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1. Multi-omics and pathway analyses of genome-wide associations implicate regulation and immunity in verbal declarative memory performance

Author

Mei, Hao, Simino, Jeannette, Li, Lianna, Jiang, Fan, Bis, Joshua C., Davies, Gail, Hill, W David, Xia, Charley, Gudnason, Vilmundur, Yang, Qiong, Lahti, Jari, Smith, Jennifer A., Kirin, Mirna, De Jager, Philip, Armstrong, Nicola J., Ghanbari, Mohsen, Kolcic, Ivana, Moran, Christopher, Teumer, Alexander, Sargurupremraj, Murali, Mahmud, Shamsed, Fornage, Myriam, Zhao, Wei, Satizabal, Claudia L., Polasek, Ozren, Räikkönen, Katri, Liewald, David C., Homuth, Georg, Callisaya, Michele, Mather, Karen A., Windham, B. Gwen, Zemunik, Tatijana, Palotie, Aarno, Pattie, Alison, van der Auwera, Sandra, Thalamuthu, Anbupalam, Knopman, David S., Rudan, Igor, Starr, John M., Wittfeld, Katharina, Kochan, Nicole A., Griswold, Michael E., Vitart, Veronique, Brodaty, Henry, Gottesman, Rebecca, Cox, Simon R., Psaty, Bruce M., Boerwinkle, Eric, Chasman, Daniel I., Grodstein, Francine, Sachdev, Perminder S., Srikanth, Velandai, Hayward, Caroline, Wilson, James F., Eriksson, Johan G., Kardia, Sharon L. R., Grabe, Hans J., Bennett, David A., Ikram, M. Arfan, Deary, Ian J., van Duijn, Cornelia M., Launer, Lenore, Fitzpatrick, Annette L., Seshadri, Sudha, Bressler, Jan, Debette, Stephanie, and Mosley, Jr, Thomas H.

Published
2024
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2. Education and Cardiovascular Health as Effect Modifiers of APOE ε4 on Dementia: The Atherosclerosis Risk in Communities Study.

Author

Lee, Mark, Hughes, Timothy M, George, Kristen M, Griswold, Michael E, Sedaghat, Sanaz, Simino, Jeannette, and Lutsey, Pamela L

Subjects
Atherosclerosis, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Genetics, Prevention, Dementia, Alzheimer's Disease, Brain Disorders, Neurosciences, Neurodegenerative, Cardiovascular, Aging, Acquired Cognitive Impairment, Heart Disease, Clinical Research, 2.3 Psychological, social and economic factors, Aetiology, 2.4 Surveillance and distribution, Neurological, Quality Education, Apolipoprotein E4, Apolipoproteins E, Cohort Studies, Female, Genotype, Humans, Male, Prospective Studies, Risk Factors, Cognitive aging, Gene by environment, Life Simple 7, Clinical Sciences, Gerontology
Abstract

Both education and cardiovascular risk factors are strongly associated with dementia risk. However, it is not clear whether these associations persist or vary among individuals with high genetic risk for Alzheimer's disease. We examined the interactive relationship between lifestyle and genetic dementia risk factors in a prospective cohort study. Our data came from the Atherosclerosis Risk in Communities study participants (n = 13 715; baseline age 45-64; 25% Black; 55% female), who were followed for incident dementia from 1987 through 2017. We used Cox proportional hazard models to estimate the risk of dementia (ascertained through in-person examination, telephone cognitive screeners, and/or hospital and death records) associated with baseline education and cardiovascular risk factors (measured using the American Heart Association's "Life Simple 7") among ε4 carriers and non-carriers separately. We also examined differences by race and sex. Two thousand two hundred and twenty-six incident dementia cases occurred over a median 25 years of follow-up. Lower educational attainment and poorer cardiovascular health were associated with greater risk of incident dementia. There was an education by apolipoprotein E (APOE) status interaction (p = .005) whereby the association of education and dementia was weaker for ε4 carriers (HR college graduates vs less than high school: 0.71 [0.59-0.84] than non-carriers (0.54 [0.47-0.63]). There was no interaction between APOE status and cardiovascular health on dementia risk. These relationships did not vary significantly by race or sex. Education and cardiovascular health were associated with lower dementia risk regardless of APOE genotype, though the protective effects of education were somewhat diminished among ε4 carriers.

Published
2022

3. Associations of mid‐to‐late‐life inflammation with late‐life mobility and the influences of chronic comorbidities, race, and social determinants of health: The Atherosclerosis Risk in Communities Study

Author

Parker, Kirby G., primary, Windham, B. Gwen, additional, Blackshear, Chad, additional, Walker, Keenan A., additional, Parker, Sara B., additional, Hoogeveen, Ron C., additional, Ballantyne, Christie M., additional, Kucharska‐Newton, Anna, additional, Palta, Priya, additional, Selvin, Elizabeth, additional, Vassilaki, Maria, additional, Mosley, Thomas H., additional, and Griswold, Michael E., additional

Published
2024
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5. Author Correction: Study of 300,486 individuals identifies 148 independent genetic loci influencing general cognitive function.

