6 results on '"Montgomery, Bailey E."'
Search Results
2. Lobar intracerebral hemorrhage and risk of subsequent uncontrolled blood pressure
- Author
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Myserlis, Evangelos Pavlos, primary, Mayerhofer, Ernst, additional, Abramson, Jessica R, additional, Teo, Kay-Cheong, additional, Montgomery, Bailey E., additional, Sugita, Lansing, additional, Warren, Andrew D, additional, Goldstein, Joshua N, additional, Gurol, Mahmut Edip, additional, Viswanathan, Anand, additional, Greenberg, Steven M, additional, Biffi, Alessandro, additional, Anderson, Christopher D, additional, and Rosand, Jonathan, additional
- Published
- 2022
- Full Text
- View/download PDF
3. sj-docx-1-wso-10.1177_17474930221095696 – Supplemental material for Shared genetic background between SARS-CoV-2 infection and large artery stroke
- Author
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Parodi, Livia, Myserlis, Evangelos Pavlos, Chung, Jaeyoon, Georgakis, Marios K, Mayerhofer, Ernst, Henry, Jonathan, Montgomery, Bailey E, Moy, Mandy, Xu, Huichun, Malik, Rainer, Langefeld, Carl D, Dichgans, Martin, Woo, Daniel, Rosand, Jonathan, and Anderson, Christopher D
- Subjects
FOS: Clinical medicine ,Cardiology ,Medicine ,110904 Neurology and Neuromuscular Diseases - Abstract
Supplemental material, sj-docx-1-wso-10.1177_17474930221095696 for Shared genetic background between SARS-CoV-2 infection and large artery stroke by Livia Parodi, Evangelos Pavlos Myserlis, Jaeyoon Chung, Marios K Georgakis, Ernst Mayerhofer, Jonathan Henry, Bailey E Montgomery, Mandy Moy, Huichun Xu, Rainer Malik, Carl D Langefeld, Martin Dichgans, Daniel Woo, Jonathan Rosand and Christopher D Anderson in International Journal of Stroke
- Published
- 2022
- Full Text
- View/download PDF
4. Shared genetic background between SARS-CoV-2 infection and large artery stroke
- Author
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Parodi, Livia, Myserlis, Evangelos Pavlos, Langefeld, Carl D, Dichgans, Martin, Network, NINDS-Stroke Genetics, Woo, Daniel, Rosand, Jonathan, Anderson, Christopher D, Consortium, International Stroke Genetics, Chung, Jaeyoon, Georgakis, Marios K, Mayerhofer, Ernst, Henry, Jonathan, Montgomery, Bailey E, Moy, Mandy, Xu, Huichun, and Malik, Rainer
- Subjects
ischaemic stroke ,Neurology ,SARS-CoV-2 ,large artery stroke ,COVID-19 ,cerebrovascular disorders ,ddc:610 ,stroke - Abstract
Background and aims: Increased risk of stroke, particularly large artery stroke (LAS), has been observed in patients with COVID-19. The biological processes underlying the observed higher risk are still unknown. We explored the association between stroke subtypes and COVID-19 susceptibility to understand whether biological mechanisms specific to SARS-CoV-2 uptake/infection could be leading to excess stroke risk in this population. Patients and methods: We constructed a polygenic risk score (PRS) of COVID-19 susceptibility and tested its association with stroke subtypes using individual- and summary-level genetic data (SiGN, MEGASTROKE). We generated co-expression networks of genes involved in SARS-CoV-2 uptake/infection ( ACE2, TMPRSS2, BEST3, ISLR2 and ADAM17) based on existing tissue expression libraries. Gene-based association testing was performed using S-PrediXcan and VEGAS2. Permutation independence tests were performed to assess SARS-CoV-2-related gene enrichment in stroke and its subtypes. Results: Our PRS demonstrated an association between COVID-19 susceptibility and LAS in SiGN (OR = 1.05 per SD increase, 95% CI: (1.00, 1.10), p = 0.04) and MEGASTROKE (β = 0.510, 95% CI: (0.242, 0.779), FDR-p = 0.0019). The SARS-CoV-2 risk-related ISLR2 co-expression gene network was significantly associated with genetic risk of LAS in aorta, tibial arteries, and multiple brain regions (P Conclusion: Presence of genetic correlation and significant pathway enrichment suggest that increases in LAS risk reported in COVID-19 patients may be intrinsic to the viral infection, rather than a more generalized response to severe illness.
