@article {1233, title = {Post hoc Parkinson{\textquoteright}s disease: identifying an uncommon disease in the Cardiovascular Health Study.}, journal = {Neuroepidemiology}, volume = {35}, year = {2010}, month = {2010}, pages = {241-9}, abstract = {

BACKGROUND: Although ongoing cohort studies offer a unique opportunity to apply existing information collected prospectively to further the scientific understanding of Parkinson{\textquoteright}s disease (PD), they typically have limited information for clinical diagnosis.

METHODS: We used combinations of self-report, International Classification of Diseases - 9th edition codes and antiparkinsonian medications to identify PD in the Cardiovascular Health Study. To determine whether the expected inverse association between smoking and PD is evident using our outcome definitions, we assessed baseline smoking characteristics for various definitions of PD.

RESULTS: We identified 60 cases with prevalent PD (1.0\%; 95\% confidence interval, CI = 0.8-1.3\%) and 154 with incident PD by year 14. Clear associations were observed for current smokers (odds ratio, OR = 0.50; 95\% CI = 0.26-0.95) and for those who smoked >=50 pack-years (OR = 0.53; 95\% CI = 0.29-0.96). Estimates for smoking were similar when >=2 data sources were required. Estimates for self-report alone were attenuated towards null.

CONCLUSIONS: Using multiple data sources to identify PD represents an alternative method of outcome identification in a cohort that would otherwise not be possible for PD research. Ongoing cohort studies can provide settings in which rapid replication and explorations of new hypotheses for PD are possible.

}, keywords = {Aged, Aged, 80 and over, Cardiovascular System, Cohort Studies, Female, Health Status, Humans, Incidence, Male, Odds Ratio, Parkinson Disease, Prevalence, Prospective Studies, Risk Factors, Smoking, Surveys and Questionnaires, United States}, issn = {1423-0208}, doi = {10.1159/000319895}, author = {Ton, T G and Jain, S and Boudreau, R and Thacker, E L and Strotmeyer, E S and Newman, A B and Longstreth, W T and Checkoway, H} } @article {1297, title = {The risk of Parkinson disease associated with urate in a community-based cohort of older adults.}, journal = {Neuroepidemiology}, volume = {36}, year = {2011}, month = {2011}, pages = {223-9}, abstract = {

BACKGROUND/AIMS: Studies suggest an inverse association between urate concentration and the risk of Parkinson disease (PD). We investigated this in the Cardiovascular Health Study in an elderly community-based cohort of adults.

METHODS: The association of baseline urate ({\textmu}mol/l) and incident PD over 14 years was assessed with locally weighted scatterplot smoothing (LOESS) regression from which categories of low (<300 {\textmu}mol/l), middle (300-500 {\textmu}mol/l), and high (>500 {\textmu}mol/l) urate ranges were derived. Multivariate logistic regression models assessed the risk of PD for each urate range. Linear and quadratic terms were tested when modeling the association between urate and the risk of PD.

RESULTS: Women had significantly lower urate concentrations than did men [316.8 {\textmu}mol/l (SD 88.0) vs. 367.4 {\textmu}mol/l (SD 87.7), p < 0.0001] and in women no associations between urate and PD risk were observed. In men, LOESS curves suggested a U-shaped or threshold effect between urate and PD risk. With the middle range as reference, the risk of developing PD was significantly increased for urate <300 {\textmu}mol/l (OR 1.69, 95\% CI 1.03-2.78) but not for urate >500 {\textmu}mol/l (OR 1.55, 95\% CI 0.72-3.32) in men. A negative linear term was significant for urate <500 {\textmu}mol/l, and across the entire range a convex quadratic term was significant.

CONCLUSIONS: Results suggest a more complex relationship than previously reported between urate levels and the risk of PD in men. Low urate concentrations were associated with a higher PD risk and high urate concentrations were not associated with a further decrease in PD risk.