Author

Davies, Gail, Lam, Max, Harris, Sarah E, Trampush, Joey W, Luciano, Michelle, Hill, W David, Hagenaars, Saskia P, Ritchie, Stuart J, Marioni, Riccardo E, Fawns-Ritchie, Chloe, Liewald, David CM, Okely, Judith A, Ahola-Olli, Ari V, Barnes, Catriona LK, Bertram, Lars, Bis, Joshua C, Burdick, Katherine E, Christoforou, Andrea, DeRosse, Pamela, Djurovic, Srdjan, Espeseth, Thomas, Giakoumaki, Stella, Giddaluru, Sudheer, Gustavson, Daniel E, Hayward, Caroline, Hofer, Edith, Ikram, M Arfan, Karlsson, Robert, Knowles, Emma, Lahti, Jari, Leber, Markus, Li, Shuo, Mather, Karen A, Melle, Ingrid, Morris, Derek, Oldmeadow, Christopher, Palviainen, Teemu, Payton, Antony, Pazoki, Raha, Petrovic, Katja, Reynolds, Chandra A, Sargurupremraj, Muralidharan, Scholz, Markus, Smith, Jennifer A, Smith, Albert V, Terzikhan, Natalie, Thalamuthu, Anbupalam, Trompet, Stella, van der Lee, Sven J, Ware, Erin B, Windham, B Gwen, Wright, Margaret J, Yang, Jingyun, Yu, Jin, Ames, David, Amin, Najaf, Amouyel, Philippe, Andreassen, Ole A, Armstrong, Nicola J, Assareh, Amelia A, Attia, John R, Attix, Deborah, Avramopoulos, Dimitrios, Bennett, David A, Böhmer, Anne C, Boyle, Patricia A, Brodaty, Henry, Campbell, Harry, Cannon, Tyrone D, Cirulli, Elizabeth T, Congdon, Eliza, Conley, Emily Drabant, Corley, Janie, Cox, Simon R, Dale, Anders M, Dehghan, Abbas, Dick, Danielle, Dickinson, Dwight, Eriksson, Johan G, Evangelou, Evangelos, Faul, Jessica D, Ford, Ian, Freimer, Nelson A, Gao, He, Giegling, Ina, Gillespie, Nathan A, Gordon, Scott D, Gottesman, Rebecca F, Griswold, Michael E, Gudnason, Vilmundur, Harris, Tamara B, Hartmann, Annette M, Hatzimanolis, Alex, Heiss, Gerardo, Holliday, Elizabeth G, Joshi, Peter K, Kähönen, Mika, Kardia, Sharon LR, Karlsson, Ida, and Kleineidam, Luca

Abstract

Christina M. Lill, who contributed to analysis of data, was inadvertently omitted from the author list in the originally published version of this article. This has now been corrected in both the PDF and HTML versions of the article.

Published
2019

6. Genetic and lifestyle risk factors for MRI-defined brain infarcts in a population-based setting

Author

Chauhan, Ganesh, Adams, Hieab HH, Satizabal, Claudia L, Bis, Joshua C, Teumer, Alexander, Sargurupremraj, Muralidharan, Hofer, Edith, Trompet, Stella, Hilal, Saima, Smith, Albert Vernon, Jian, Xueqiu, Malik, Rainer, Traylor, Matthew, Pulit, Sara L, Amouyel, Philippe, Mazoyer, Bernard, Zhu, Yi-Cheng, Kaffashian, Sara, Schilling, Sabrina, Beecham, Gary W, Montine, Thomas J, Schellenberg, Gerard D, Kjartansson, Olafur, Guðnason, Vilmundur, Knopman, David S, Griswold, Michael E, Windham, B Gwen, Gottesman, Rebecca F, Mosley, Thomas H, Schmidt, Reinhold, Saba, Yasaman, Schmidt, Helena, Takeuchi, Fumihiko, Yamaguchi, Shuhei, Nabika, Toru, Kato, Norihiro, Rajan, Kumar B, Aggarwal, Neelum T, De Jager, Philip L, Evans, Denis A, Psaty, Bruce M, Rotter, Jerome I, Rice, Kenneth, Lopez, Oscar L, Liao, Jiemin, Chen, Christopher, Cheng, Ching-Yu, Wong, Tien Y, Ikram, Mohammad K, van der Lee, Sven J, Amin, Najaf, Chouraki, Vincent, DeStefano, Anita L, Aparicio, Hugo J, Romero, Jose R, Maillard, Pauline, DeCarli, Charles, Wardlaw, Joanna M, del C. Valdés Hernández, Maria, Luciano, Michelle, Liewald, David, Deary, Ian J, Starr, John M, Bastin, Mark E, Maniega, Susana Muñoz, Slagboom, P Eline, Beekman, Marian, Deelen, Joris, Uh, Hae-Won, Lemmens, Robin, Brodaty, Henry, Wright, Margaret J, Ames, David, Boncoraglio, Giorgio B, Hopewell, Jemma C, Beecham, Ashley H, Blanton, Susan H, Wright, Clinton B, Sacco, Ralph L, Wen, Wei, Thalamuthu, Anbupalam, Armstrong, Nicola J, Chong, Elizabeth, Schofield, Peter R, Kwok, John B, van der Grond, Jeroen, Stott, David J, Ford, Ian, Jukema, J Wouter, Vernooij, Meike W, Hofman, Albert, Uitterlinden, André G, van der Lugt, Aad, Wittfeld, Katharina, Grabe, Hans J, Hosten, Norbert, von Sarnowski, Bettina, Völker, Uwe, Levi, Christopher, and Jimenez-Conde, Jordi

Subjects
Biomedical and Clinical Sciences, Neurosciences, Clinical Sciences, Brain Disorders, Genetics, Cardiovascular, Prevention, Aging, Cerebrovascular, Stroke, Human Genome, 2.1 Biological and endogenous factors, Good Health and Well Being, Stroke Genetics Network (SiGN), the International Stroke Genetics Consortium (ISGC), METASTROKE, Alzheimer's Disease Genetics Consortium (ADGC), and the Neurology Working Group of the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) Consortium, Cognitive Sciences, Neurology & Neurosurgery, Clinical sciences
Abstract

