The Frequency of Idiopathic Parkinson's Disease by Age, Ethnic Group, and Sex in Northern Manhattan, 1988-1993

Department of Neurology, College of Physicians and Surgeons, Columbia University, New York, NY, USA.
American Journal of Epidemiology (Impact Factor: 5.23). 11/1995; 142(8).
Source: OAI


Sex and ethnic differences in the frequency of Parkinson's disease have become increasingly important, because putative genetic and environmental risk factors have been identified. The authors estimated the prevalence and incidence of Parkinson's disease in a culturally diverse community in New York City over a 4-year period (January 1, 1988–December 31, 1991) using a disease registry substantiated, for older individuals, by a subsequent survey of a random sample of Medicare recipients between January 1, 1992, and December 31, 1993. The prevalence rate was 107 per 100,000 persons, and over a 3-year period the average incidence rate was 13 per 100,000 person-years. Age-adjusted prevalence rates were lower for women than for men in each ethnic group and were lower for blacks than for whites and Hispanics. Incidence rates were highest among black men, but they were otherwise comparable across the sex and ethnic groups. The estimated cumulative incidence of Parkinson's disease up to age 90 years was lower for women than for men, which could partially explain the lower prevalence rate. By ethnic group, the cumulative incidence was higher for blacks than for whites and Hispanics, but more deaths occurred among incident black cases. Discrepant prevalence and incidence rates of Parkinson's disease among blacks and women warrant further investigation. While selective mortality could partially account for this paradox, it is also possible that a delay in diagnosis due to limited access to appropriate health services among these individuals could have resulted in the observed discordant rates of disease.

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    • "Characterized by motor impairment and, with time, cognitive deficits, Parkinson’s disease (PD) affects ~1% of people over the age of 65 [1]. Histopathological features include loss of dopaminergic neurons, predominantly in the substantia nigra pars compacta, often accompanied by intracellular inclusions called Lewy bodies [2,3]. "
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    ABSTRACT: Mutations in the gene encoding parkin, a neuroprotective protein with dual functions as an E3 ubiquitin ligase and transcriptional repressor of p53, are linked to familial forms of Parkinson's disease (PD). We hypothesized that oxidative posttranslational modification of parkin by environmental toxins may contribute to sporadic PD. We first demonstrated that S-nitrosylation of parkin decreased its activity as a repressor of p53 gene expression, leading to upregulation of p53. Chromatin immunoprecipitation as well as gel-shift assays showed that parkin bound to the p53 promoter, and this binding was inhibited by S-nitrosylation of parkin. Additionally, nitrosative stress induced apoptosis in cells expressing parkin, and this death was, at least in part, dependent upon p53. In primary mesencephalic cultures, pesticide-induced apoptosis was prevented by inhibition of nitric oxide synthase (NOS). In a mouse model of pesticide-induced PD, both S-nitrosylated (SNO-)parkin and p53 protein levels were increased, while administration of a NOS inhibitor mitigated neuronal death in these mice. Moreover, the levels of SNO-parkin and p53 were simultaneously elevated in postmortem human PD brain compared to controls. Taken together, our data indicate that S-nitrosylation of parkin, leading to p53-mediated neuronal cell death, contributes to the pathophysiology of sporadic PD.
    Molecular Neurodegeneration 08/2013; 8(1):29. DOI:10.1186/1750-1326-8-29 · 6.56 Impact Factor
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    • "Parkinson's disease (PD) is a common neurodegenerative disorder, affecting 2% of those over the age of 75 years (Mayeux et al., 1995). Neuropathologically, it is characterized by a progressive loss of dopaminergic neurons of the substantia nigra, associated with the formation of fibrillar aggregates composed of α-synuclein and other proteins (Lewy bodies and Lewy neurites) (Braak et al., 2003). "
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    ABSTRACT: Recently 2 groups have independently identified a mutation in the gene 'vacuolar protein sorting 35 homolog' (VPS35 c.1858G>A; p.Asp620Asn) as a possible cause of autosomal dominant Parkinson's disease (PD). In order to assess the frequency of the reported mutation and to search for other possible disease-causing variants in this gene, we sequenced all 17 exons of VPS35 in 96 familial PD cases, and exon 15 (in which the reported mutation is found) in an additional 64 familial PD cases, 175 young-onset PD cases, and 262 sporadic, neuropathologically confirmed PD cases. We identified 1 individual with the p.Asp620Asn mutation and an autosomal dominant family history of PD. Subsequent follow-up of the family confirmed an affected sibling and cousin who also carried the same mutation. No other potentially disease-causing mutations were identified. We conclude that the VPS35 c.1858G>A mutation is an uncommon cause of familial Parkinson's disease in our population.
    Neurobiology of aging 12/2011; 33(4):838.e1-5. DOI:10.1016/j.neurobiolaging.2011.10.032 · 5.01 Impact Factor
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    • "There are sex differences in dopaminergic (DA) degeneration, as observed in animal models as well as clinical and epidemiological reports on Parkinson's disease (PD). The higher risk of developing PD in men than in premenopausal women of the same age is well-established; men are approximately two times as likely as women to develop the disease [1-3]. However, the mechanisms responsible for this difference have not been clarified [4]. "
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    ABSTRACT: There are sex differences in dopaminergic degeneration. Men are approximately two times as likely as premenopausal women of the same age to develop Parkinson's disease (PD). It has been shown that the local renin angiotensin system (RAS) plays a prominent role in sex differences in the development of chronic renal and cardiovascular diseases, and there is a local RAS in the substantia nigra and dopaminergic cell loss is enhanced by angiotensin via type 1 (AT1) receptors. In the present study, we observed that intrastriatal injection of 6-hydroxydopamine induced a marked loss of dopaminergic neurons in the substantia nigra of male rats, which was significantly higher than the loss induced in ovariectomized female rats given estrogen implants (i.e. rats with estrogen). However, the loss of dopaminergic neurons was significantly lower in male rats treated with the AT1 antagonist candesartan, and similar to that observed in female rats with estrogen. The involvement of the RAS in gender differences in dopaminergic degeneration was confirmed with AT1a-null mice lesioned with the dopaminergic neurotoxin MPTP. Significantly higher expression of AT1 receptors, angiotensin converting enzyme activity, and NADPH-oxidase complex activity, and much lower levels of AT2 receptors were observed in male rats than in female rats with estrogen. The results suggest that brain RAS plays a major role in the increased risk of developing PD in men, and that manipulation of brain RAS may be an efficient approach for neuroprotective treatment of PD in men, without the feminizing effects of estrogen.
    Molecular Neurodegeneration 08/2011; 6(1):58. DOI:10.1186/1750-1326-6-58 · 6.56 Impact Factor
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