Sonya S. Kaur
Research Subjects
Sonya S. Kaur has a total of 24 co-authors. Here are the top co-authors by number of shared publications:
- Ariana M. Stickel
Department of Psychology, San Diego State University, CA
1 shared publication - Bharat Thyagarajan
Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis
1 shared publication - Carmen R. Isasi
Department of Epidemiology and Population Health, Albert Einstein College of Medicine, Bronx, USA
1 shared publication - Charles DeCarli
Department of Neurology, University of California, Davis
1 shared publication - Christian Agudelo
University of Miami
1 shared publication - Chuanhui Dong
Department of Neurology, Miller School of Medicine, University of Miami, Miami, FL, United States
1 shared publication
Latest Publications
- 25 August 2026
- Published by Wolters Kluwer Health in Neurology
- Vol. 107 (4) , e218305
Association Between White Matter Integrity and Cognitive Performance Among Diverse Older Hispanic/Latino Adults in SOL-INCA MRI
Background and ObjectivesHispanic/Latino Americans are disproportionately affected by vascular risk factors (VRFs) linked to cognitive decline, yet they remain underrepresented in neuroimaging rese...
- 25 August 2026
- Published by Wolters Kluwer Health in Neurology
- Vol. 107 (4) , e218305
Association Between White Matter Integrity and Cognitive Performance Among Diverse Older Hispanic/Latino Adults in SOL-INCA MRI
Background and ObjectivesHispanic/Latino Americans are disproportionately affected by vascular risk factors (VRFs) linked to cognitive decline, yet they remain underrepresented in neuroimaging rese...
- Open Access
- 21 January 2025
- Published by Wolters Kluwer Health in Journal of the American Heart Association
- Vol. 14 (2) , e034033
Hypermethylation of PM20D1 Is Associated With Carotid Bifurcation Intima‐Media Thickness in Dominican Republic Families
Background: Carotid intima‐media thickness (IMT) is a measure of atherosclerosis and a predictor of vascular diseases. Traditional vascular risk factors and genetic variants do not completely explain the variation in carotid IMT. We sought to identify epigenetic factors that may contribute to the remaining carotid IMT variability. Methods and Results: An epigenome‐wide association study was performed in 61 Dominican families with 769 individuals. A cytosine nucleotide that precedes a guanine nucleotide methylation in blood‐derived DNA was measured using the Human MethylationEPIC BeadChip. Linear mixed model analyses were performed regressing bifurcation carotid IMT (bIMT) on beta values for cytosine nucleotide that precedes a guanine nucleotide sites, adjusting for covariates, followed by differentially methylated region (DMR) analysis. One‐sample Mendelian randomization analysis was conducted to investigate causal associations between DMRs and bIMT. Twenty‐five DMRs were associated with bIMT (Sidak P P =2.45×10 −17 ) overlapping with the promoter of PM20D1 . All 11 cytosine nucleotides that precede a guanine nucleotide within the PM20D1 DMR were positively associated with bIMT ( P =0.0007–0.00006). Methylation of the PM20D1 DMR was associated with cis variants, including rs823154 (β=0.26; P =1.1×10 −121 ). As reported in GTEx (Genotype‐Tissue Expression project), rs823154 is an expression quantitative trait locus for PM20D1 in multiple tissues, including the aorta ( P =2.3×10 −60 ) and blood ( P =4.0×10 −73 ), suggesting that hypermethylation of the PM20D1 DMR directs lower expression of the gene. Mendelian randomization analysis supported a causal role for PM20D1 DMR in bIMT ( P =0.049). Conclusions: Our study and previous expression quantitative trait locus studies provide converging evidence that reduced PM20D1 expression via hypermethylation of the promoter is associated with increased atherosclerosis.
- 21 January 2025
- Published by Wolters Kluwer Health in Journal of the American Heart Association
- Vol. 14 (2) , e034033
Open AccessHypermethylation of PM20D1 Is Associated With Carotid Bifurcation Intima‐Media Thickness in Dominican Republic Families
Background: Carotid intima‐media thickness (IMT) is a measure of atherosclerosis and a predictor of vascular diseases. Traditional vascular risk factors and genetic variants do not completely explain the variation in carotid IMT. We sought to identify epigenetic factors that may contribute to the remaining carotid IMT variability. Methods and Results: An epigenome‐wide association study was performed in 61 Dominican families with 769 individuals. A cytosine nucleotide that precedes a guanine nucleotide methylation in blood‐derived DNA was measured using the Human MethylationEPIC BeadChip. Linear mixed model analyses were performed regressing bifurcation carotid IMT (bIMT) on beta values for cytosine nucleotide that precedes a guanine nucleotide sites, adjusting for covariates, followed by differentially methylated region (DMR) analysis. One‐sample Mendelian randomization analysis was conducted to investigate causal associations between DMRs and bIMT. Twenty‐five DMRs were associated with bIMT (Sidak P P =2.45×10 −17 ) overlapping with the promoter of PM20D1 . All 11 cytosine nucleotides that precede a guanine nucleotide within the PM20D1 DMR were positively associated with bIMT ( P =0.0007–0.00006). Methylation of the PM20D1 DMR was associated with cis variants, including rs823154 (β=0.26; P =1.1×10 −121 ). As reported in GTEx (Genotype‐Tissue Expression project), rs823154 is an expression quantitative trait locus for PM20D1 in multiple tissues, including the aorta ( P =2.3×10 −60 ) and blood ( P =4.0×10 −73 ), suggesting that hypermethylation of the PM20D1 DMR directs lower expression of the gene. Mendelian randomization analysis supported a causal role for PM20D1 DMR in bIMT ( P =0.049). Conclusions: Our study and previous expression quantitative trait locus studies provide converging evidence that reduced PM20D1 expression via hypermethylation of the promoter is associated with increased atherosclerosis.