ObjectiveTo explore genetic and lifestyle risk factors of MRI-defined brain infarcts (BI) in large population-based cohorts.MethodsWe performed meta-analyses of genome-wide association studies (GWAS) and examined associations of vascular risk factors and their genetic risk scores (GRS) with MRI-defined BI and a subset of BI, namely, small subcortical BI (SSBI), in 18 population-based cohorts (n = 20,949) from 5 ethnicities (3,726 with BI, 2,021 with SSBI). Top loci were followed up in 7 population-based cohorts (n = 6,862; 1,483 with BI, 630 with SBBI), and we tested associations with related phenotypes including ischemic stroke and pathologically defined BI.ResultsThe mean prevalence was 17.7% for BI and 10.5% for SSBI, steeply rising after age 65. Two loci showed genome-wide significant association with BI: FBN2, p = 1.77 × 10-8; and LINC00539/ZDHHC20, p = 5.82 × 10-9. Both have been associated with blood pressure (BP)-related phenotypes, but did not replicate in the smaller follow-up sample or show associations with related phenotypes. Age- and sex-adjusted associations with BI and SSBI were observed for BP traits (p value for BI, p [BI] = 9.38 × 10-25; p [SSBI] = 5.23 × 10-14 for hypertension), smoking (p [BI] = 4.4 × 10-10; p [SSBI] = 1.2 × 10-4), diabetes (p [BI] = 1.7 × 10-8; p [SSBI] = 2.8 × 10-3), previous cardiovascular disease (p [BI] = 1.0 × 10-18; p [SSBI] = 2.3 × 10-7), stroke (p [BI] = 3.9 × 10-69; p [SSBI] = 3.2 × 10-24), and MRI-defined white matter hyperintensity burden (p [BI] = 1.43 × 10-157; p [SSBI] = 3.16 × 10-106), but not with body mass index or cholesterol. GRS of BP traits were associated with BI and SSBI (p ≤ 0.0022), without indication of directional pleiotropy.ConclusionIn this multiethnic GWAS meta-analysis, including over 20,000 population-based participants, we identified genetic risk loci for BI requiring validation once additional large datasets become available. High BP, including genetically determined, was the most significant modifiable, causal risk factor for BI.

Published
2019

7. Study of 300,486 individuals identifies 148 independent genetic loci influencing general cognitive function.

Author

Davies, Gail, Lam, Max, Harris, Sarah E, Trampush, Joey W, Luciano, Michelle, Hill, W David, Hagenaars, Saskia P, Ritchie, Stuart J, Marioni, Riccardo E, Fawns-Ritchie, Chloe, Liewald, David CM, Okely, Judith A, Ahola-Olli, Ari V, Barnes, Catriona LK, Bertram, Lars, Bis, Joshua C, Burdick, Katherine E, Christoforou, Andrea, DeRosse, Pamela, Djurovic, Srdjan, Espeseth, Thomas, Giakoumaki, Stella, Giddaluru, Sudheer, Gustavson, Daniel E, Hayward, Caroline, Hofer, Edith, Ikram, M Arfan, Karlsson, Robert, Knowles, Emma, Lahti, Jari, Leber, Markus, Li, Shuo, Mather, Karen A, Melle, Ingrid, Morris, Derek, Oldmeadow, Christopher, Palviainen, Teemu, Payton, Antony, Pazoki, Raha, Petrovic, Katja, Reynolds, Chandra A, Sargurupremraj, Muralidharan, Scholz, Markus, Smith, Jennifer A, Smith, Albert V, Terzikhan, Natalie, Thalamuthu, Anbupalam, Trompet, Stella, van der Lee, Sven J, Ware, Erin B, Windham, B Gwen, Wright, Margaret J, Yang, Jingyun, Yu, Jin, Ames, David, Amin, Najaf, Amouyel, Philippe, Andreassen, Ole A, Armstrong, Nicola J, Assareh, Amelia A, Attia, John R, Attix, Deborah, Avramopoulos, Dimitrios, Bennett, David A, Böhmer, Anne C, Boyle, Patricia A, Brodaty, Henry, Campbell, Harry, Cannon, Tyrone D, Cirulli, Elizabeth T, Congdon, Eliza, Conley, Emily Drabant, Corley, Janie, Cox, Simon R, Dale, Anders M, Dehghan, Abbas, Dick, Danielle, Dickinson, Dwight, Eriksson, Johan G, Evangelou, Evangelos, Faul, Jessica D, Ford, Ian, Freimer, Nelson A, Gao, He, Giegling, Ina, Gillespie, Nathan A, Gordon, Scott D, Gottesman, Rebecca F, Griswold, Michael E, Gudnason, Vilmundur, Harris, Tamara B, Hartmann, Annette M, Hatzimanolis, Alex, Heiss, Gerardo, Holliday, Elizabeth G, Joshi, Peter K, Kähönen, Mika, Kardia, Sharon LR, Karlsson, Ida, and Kleineidam, Luca

Subjects
Humans, Neurodegenerative Diseases, Genetic Predisposition to Disease, Cognition, Reaction Time, Mental Disorders, Multifactorial Inheritance, Polymorphism, Single Nucleotide, Adolescent, Adult, Aged, Aged, 80 and over, Middle Aged, Young Adult, Genetic Loci, Neurodevelopmental Disorders, Prevention, Behavioral and Social Science, Mental Health, Neurosciences, Biotechnology, Genetics, Human Genome, Neurological, Mental health
Abstract

General cognitive function is a prominent and relatively stable human trait that is associated with many important life outcomes. We combine cognitive and genetic data from the CHARGE and COGENT consortia, and UK Biobank (total N = 300,486; age 16-102) and find 148 genome-wide significant independent loci (P

Published
2018

8. Gene-by-Psychosocial Factor Interactions Influence Diastolic Blood Pressure in European and African Ancestry Populations: Meta-Analysis of Four Cohort Studies

Author

Smith, Jennifer A, Zhao, Wei, Yasutake, Kalyn, August, Carmella, Ratliff, Scott M, Faul, Jessica D, Boerwinkle, Eric, Chakravarti, Aravinda, Roux, Ana V Diez, Gao, Yan, Griswold, Michael E, Heiss, Gerardo, Kardia, Sharon LR, Morrison, Alanna C, Musani, Solomon K, Mwasongwe, Stanford, North, Kari E, Rose, Kathryn M, Sims, Mario, Sun, Yan V, Weir, David R, and Needham, Belinda L

Subjects
Mental Health, Behavioral and Social Science, Human Genome, Genetics, Depression, Clinical Research, 2.1 Biological and endogenous factors, Aetiology, Black or African American, Blood Pressure, Cohort Studies, Gene-Environment Interaction, Humans, Psychology, Risk Factors, Socioeconomic Factors, United States, White People, blood pressure, hypertension, genetics, gene-by-environment interaction, non-burden test, socioeconomic status, psychosocial factors, depression, chronic burden, Toxicology
Abstract

