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      Diabetes and Risk of Parkinson’s Disease

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      Author(s): , MD, PHD 1 , , SCD 2 , , MD, PHD 3 , , PHD 4 , , PHD 5 , , MD, PHD 2 , , MD, PHD 1
      Publication date (Electronic):
      Journal: Diabetes Care
      Publisher: American Diabetes Association

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          Abstract

          OBJECTIVE

          To investigate the relationship between diabetes and future risk of Parkinson’s disease (PD) among older U.S. adults.

          RESEARCH DESIGN AND METHODS

          A prospective study of self-reported diabetes in 1995 and 1996 in relation to PD diagnosed after 1995 among 288,662 participants of the National Institutes of Health-AARP Diet and Health Study. Multivariate odds ratio (OR) and 95% CI were derived from logistic regression models.

          RESULTS

          A total of 1,565 participants with PD diagnosed after 1995 were included in the analysis. After adjustment for potential confounders, PD risk was ∼40% higher (OR = 1.41 [95% CI 1.20–1.66]) among diabetic patients than among participants without diabetes. Further analysis showed that the risk elevation was largely limited to individuals who had diabetes for more than 10 years at the time of baseline survey (1.75 [1.36–2.25]). The association with diabetes was seen for both participants with PD diagnosed between 1995 and 1999 and participants with PD diagnosed after 2000. In addition, similar results were obtained after excluding participants with stroke, heart disease, cancers, or poor or fair health status and in subgroup analyses by age, sex, smoking status, and coffee consumption.

          CONCLUSIONS

          This large study showed that diabetes was associated with a higher future risk of PD and the nature of this association warrants further investigation.

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          Agreement between self-report questionnaires and medical record data was substantial for diabetes, hypertension, myocardial infarction and stroke but not for heart failure.

          Yuji Okura, Lynn H. Urban, Douglas Mahoney … (2004)
          Questionnaires are used to estimate disease burden. Agreement between questionnaire responses and a criterion standard is important for optimal disease prevalence estimates. We measured the agreement between self-reported disease and medical record diagnosis of disease. A total of 2,037 Olmsted County, Minnesota residents > or =45 years of age were randomly selected. Questionnaires asked if subjects had ever had heart failure, diabetes, hypertension, myocardial infarction (MI), or stroke. Medical records were abstracted. Self-report of disease showed >90% specificity for all these diseases, but sensitivity was low for heart failure (69%) and diabetes (66%). Agreement between self-report and medical record was substantial (kappa 0.71-0.80) for diabetes, hypertension, MI, and stroke but not for heart failure (kappa 0.46). Factors associated with high total agreement by multivariate analysis were age 12 years, and zero Charlson Index score (P < .05). Questionnaire data are of greatest value in life-threatening, acute-onset diseases (e.g., MI and stroke) and chronic disorders requiring ongoing management (e.g.,diabetes and hypertension). They are more accurate in young women and better-educated subjects.
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            Prevalence of diabetes and impaired fasting glucose in adults in the U.S. population: National Health And Nutrition Examination Survey 1999-2002.

