scholarly journals Validation of a polygenic risk score for dementia in black and white individuals

2014 ◽  
Vol 4 (5) ◽  
pp. 687-697 ◽  
Author(s):  
Jessica R. Marden ◽  
Stefan Walter ◽  
Eric J. Tchetgen Tchetgen ◽  
Ichiro Kawachi ◽  
M. Maria Glymour
2016 ◽  
Vol 30 (3) ◽  
pp. 195-202 ◽  
Author(s):  
Jessica R. Marden ◽  
Elizabeth R. Mayeda ◽  
Stefan Walter ◽  
Alexandre Vivot ◽  
Eric J. Tchetgen Tchetgen ◽  
...  

2019 ◽  
pp. e000183
Author(s):  
Shervin Assari ◽  
Arash Javanbakht ◽  
Mohammed Saqib ◽  
Hamid Helmi ◽  
Mohsen Bazargan ◽  
...  

Background. Black-White differences are reported in social, psychological, behavioral, medical, and biological correlates of depression. This study was conducted to compare Black and White older adults for the association between neuroticism polygenic risk score (N-PRS) and chronicity of depressive symptoms over 20 years. Methods. Data came from the Health and Retirement Study (HRS), 1990 – 2012, a nationally representative sample of Americans above age 50. Current analysis followed 9,249 individuals (7,924 Whites and 1,325 Blacks) for up to 22 years. Depressive symptoms were measured every two years between 1992 and 2012 using the 8-item Center for Epidemiological Studies-Depression Scale (CES-D-8). The independent variable was N-PRS. The dependent variable was average depressive symptoms between 1992 and 2012. Linear regression was used for data analysis. Results. In the pooled sample, higher N-PRS was associated with higher average depressive symptoms over the 20-year follow up period [b=0.01, 95%CI=0.00 to 0.04], net of all covariates. We also found an interaction between race and N-PRS [b=-0.02, 95%CI=-0.03 to 0.00], suggesting a stronger effect of N-PRS on 20-year average depressive symptoms for Whites than Blacks. Based on our race-specific linear regression models, higher N-PRS was associated with higher depressive symptoms from 1992 to 2012 for Whites [b=0.01, 95%CI=0.01 to 0.02] but not Blacks [b=0.00, 95%CI=-0.02 to 0.02]. Conclusion. Black and White older adults may differ in the salience of the existing N-PRS for depressive symptoms, which better reflects the burden of depression for Whites than Blacks. This may be because the existing PRSs are derived from mostly or exclusively White samples, limiting their applicability in other race groups. Racial variation in psychosocial, clinical, and biological correlates of depression needs further research.


Diabetes ◽  
2020 ◽  
Vol 69 (Supplement 1) ◽  
pp. 1645-P
Author(s):  
JOHANNE TREMBLAY ◽  
REDHA ATTAOUA ◽  
MOUNSIF HALOUI ◽  
RAMZAN TAHIR ◽  
CAROLE LONG ◽  
...  

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 304-OR
Author(s):  
MICHAEL L. MULTHAUP ◽  
RYOSUKE KITA ◽  
NICHOLAS ERIKSSON ◽  
STELLA ASLIBEKYAN ◽  
JANIE SHELTON ◽  
...  

2015 ◽  
Vol 11 (7S_Part_19) ◽  
pp. P872-P872 ◽  
Author(s):  
Valentina Escott-Price ◽  
Rebecca Sims ◽  
Denise Harold ◽  
Maria Vronskaya ◽  
Peter Holmans ◽  
...  

2020 ◽  
Vol 7 (1) ◽  
pp. e000755
Author(s):  
Matthew Moll ◽  
Sharon M. Lutz ◽  
Auyon J. Ghosh ◽  
Phuwanat Sakornsakolpat ◽  
Craig P. Hersh ◽  
...  

IntroductionFamily history is a risk factor for chronic obstructive pulmonary disease (COPD). We previously developed a COPD risk score from genome-wide genetic markers (Polygenic Risk Score, PRS). Whether the PRS and family history provide complementary or redundant information for predicting COPD and related outcomes is unknown.MethodsWe assessed the predictive capacity of family history and PRS on COPD and COPD-related outcomes in non-Hispanic white (NHW) and African American (AA) subjects from COPDGene and ECLIPSE studies. We also performed interaction and mediation analyses.ResultsIn COPDGene, family history and PRS were significantly associated with COPD in a single model (PFamHx <0.0001; PPRS<0.0001). Similar trends were seen in ECLIPSE. The area under the receiver operator characteristic curve for a model containing family history and PRS was significantly higher than a model with PRS (p=0.00035) in NHWs and a model with family history (p<0.0001) alone in NHWs and AAs. Both family history and PRS were significantly associated with measures of quantitative emphysema and airway thickness. There was a weakly positive interaction between family history and the PRS under the additive, but not multiplicative scale in NHWs (relative excess risk due to interaction=0.48, p=0.04). Mediation analyses found that a significant proportion of the effect of family history on COPD was mediated through PRS in NHWs (16.5%, 95% CI 9.4% to 24.3%), but not AAs.ConclusionFamily history and the PRS provide complementary information for predicting COPD and related outcomes. Future studies can address the impact of obtaining both measures in clinical practice.


Leukemia ◽  
2021 ◽  
Author(s):  
Geffen Kleinstern ◽  
J. Brice Weinberg ◽  
Sameer A. Parikh ◽  
Esteban Braggio ◽  
Sara J. Achenbach ◽  
...  

AbstractMonoclonal B-cell lymphocytosis (MBL) is a precursor to CLL. Other than age, sex, and CLL family-history, little is known about factors associated with MBL risk. A polygenic-risk-score (PRS) of 41 CLL-susceptibility variants has been found to be associated with CLL risk among individuals of European-ancestry(EA). Here, we evaluate these variants, the PRS, and environmental factors for MBL risk. We also evaluate these variants and the CLL-PRS among African-American (AA) and EA-CLL cases and controls. Our study included 560 EA MBLs, 869 CLLs (696 EA/173 AA), and 2866 controls (2631 EA/235 AA). We used logistic regression, adjusting for age and sex, to estimate odds ratios (OR) and 95% confidence intervals within each race. We found significant associations with MBL risk among 21 of 41 variants and with the CLL-PRS (OR = 1.86, P = 1.9 × 10−29, c-statistic = 0.72). Little evidence of any association between MBL risk and environmental factors was observed. We observed significant associations of the CLL-PRS with EA-CLL risk (OR = 2.53, P = 4.0 × 10−63, c-statistic = 0.77) and AA-CLL risk (OR = 1.76, P = 5.1 × 10−5, c-statistic = 0.62). Inherited genetic factors and not environmental are associated with MBL risk. In particular, the CLL-PRS is a strong predictor for both risk of MBL and EA-CLL, but less so for AA-CLL supporting the need for further work in this population.


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