}, keywords = {Aged, California, Cohort Studies, Female, Humans, Male, Maryland, North Carolina, Parkinson Disease, Pennsylvania, Prospective Studies, Risk Factors, Sex Distribution, Sex Factors, Uric Acid}, issn = {1423-0208}, doi = {10.1159/000327748}, author = {Jain, S and Ton, T G and Boudreau, R M and Yang, M and Thacker, E L and Studenski, S and Longstreth, W T and Strotmeyer, E S and Newman, A B} } @article {6804, title = {Genome-wide meta-analyses of smoking behaviors in African Americans.}, journal = {Transl Psychiatry}, volume = {2}, year = {2012}, month = {2012}, pages = {e119}, abstract = {

The identification and exploration of genetic loci that influence smoking behaviors have been conducted primarily in populations of the European ancestry. Here we report results of the first genome-wide association study meta-analysis of smoking behavior in African Americans in the Study of Tobacco in Minority Populations Genetics Consortium (n = 32,389). We identified one non-coding single-nucleotide polymorphism (SNP; rs2036527[A]) on chromosome 15q25.1 associated with smoking quantity (cigarettes per day), which exceeded genome-wide significance (β = 0.040, s.e. = 0.007, P = 1.84 {\texttimes} 10(-8)). This variant is present in the 5{\textquoteright}-distal enhancer region of the CHRNA5 gene and defines the primary index signal reported in studies of the European ancestry. No other SNP reached genome-wide significance for smoking initiation (SI, ever vs never smoking), age of SI, or smoking cessation (SC, former vs current smoking). Informative associations that approached genome-wide significance included three modestly correlated variants, at 15q25.1 within PSMA4, CHRNA5 and CHRNA3 for smoking quantity, which are associated with a second signal previously reported in studies in European ancestry populations, and a signal represented by three SNPs in the SPOCK2 gene on chr10q22.1. The association at 15q25.1 confirms this region as an important susceptibility locus for smoking quantity in men and women of African ancestry. Larger studies will be needed to validate the suggestive loci that did not reach genome-wide significance and further elucidate the contribution of genetic variation to disparities in cigarette consumption, SC and smoking-attributable disease between African Americans and European Americans.

}, keywords = {Adult, African Americans, Aged, Chromosomes, Human, Pair 10, Chromosomes, Human, Pair 15, Female, Genetic Loci, Genetic Predisposition to Disease, Genetic Variation, Genome-Wide Association Study, Genotype, Humans, Male, Middle Aged, Nerve Tissue Proteins, Phenotype, Polymorphism, Single Nucleotide, Proteoglycans, Receptors, Nicotinic, Smoking, Statistics as Topic}, issn = {2158-3188}, doi = {10.1038/tp.2012.41}, author = {David, S P and Hamidovic, A and Chen, G K and Bergen, A W and Wessel, J and Kasberger, J L and Brown, W M and Petruzella, S and Thacker, E L and Kim, Y and Nalls, M A and Tranah, G J and Sung, Y J and Ambrosone, C B and Arnett, D and Bandera, E V and Becker, D M and Becker, L and Berndt, S I and Bernstein, L and Blot, W J and Broeckel, U and Buxbaum, S G and Caporaso, N and Casey, G and Chanock, S J and Deming, S L and Diver, W R and Eaton, C B and Evans, D S and Evans, M K and Fornage, M and Franceschini, N and Harris, T B and Henderson, B E and Hernandez, D G and Hitsman, B and Hu, J J and Hunt, S C and Ingles, S A and John, E M and Kittles, R and Kolb, S and Kolonel, L N and Le Marchand, L and Liu, Y and Lohman, K K and McKnight, B and Millikan, R C and Murphy, A and Neslund-Dudas, C and Nyante, S and Press, M and Psaty, B M and Rao, D C and Redline, S and Rodriguez-Gil, J L and Rybicki, B A and Signorello, L B and Singleton, A B and Smoller, J and Snively, B and Spring, B and Stanford, J L and Strom, S S and Swan, G E and Taylor, K D and Thun, M J and Wilson, A F and Witte, J S and Yamamura, Y and Yanek, L R and Yu, K and Zheng, W and Ziegler, R G and Zonderman, A B and Jorgenson, E and Haiman, C A and Furberg, H} }