Inter-individual variability in blood pressure (BP) is influenced by both genetic and non-genetic factors including socioeconomic and psychosocial stressors. A deeper understanding of the gene-by-socioeconomic/psychosocial factor interactions on BP may help to identify individuals that are genetically susceptible to high BP in specific social contexts. In this study, we used a genomic region-based method for longitudinal analysis, Longitudinal Gene-Environment-Wide Interaction Studies (LGEWIS), to evaluate the effects of interactions between known socioeconomic/psychosocial and genetic risk factors on systolic and diastolic BP in four large epidemiologic cohorts of European and/or African ancestry. After correction for multiple testing, two interactions were significantly associated with diastolic BP. In European ancestry participants, outward/trait anger score had a significant interaction with the C10orf107 genomic region (p = 0.0019). In African ancestry participants, depressive symptom score had a significant interaction with the HFE genomic region (p = 0.0048). This study provides a foundation for using genomic region-based longitudinal analysis to identify subgroups of the population that may be at greater risk of elevated BP due to the combined influence of genetic and socioeconomic/psychosocial risk factors.

Published
2017

10. Novel genetic loci associated with hippocampal volume.

Author

Hibar, Derrek P, Adams, Hieab HH, Jahanshad, Neda, Chauhan, Ganesh, Stein, Jason L, Hofer, Edith, Renteria, Miguel E, Bis, Joshua C, Arias-Vasquez, Alejandro, Ikram, M Kamran, Desrivières, Sylvane, Vernooij, Meike W, Abramovic, Lucija, Alhusaini, Saud, Amin, Najaf, Andersson, Micael, Arfanakis, Konstantinos, Aribisala, Benjamin S, Armstrong, Nicola J, Athanasiu, Lavinia, Axelsson, Tomas, Beecham, Ashley H, Beiser, Alexa, Bernard, Manon, Blanton, Susan H, Bohlken, Marc M, Boks, Marco P, Bralten, Janita, Brickman, Adam M, Carmichael, Owen, Chakravarty, M Mallar, Chen, Qiang, Ching, Christopher RK, Chouraki, Vincent, Cuellar-Partida, Gabriel, Crivello, Fabrice, Den Braber, Anouk, Doan, Nhat Trung, Ehrlich, Stefan, Giddaluru, Sudheer, Goldman, Aaron L, Gottesman, Rebecca F, Grimm, Oliver, Griswold, Michael E, Guadalupe, Tulio, Gutman, Boris A, Hass, Johanna, Haukvik, Unn K, Hoehn, David, Holmes, Avram J, Hoogman, Martine, Janowitz, Deborah, Jia, Tianye, Jørgensen, Kjetil N, Karbalai, Nazanin, Kasperaviciute, Dalia, Kim, Sungeun, Klein, Marieke, Kraemer, Bernd, Lee, Phil H, Liewald, David CM, Lopez, Lorna M, Luciano, Michelle, Macare, Christine, Marquand, Andre F, Matarin, Mar, Mather, Karen A, Mattheisen, Manuel, McKay, David R, Milaneschi, Yuri, Muñoz Maniega, Susana, Nho, Kwangsik, Nugent, Allison C, Nyquist, Paul, Loohuis, Loes M Olde, Oosterlaan, Jaap, Papmeyer, Martina, Pirpamer, Lukas, Pütz, Benno, Ramasamy, Adaikalavan, Richards, Jennifer S, Risacher, Shannon L, Roiz-Santiañez, Roberto, Rommelse, Nanda, Ropele, Stefan, Rose, Emma J, Royle, Natalie A, Rundek, Tatjana, Sämann, Philipp G, Saremi, Arvin, Satizabal, Claudia L, Schmaal, Lianne, Schork, Andrew J, Shen, Li, Shin, Jean, Shumskaya, Elena, Smith, Albert V, Sprooten, Emma, Strike, Lachlan T, and Teumer, Alexander

Subjects
Hippocampus, Humans, Alzheimer Disease, Genetic Predisposition to Disease, Protein-Serine-Threonine Kinases, Glycoproteins, Microtubule-Associated Proteins, Nerve Tissue Proteins, Organ Size, Cohort Studies, Adolescent, Adult, Aged, Aged, 80 and over, Middle Aged, Child, Female, Male, Genome-Wide Association Study, Young Adult, Methionine Sulfoxide Reductases, Genetic Loci, Dipeptidyl Peptidase 4, Human Genome, Aging, Brain Disorders, Clinical Research, Acquired Cognitive Impairment, Neurodegenerative, Dementia, Neurosciences, Prevention, Genetics, Alzheimer's Disease, Alzheimer's Disease including Alzheimer's Disease Related Dementias (AD/ADRD), Mental Health, 2.1 Biological and endogenous factors, Mental health, Neurological
Abstract

The hippocampal formation is a brain structure integrally involved in episodic memory, spatial navigation, cognition and stress responsiveness. Structural abnormalities in hippocampal volume and shape are found in several common neuropsychiatric disorders. To identify the genetic underpinnings of hippocampal structure here we perform a genome-wide association study (GWAS) of 33,536 individuals and discover six independent loci significantly associated with hippocampal volume, four of them novel. Of the novel loci, three lie within genes (ASTN2, DPP4 and MAST4) and one is found 200 kb upstream of SHH. A hippocampal subfield analysis shows that a locus within the MSRB3 gene shows evidence of a localized effect along the dentate gyrus, subiculum, CA1 and fissure. Further, we show that genetic variants associated with decreased hippocampal volume are also associated with increased risk for Alzheimer's disease (rg=-0.155). Our findings suggest novel biological pathways through which human genetic variation influences hippocampal volume and risk for neuropsychiatric illness.

