1 found in previous twin studies provided no evidence of a significant genetic risk (Ward et al 1983 ;Barucha et al 1986 ;Marsden, 1987 ;Tanner, 1992 ;Vieregge et al 1992). However, these cross-sectional studies do not allow detection of cases with subclinical disease.…”

Section: Twin Studies and The Role Of Positron Emission Tomographymentioning

confidence: 81%

Genetics of Parkinsonism: a review

VAUGHAN¹,

DAVIS²,

WOOD³

2001

Annals of Human Genetics

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Idiopathic Parkinson's disease (IPD), a progressive neurodegenerative disorder, is a common cause of disability. No current therapies modify disease progression. The pathological hallmarks are the presence of Lewy bodies and massive loss of dopaminergic neurons in the pars compacta of the substantia nigra. Two genes (SNCA and parkin) as well as two gene loci have now been implicated in the pathogenesis of familial PD. These represent significant progress in our understanding of the disease, considering the rarity of large families, low heritability in the general population and genetic heterogeneity. Mutations in a further gene, UCHL1, have been described in familial PD although the evidence for its role in PD is less clear. Knowledge of the genes described in PD to date should help to define molecular mechanisms of neurodegeneration in PD, as well as in other diseases where defects in protein handling may be a common feature. Nigral degeneration with Lewy body formation and the resulting clinical picture of PD may represent a final common pathway of a multifactorial disease process in which both environmental and genetic factors have a role. This review discusses the major advances in the field to date and illustrates how the existence of genetic factors has now become firmly established.

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“…However, the existence of "susceptibility" genes has been suggested (Martin et al, 2001), particularly in the context of the alleged disease-causing role of environmental toxins (Checkoway and Nelson, 1999). Several twin studies have so far been unable to identify genetic factors (Ward et al, 1983;Tanner et al, 1999). Surprisingly, patients with Parkinson often have peculiar premorbid personality traits (e.g., industriousness, punctuality, lack of novelty seeking, low life-time risk for cigarette smoking) whose relevance for the disease onset is entirely unclear (Menza, 2000).…”

Section: Introductionmentioning

confidence: 99%

Functional genomics of neural and behavioral plasticity

2002

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How does the environment, particularly the social environment, influence brain and behavior and what are the underlying physiologic, molecular, and genetic mechanisms? Adaptations of brain and behavior to changes in the social or physical environment are common in the animal world, either as short-term (i.e., modulatory) or as long-term modifications (e.g., via gene expression changes) in behavioral or physiologic properties. The study of the mechanisms and constraints underlying these dynamic changes requires model systems that offer plastic phenotypes as well as a sufficient level of quantifiable behavioral complexity while being accessible at the physiological and molecular level. In this article, I explore how the new field of functional genomics can contribute to an understanding of the complex relationship between genome and environment that results in highly plastic phenotypes. This approach will lead to the discovery of genes under environmental control and provide the basis for the study of the interrelationship between an individual's gene expression profile and its social phenotype in a given environmental context.

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Parkinson's disease in 65 pairs of twins and in a set of quadruplets

Cited by 332 publications

References 0 publications

Epidemiology and etiology of Parkinson’s disease: a review of the evidence

Epidemiology and etiology of Parkinson’s disease: a review of the evidence

Genetics of Parkinsonism: a review

Functional genomics of neural and behavioral plasticity

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