            Catherine C Cowie, Keith F. Rust, Danita D. Byrd-Holt … (2006)
            The purpose of this study was to examine the prevalences of diagnosed and undiagnosed diabetes, and impaired fasting glucose (IFG) in U.S. adults during 1999-2002, and compare prevalences to those in 1988-1994. The National Health and Nutrition Examination Survey (NHANES) contains a probability sample of adults aged > or =20 years. In the NHANES 1999-2002, 4,761 adults were classified on glycemic status using standard criteria, based on an interview for diagnosed diabetes and fasting plasma glucose measured in a subsample. The crude prevalence of total diabetes in 1999-2002 was 9.3% (19.3 million, 2002 U.S. population), consisting of 6.5% diagnosed and 2.8% undiagnosed. An additional 26.0% had IFG, totaling 35.3% (73.3 million) with either diabetes or IFG. The prevalence of total diabetes rose with age, reaching 21.6% for those aged > or =65 years. The prevalence of diagnosed diabetes was twice as high in non-Hispanic blacks and Mexican Americans compared with non-Hispanic whites (both P < 0.00001), whereas the prevalence of undiagnosed diabetes was similar by race/ethnicity, adjusted for age and sex. The prevalence of diagnosed diabetes was similar by sex, but prevalences of undiagnosed diabetes and IFG were significantly higher in men. The crude prevalence of diagnosed diabetes rose significantly from 5.1% in 1988-1994 to 6.5% in 1999-2002, but the crude prevalences were stable for undiagnosed diabetes (from 2.7 to 2.8%) and IFG (from 24.7 to 26.0%). Results were similar after adjustment for age and sex. Although the prevalence of diagnosed diabetes has increased significantly over the last decade, the prevalences of undiagnosed diabetes and IFG have remained relatively stable. Minority groups remain disproportionately affected.
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              Mitochondrial biology and oxidative stress in Parkinson disease pathogenesis.

              Claire Henchcliffe, M. Beal (2008)
              Parkinson disease (PD) is associated with progressive loss of dopaminergic neurons in the substantia nigra, as well as with more-widespread neuronal changes that cause complex and variable motor and nonmotor symptoms. Recent rapid advances in PD genetics have revealed a prominent role for mitochondrial dysfunction in the pathogenesis of the disease, and the products of several PD-associated genes, including SNCA, Parkin, PINK1, DJ-1, LRRK2 and HTR2A, show a degree of localization to the mitochondria under certain conditions. Impaired mitochondrial function is likely to increase oxidative stress and might render cells more vulnerable to this and other related processes, including excitotoxicity. The mitochondria, therefore, represent a highly promising target for the development of disease biomarkers by use of genetic, biochemical and bioimaging approaches. Novel therapeutic interventions that modify mitochondrial function are currently under development, and a large phase III clinical trial is underway to examine whether high-dose oral coenzyme Q10 will slow disease progression. In this Review, we examine evidence for the roles of mitochondrial dysfunction and increased oxidative stress in the neuronal loss that leads to PD and discuss how this knowledge might further improve patient management and aid in the development of 'mitochondrial therapy' for PD.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Diabetes Care
                Journal ID (hwp): diacare
                Journal ID (pmc): dcare
                Journal ID (publisher-id): Diabetes Care
                Title: Diabetes Care
                Publisher: American Diabetes Association
                ISSN (Print): 0149-5992
                ISSN (Electronic): 1935-5548
                Publication date (Print): April 2011
                Publication date (Electronic): 21 March 2011
                Volume: 34
                Issue: 4
                Pages: 910-915
                Affiliations
                [1] 1Epidemiology Branch, National Institute of Environmental Health Sciences, Research Triangle Park, North Carolina
                [2] 2Nutritional Epidemiology Branch, National Cancer Institute, Rockville, Maryland
                [3] 3Department of Neurology, Pennsylvania State University-Milton S. Hershey Medical Center, Hershey, Pennsylvania
                [4] 4AARP, Washington, District of Columbia
                [5] 5Occupational and Environmental Epidemiology Branch, National Cancer Institute, Rockville, Maryland
                Author notes
                Corresponding author: Honglei Chen, chenh2@ 123456niehs.nih.gov .
                Article
                Publisher ID: 1922
                DOI: 10.2337/dc10-1922
                PMC ID: 3064050
                PubMed ID: 21378214
                SO-VID: 84324bdf-0fe3-4902-8689-26684ee511a8
                Copyright © © 2011 by the American Diabetes Association.
                License:

                Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

                History
                Date received : 7 October 2010
                Date accepted : 30 January 2011
                Categories
                Subject: Original Research
                Subject: Epidemiology/Health Services Research

                ScienceOpen disciplines: Endocrinology & Diabetes
                Data availability:
                ScienceOpen disciplines: Endocrinology & Diabetes

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