Published
2017

11. Novel genetic loci underlying human intracranial volume identified through genome-wide association

Author

Adams, Hieab HH, Hibar, Derrek P, Chouraki, Vincent, Stein, Jason L, Nyquist, Paul A, Rentería, Miguel E, Trompet, Stella, Arias-Vasquez, Alejandro, Seshadri, Sudha, Desrivières, Sylvane, Beecham, Ashley H, Jahanshad, Neda, Wittfeld, Katharina, Van der Lee, Sven J, Abramovic, Lucija, Alhusaini, Saud, Amin, Najaf, Andersson, Micael, Arfanakis, Konstantinos, Aribisala, Benjamin S, Armstrong, Nicola J, Athanasiu, Lavinia, Axelsson, Tomas, Beiser, Alexa, Bernard, Manon, Bis, Joshua C, Blanken, Laura ME, Blanton, Susan H, Bohlken, Marc M, Boks, Marco P, Bralten, Janita, Brickman, Adam M, Carmichael, Owen, Chakravarty, M Mallar, Chauhan, Ganesh, Chen, Qiang, Ching, Christopher RK, Cuellar-Partida, Gabriel, Braber, Anouk Den, Doan, Nhat Trung, Ehrlich, Stefan, Filippi, Irina, Ge, Tian, Giddaluru, Sudheer, Goldman, Aaron L, Gottesman, Rebecca F, Greven, Corina U, Grimm, Oliver, Griswold, Michael E, Guadalupe, Tulio, Hass, Johanna, Haukvik, Unn K, Hilal, Saima, Hofer, Edith, Hoehn, David, Holmes, Avram J, Hoogman, Martine, Janowitz, Deborah, Jia, Tianye, Kasperaviciute, Dalia, Kim, Sungeun, Klein, Marieke, Kraemer, Bernd, Lee, Phil H, Liao, Jiemin, Liewald, David CM, Lopez, Lorna M, Luciano, Michelle, Macare, Christine, Marquand, Andre, Matarin, Mar, Mather, Karen A, Mattheisen, Manuel, Mazoyer, Bernard, McKay, David R, McWhirter, Rebekah, Milaneschi, Yuri, Mirza-Schreiber, Nazanin, Muetzel, Ryan L, Maniega, Susana Muñoz, Nho, Kwangsik, Nugent, Allison C, Loohuis, Loes M Olde, Oosterlaan, Jaap, Papmeyer, Martina, Pappa, Irene, Pirpamer, Lukas, Pudas, Sara, Pütz, Benno, Rajan, Kumar B, Ramasamy, Adaikalavan, Richards, Jennifer S, Risacher, Shannon L, Roiz-Santiañez, Roberto, Rommelse, Nanda, Rose, Emma J, Royle, Natalie A, Rundek, Tatjana, Sämann, Philipp G, and Satizabal, Claudia L

Subjects
Biological Psychology, Biomedical and Clinical Sciences, Neurosciences, Psychology, Human Genome, Biotechnology, Brain Disorders, Clinical Research, Aging, Prevention, Neurodegenerative, Genetics, 2.1 Biological and endogenous factors, Brain, Cognition, Genetic Loci, Genetic Predisposition to Disease, Genome-Wide Association Study, Humans, Oncogene Protein v-akt, Parkinson Disease, Phenotype, Phosphatidylinositol 3-Kinases, Polymorphism, Single Nucleotide, White People, Cognitive Sciences, Neurology & Neurosurgery, Biological psychology
Abstract

Intracranial volume reflects the maximally attained brain size during development, and remains stable with loss of tissue in late life. It is highly heritable, but the underlying genes remain largely undetermined. In a genome-wide association study of 32,438 adults, we discovered five previously unknown loci for intracranial volume and confirmed two known signals. Four of the loci were also associated with adult human stature, but these remained associated with intracranial volume after adjusting for height. We found a high genetic correlation with child head circumference (ρgenetic = 0.748), which indicates a similar genetic background and allowed us to identify four additional loci through meta-analysis (Ncombined = 37,345). Variants for intracranial volume were also related to childhood and adult cognitive function, and Parkinson's disease, and were enriched near genes involved in growth pathways, including PI3K-AKT signaling. These findings identify the biological underpinnings of intracranial volume and their link to physiological and pathological traits.

Published
2016

13. Association Between Periodontal Disease and Kidney Function Decline in African Americans: The Jackson Heart Study

Author

Grubbs, Vanessa, Vittinghoff, Eric, Beck, James D, Kshirsagar, Abhijit V, Wang, Wei, Griswold, Michael E, Powe, Neil R, Correa, Adolfo, and Young, Bessie

Subjects
Biomedical and Clinical Sciences, Dentistry, Kidney Disease, Clinical Research, Prevention, Infectious Diseases, Aging, Cardiovascular, Dental/Oral and Craniofacial Disease, Renal and urogenital, Black or African American, Age Factors, Aged, Cohort Studies, Creatinine, Diabetes Complications, Disease Progression, Female, Follow-Up Studies, Gingival Recession, Glomerular Filtration Rate, Humans, Hypertension, Income, Male, Middle Aged, Periodontal Attachment Loss, Periodontal Diseases, Periodontal Index, Periodontal Pocket, Renal Insufficiency, Chronic, Retrospective Studies, Risk Factors, Sex Factors, Smoking, African Americans, disease progression, health status disparities, periodontal disease, renal insufficiency, chronic, risk factors
Abstract

BackgroundChronic kidney disease (CKD) remains a prevalent public health problem that disproportionately affects African Americans, despite intense efforts targeting traditional risk factors. Periodontal disease, a chronic bacterial infection of the oral cavity, is both common and modifiable and has been implicated as a novel potential CKD risk factor. The authors seek to examine to what extent periodontal disease is associated with kidney function decline.MethodsThis retrospective cohort study examines 699 African American participants with preserved kidney function (defined by estimated glomerular filtration rate (eGFR) >60 mL/minute/1.73 m(2) at baseline) who underwent complete dental examinations as part of the Dental-Atherosclerosis Risk in Communities study (1996 to 1998) and subsequently enrolled in the Jackson Heart Study (2000 to 2004). Using multivariable Poisson regression, the authors examined the association of periodontal disease (severe versus non-severe) with incident CKD, defined as incident eGFR

Published
2015

15. Association of Low-Frequency and Rare Coding-Sequence Variants with Blood Lipids and Coronary Heart Disease in 56,000 Whites and Blacks