- Published
- 2022
5. Mendelian Randomization Study of Obesity and Cerebrovascular Disease.
- Author
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Marini, Sandro, Merino, Jordi, Montgomery, Bailey E., Malik, Rainer, Sudlow, Catherine L., Dichgans, Martin, Florez, Jose C., Rosand, Jonathan, Gill, Dipender, Anderson, Christopher D., and International Stroke Genetics Consortium
- Subjects
CEREBROVASCULAR disease ,SYSTOLIC blood pressure ,WAIST-hip ratio ,CEREBRAL hemorrhage ,BLOOD sugar ,BODY mass index ,OBESITY ,BRAIN ,CEREBRAL small vessel diseases ,BLOOD pressure ,RESEARCH ,STROKE ,RESEARCH methodology ,EVALUATION research ,MEDICAL cooperation ,COMPARATIVE studies ,RESEARCH funding - Abstract
Objective: To systematically investigate causal relationships between obesity and cerebrovascular disease and the extent to which hypertension and hyperglycemia mediate the effect of obesity on cerebrovascular disease.Methods: We used summary statistics from genome-wide association studies for body mass index (BMI), waist-to-hip ratio (WHR), and multiple cerebrovascular disease phenotypes. We explored causal associations with 2-sample Mendelian randomization (MR) accounting for genetic covariation between BMI and WHR, and we assessed what proportion of the association between obesity and cerebrovascular disease was mediated by systolic blood pressure (SBP) and blood glucose levels, respectively.Results: Genetic predisposition to higher BMI did not increase the risk of cerebrovascular disease. In contrast, for each 10% increase in WHR there was a 75% increase (95% confidence interval [CI] = 44-113%) in risk for large artery ischemic stroke, a 57% (95% CI = 29-91%) increase in risk for small vessel ischemic stroke, a 197% increase (95% CI = 59-457%) in risk of intracerebral hemorrhage, and an increase in white matter hyperintensity volume (β = 0.11, 95% CI = 0.01-0.21). These WHR associations persisted after adjusting for genetic determinants of BMI. Approximately one-tenth of the observed effect of WHR was mediated by SBP for ischemic stroke (proportion mediated: 12%, 95% CI = 4-20%), but no evidence of mediation was found for average blood glucose.Interpretation: Abdominal adiposity may trigger causal pathological processes, partially independent from blood pressure and totally independent from glucose levels, that lead to cerebrovascular disease. Potential targets of these pathological processes could represent novel therapeutic opportunities for stroke. ANN NEUROL 2020;87:516-524. [ABSTRACT FROM AUTHOR]- Published
- 2020
- Full Text
- View/download PDF
6. Shared genetic background between SARS-CoV-2 infection and large artery stroke.
- Author
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Parodi L, Myserlis EP, Chung J, Georgakis MK, Mayerhofer E, Henry J, Montgomery BE, Moy M, Xu H, Malik R, Langefeld CD, Dichgans M, Woo D, Rosand J, and Anderson CD
- Abstract
Background and Aims: Increased risk of stroke, particularly large artery stroke (LAS), has been observed in patients with COVID-19. The biological processes underlying the observed higher risk are still unknown. We explored the association between stroke subtypes and COVID-19 susceptibility to understand whether biological mechanisms specific to SARS-CoV-2 uptake/infection could be leading to excess stroke risk in this population., Patients and Methods: We constructed a polygenic risk score (PRS) of COVID-19 susceptibility and tested its association with stroke subtypes using individual- and summary-level genetic data (SiGN, MEGASTROKE). We generated co-expression networks of genes involved in SARS-CoV-2 uptake/infection ( ACE2 , TMPRSS2 , BEST3 , ISLR2 and ADAM17 ) based on existing tissue expression libraries. Gene-based association testing was performed using S-PrediXcan and VEGAS2. Permutation independence tests were performed to assess SARS-CoV-2-related gene enrichment in stroke and its subtypes., Results: Our PRS demonstrated an association between COVID-19 susceptibility and LAS in SiGN (OR = 1.05 per SD increase, 95% CI: (1.00, 1.10), p = 0.04) and MEGASTROKE (β = 0.510, 95% CI: (0.242, 0.779), FDR-p = 0.0019). The SARS-CoV-2 risk-related ISLR2 co-expression gene network was significantly associated with genetic risk of LAS in aorta, tibial arteries, and multiple brain regions (P < 0.05)., Conclusion: Presence of genetic correlation and significant pathway enrichment suggest that increases in LAS risk reported in COVID-19 patients may be intrinsic to the viral infection, rather than a more generalized response to severe illness.
- Published
- 2022
- Full Text
- View/download PDF
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