Author

Peloso, Gina M, Auer, Paul L, Bis, Joshua C, Voorman, Arend, Morrison, Alanna C, Stitziel, Nathan O, Brody, Jennifer A, Khetarpal, Sumeet A, Crosby, Jacy R, Fornage, Myriam, Isaacs, Aaron, Jakobsdottir, Johanna, Feitosa, Mary F, Davies, Gail, Huffman, Jennifer E, Manichaikul, Ani, Davis, Brian, Lohman, Kurt, Joon, Aron Y, Smith, Albert V, Grove, Megan L, Zanoni, Paolo, Redon, Valeska, Demissie, Serkalem, Lawson, Kim, Peters, Ulrike, Carlson, Christopher, Jackson, Rebecca D, Ryckman, Kelli K, Mackey, Rachel H, Robinson, Jennifer G, Siscovick, David S, Schreiner, Pamela J, Mychaleckyj, Josyf C, Pankow, James S, Hofman, Albert, Uitterlinden, Andre G, Harris, Tamara B, Taylor, Kent D, Stafford, Jeanette M, Reynolds, Lindsay M, Marioni, Riccardo E, Dehghan, Abbas, Franco, Oscar H, Patel, Aniruddh P, Lu, Yingchang, Hindy, George, Gottesman, Omri, Bottinger, Erwin P, Melander, Olle, Orho-Melander, Marju, Loos, Ruth JF, Duga, Stefano, Merlini, Piera Angelica, Farrall, Martin, Goel, Anuj, Asselta, Rosanna, Girelli, Domenico, Martinelli, Nicola, Shah, Svati H, Kraus, William E, Li, Mingyao, Rader, Daniel J, Reilly, Muredach P, McPherson, Ruth, Watkins, Hugh, Ardissino, Diego, Project, NHLBI GO Exome Sequencing, Zhang, Qunyuan, Wang, Judy, Tsai, Michael Y, Taylor, Herman A, Correa, Adolfo, Griswold, Michael E, Lange, Leslie A, Starr, John M, Rudan, Igor, Eiriksdottir, Gudny, Launer, Lenore J, Ordovas, Jose M, Levy, Daniel, Chen, Y-D Ida, Reiner, Alexander P, Hayward, Caroline, Polasek, Ozren, Deary, Ian J, Borecki, Ingrid B, Liu, Yongmei, Gudnason, Vilmundur, Wilson, James G, van Duijn, Cornelia M, Kooperberg, Charles, Rich, Stephen S, Psaty, Bruce M, Rotter, Jerome I, O’Donnell, Christopher J, Rice, Kenneth, Boerwinkle, Eric, Kathiresan, Sekar, and Cupples, L Adrienne

Subjects
Biological Sciences, Biomedical and Clinical Sciences, Genetics, Heart Disease - Coronary Heart Disease, Human Genome, Cardiovascular, Heart Disease, Atherosclerosis, Aetiology, 2.1 Biological and endogenous factors, 1-Alkyl-2-acetylglycerophosphocholine Esterase, Adult, Aged, Alleles, Animals, Black People, Cholesterol, HDL, Cholesterol, LDL, Cohort Studies, Coronary Disease, Female, Gene Frequency, Genetic Association Studies, Genetic Code, Genetic Variation, Humans, Linear Models, Male, Mice, Mice, Inbred C57BL, Microtubule-Associated Proteins, Middle Aged, Phenotype, Sequence Analysis, DNA, Subtilisins, Triglycerides, White People, NHLBI GO Exome Sequencing Project, Medical and Health Sciences, Genetics & Heredity, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

Low-frequency coding DNA sequence variants in the proprotein convertase subtilisin/kexin type 9 gene (PCSK9) lower plasma low-density lipoprotein cholesterol (LDL-C), protect against risk of coronary heart disease (CHD), and have prompted the development of a new class of therapeutics. It is uncertain whether the PCSK9 example represents a paradigm or an isolated exception. We used the "Exome Array" to genotype >200,000 low-frequency and rare coding sequence variants across the genome in 56,538 individuals (42,208 European ancestry [EA] and 14,330 African ancestry [AA]) and tested these variants for association with LDL-C, high-density lipoprotein cholesterol (HDL-C), and triglycerides. Although we did not identify new genes associated with LDL-C, we did identify four low-frequency (frequencies between 0.1% and 2%) variants (ANGPTL8 rs145464906 [c.361C>T; p.Gln121*], PAFAH1B2 rs186808413 [c.482C>T; p.Ser161Leu], COL18A1 rs114139997 [c.331G>A; p.Gly111Arg], and PCSK7 rs142953140 [c.1511G>A; p.Arg504His]) with large effects on HDL-C and/or triglycerides. None of these four variants was associated with risk for CHD, suggesting that examples of low-frequency coding variants with robust effects on both lipids and CHD will be limited.

Published
2014

16. Whole-Exome Sequencing Identifies Rare and Low-Frequency Coding Variants Associated with LDL Cholesterol

Author

Lange, Leslie A, Hu, Youna, Zhang, He, Xue, Chenyi, Schmidt, Ellen M, Tang, Zheng-Zheng, Bizon, Chris, Lange, Ethan M, Smith, Joshua D, Turner, Emily H, Jun, Goo, Kang, Hyun Min, Peloso, Gina, Auer, Paul, Li, Kuo-ping, Flannick, Jason, Zhang, Ji, Fuchsberger, Christian, Gaulton, Kyle, Lindgren, Cecilia, Locke, Adam, Manning, Alisa, Sim, Xueling, Rivas, Manuel A, Holmen, Oddgeir L, Gottesman, Omri, Lu, Yingchang, Ruderfer, Douglas, Stahl, Eli A, Duan, Qing, Li, Yun, Durda, Peter, Jiao, Shuo, Isaacs, Aaron, Hofman, Albert, Bis, Joshua C, Correa, Adolfo, Griswold, Michael E, Jakobsdottir, Johanna, Smith, Albert V, Schreiner, Pamela J, Feitosa, Mary F, Zhang, Qunyuan, Huffman, Jennifer E, Crosby, Jacy, Wassel, Christina L, Do, Ron, Franceschini, Nora, Martin, Lisa W, Robinson, Jennifer G, Assimes, Themistocles L, Crosslin, David R, Rosenthal, Elisabeth A, Tsai, Michael, Rieder, Mark J, Farlow, Deborah N, Folsom, Aaron R, Lumley, Thomas, Fox, Ervin R, Carlson, Christopher S, Peters, Ulrike, Jackson, Rebecca D, van Duijn, Cornelia M, Uitterlinden, André G, Levy, Daniel, Rotter, Jerome I, Taylor, Herman A, Gudnason, Vilmundur, Siscovick, David S, Fornage, Myriam, Borecki, Ingrid B, Hayward, Caroline, Rudan, Igor, Chen, Y Eugene, Bottinger, Erwin P, Loos, Ruth JF, Sætrom, Pål, Hveem, Kristian, Boehnke, Michael, Groop, Leif, McCarthy, Mark, Meitinger, Thomas, Ballantyne, Christie M, Gabriel, Stacey B, O’Donnell, Christopher J, Post, Wendy S, North, Kari E, Reiner, Alexander P, Boerwinkle, Eric, Psaty, Bruce M, Altshuler, David, Kathiresan, Sekar, Lin, Dan-Yu, Jarvik, Gail P, Cupples, L Adrienne, Kooperberg, Charles, Wilson, James G, Nickerson, Deborah A, Abecasis, Goncalo R, and Rich, Stephen S

Subjects
Epidemiology, Biological Sciences, Health Sciences, Genetics, Human Genome, Prevention, Clinical Research, Heart Disease, Cardiovascular, Atherosclerosis, Aetiology, 2.1 Biological and endogenous factors, Adult, Aged, Apolipoproteins E, Cholesterol, LDL, Cohort Studies, Dyslipidemias, Exome, Female, Follow-Up Studies, Gene Frequency, Genetic Code, Genome-Wide Association Study, Genotype, Humans, Lipase, Male, Middle Aged, Phenotype, Polymorphism, Single Nucleotide, Proprotein Convertase 9, Proprotein Convertases, Receptors, LDL, Sequence Analysis, DNA, Serine Endopeptidases, NHLBI Grand Opportunity Exome Sequencing Project, Medical and Health Sciences, Genetics & Heredity, Biological sciences, Biomedical and clinical sciences, Health sciences
Abstract

Elevated low-density lipoprotein cholesterol (LDL-C) is a treatable, heritable risk factor for cardiovascular disease. Genome-wide association studies (GWASs) have identified 157 variants associated with lipid levels but are not well suited to assess the impact of rare and low-frequency variants. To determine whether rare or low-frequency coding variants are associated with LDL-C, we exome sequenced 2,005 individuals, including 554 individuals selected for extreme LDL-C (>98(th) or

Published
2014

17. Type 2 Diabetes and Cognitive Decline Over 14 Years in Middle-Aged African Americans and Whites: The ARIC Brain MRI Study

Author

Mayeda, Elizabeth R, Haan, Mary N, Neuhaus, John, Yaffe, Kristine, Knopman, David S, Sharrett, A Richey, Griswold, Michael E, and Mosley, Thomas H

Subjects
Epidemiology, Health Services and Systems, Health Sciences, Dementia, Aging, Neurosciences, Acquired Cognitive Impairment, Prevention, Atherosclerosis, Clinical Research, Brain Disorders, Cardiovascular, Behavioral and Social Science, Diabetes, Metabolic and endocrine, Black or African American, Aged, Cognition Disorders, Diabetes Mellitus, Type 2, Female, Humans, Incidence, Male, Memory, Middle Aged, Neuropsychological Tests, Prevalence, Risk Factors, White People, Cognitive decline, Ethnicity, Public Health and Health Services, Clinical sciences
Abstract

BackgroundDiabetes predicts late-life dementia, but the association with rate of cognitive decline is inconsistent and has rarely been examined in non-white populations, despite the high prevalence of diabetes in African Americans. We evaluated the effect of diabetes on cognitive decline in middle-aged African Americans and whites.MethodsAtherosclerosis Risk in Communities (ARIC) Brain MRI Study participants (n = 1,886, mean age = 60, 49% African American) underwent assessments of verbal memory, processing speed, and verbal fluency four times over 14 years. Using race-stratified mixed linear effects models, we examined cognitive change for participants with prevalent (baseline) diabetes and incident (diagnosed after baseline) diabetes versus those without diabetes.ResultsAfrican Americans had more advanced diabetes, as indicated by fasting blood glucose levels, anti-diabetes medication use, and cardiovascular risk profiles. African Americans with prevalent diabetes experienced 41% greater annual decline in processing speed scores (p = 0.048) and 50% greater annual decline in verbal fluency scores (p = 0.042) than those without diabetes; incident diabetes was not associated with cognitive decline. Among whites, diabetes was not associated with cognitive decline.ConclusionsPrevalent diabetes was associated with greater cognitive decline in middle-aged African Americans, possibly reflecting adverse effects of longer duration and more advanced diabetes.

Published
2014

19. Serum Proteomic Signatures of Common Health Outcomes among Older Adults.

Author

Roberts, Jackson A., Basu-Roy, Sayantani, Shin, Jong, Varma, Vijay R., Williamson, Andrew, Blackshear, Chad, Griswold, Michael E., Candia, Julián, Elango, Palchamy, Karikkineth, Ajoy C., Tanaka, Toshiko, Ferrucci, Luigi, and Thambisetty, Madhav

Subjects
OLDER people, HEALTH outcome assessment, LEAN body mass, PROTEOMICS, BLOOD proteins
Abstract

Introduction: In aging populations, the coexistence of multiple health comorbidities represents a significant challenge for clinicians and researchers. Leveraging advances in omics techniques to characterize these health conditions may provide insight into disease pathogenesis as well as reveal biomarkers for monitoring, prognostication, and diagnosis. Researchers have previously established the utility of big data approaches with respect to comprehensive health outcome measurements in younger populations, identifying protein markers that may provide significant health information with a single blood sample. Methods: Here, we employed a similar approach in two cohorts of older adults, the Baltimore Longitudinal Study of Aging (mean age = 76.12 years) and InCHIANTI Study (mean age = 66.05 years), examining the relationship between levels of serum proteins and 5 key health outcomes: kidney function, fasting glucose, physical activity, lean body mass, and percent body fat. Results: Correlations between proteins and health outcomes were primarily shared across both older adult cohorts. We further identified that most proteins associated with health outcomes in the older adult cohorts were not associated with the same outcomes in a prior study of a younger population. A subset of proteins, adiponectin, MIC-1, and NCAM-120, were associated with at least three health outcomes in both older adult cohorts but not in the previously published younger cohort, suggesting that they may represent plausible markers of general health in older adult populations. Conclusion: Taken together, these findings suggest that comprehensive protein health markers have utility in aging populations and are distinct from those identified in younger adults, indicating unique mechanisms of disease with aging. [ABSTRACT FROM AUTHOR]

Published
2024
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20. Calorie restriction modulates the transcription of genes related to stress response and longevity in human muscle: The CALERIE study

Author

Das, Jayanta Kumar, primary, Banskota, Nirad, additional, Candia, Julián, additional, Griswold, Michael E., additional, Orenduff, Melissa, additional, de Cabo, Rafael, additional, Corcoran, David L., additional, Das, Sai Krupa, additional, De, Supriyo, additional, Huffman, Kim Marie, additional, Kraus, Virginia B., additional, Kraus, William E., additional, Martin, Corby K., additional, Racette, Susan B., additional, Redman, Leanne M., additional, Schilling, Birgit, additional, Belsky, Daniel W., additional, and Ferrucci, Luigi, additional

Published
2023
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21. Association of Olfaction and Microstructural Integrity of Brain Tissue in Community-Dwelling Adults

Author

Shrestha, Srishti, primary, Zhu, Xiaoqian, additional, Sullivan, Kevin J., additional, Blackshear, Chad, additional, Deal, Jennifer A., additional, Sharrett, A. Richey, additional, Kamath, Vidyulata, additional, Schneider, Andrea L.C., additional, Jack, Clifford R., additional, Huang, Juebin, additional, Palta, Priya, additional, Reid, Robert I., additional, Knopman, David S., additional, Gottesman, Rebecca F., additional, Chen, Honglei, additional, Windham, B. Gwen, additional, Griswold, Michael E., additional, and Mosley, Thomas H., additional

Published
2023
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23. Systematic Review for the 2017 ACC/AHA/AAPA/ABC/ACPM/AGS/APhA/ASH/ASPC/NMA/PCNA Guideline for the Prevention, Detection, Evaluation, and Management of High Blood Pressure in Adults: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines

Author

Reboussin, David M., Allen, Norrina B., Griswold, Michael E., Guallar, Eliseo, Hong, Yuling, Lackland, Daniel T., Miller, Edgar (Pete) R., III, Polonsky, Tamar, Thompson-Paul, Angela M., and Vupputuri, Suma

Published
2018
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24. Genetics of coronary artery calcification among African Americans, a meta-analysis

Author

Wojczynski, Mary K, Li, Mingyao, Bielak, Lawrence F, Kerr, Kathleen F, Reiner, Alex P, Wong, Nathan D, Yanek, Lisa R, Qu, Liming, White, Charles C, Lange, Leslie A, Ferguson, Jane F, He, Jing, Young, Taylor, Mosley, Thomas H, Smith, Jennifer A, Kral, Brian G, Guo, Xiuqing, Wong, Quenna, Ganesh, Santhi K, Heckbert, Susan R, Griswold, Michael E, O’Leary, Daniel H, Budoff, Matthew, Carr, J, Taylor,, Herman A, Bluemke, David A, Demissie, Serkalem, Hwang, Shih-Jen, Paltoo, Dina N, Polak, Joseph F, Psaty, Bruce M, Becker, Diane M, Province, Michael A, Post, Wendy S, O’Donnell, Christopher J, Wilson, James G, Harris, Tamara B, Kavousi, Maryam, Cupples, L, Rotter, Jerome I, Fornage, Myriam, Becker, Lewis C, Peyser, Patricia A, Borecki, Ingrid B, and Reilly, Muredach P

Abstract

Abstract Background Coronary heart disease (CHD) is the major cause of death in the United States. Coronary artery calcification (CAC) scores are independent predictors of CHD. African Americans (AA) have higher rates of CHD but are less well-studied in genomic studies. We assembled the largest AA data resource currently available with measured CAC to identify associated genetic variants. Methods We analyzed log transformed CAC quantity (ln(CAC + 1)), for association with ~2.5 million single nucleotide polymorphisms (SNPs) and performed an inverse-variance weighted meta-analysis on results for 5,823 AA from 8 studies. Heritability was calculated using family studies. The most significant SNPs among AAs were evaluated in European Ancestry (EA) CAC data; conversely, the significance of published SNPs for CAC/CHD in EA was queried within our AA meta-analysis. Results Heritability of CAC was lower in AA (~30%) than previously reported for EA (~50%). No SNP reached genome wide significance (p

Published
2013

25. Factors Associated with Poor Olfaction and Olfactory Decline in Older Adults in the ARIC Neurocognitive Study

Author

Shrestha, Srishti, primary, Zhu, Xiaoqian, additional, Kamath, Vidyulata, additional, Sullivan, Kevin J., additional, Deal, Jennifer A., additional, Sharrett, A. Richey, additional, Schneider, Andrea L. C., additional, Palta, Priya, additional, Gottesman, Rebecca F., additional, Windham, B. Gwen, additional, Mosley, Thomas H., additional, Griswold, Michael E., additional, and Chen, Honglei, additional

Published
2023
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29. Mid-Life Vascular Risk and Rate of Physical Function Decline Among Older Adults: The Atherosclerosis Risk in Communities (ARIC) Study.

Author

Skow, Laura F, Sharrett, A Richey, Gottesman, Rebecca F, Coresh, Josef, Deal, Jennifer A, Palta, Priya, Sullivan, Kevin J, Griswold, Michael E, Schrack, Jennifer A, and Windham, B Gwen

Subjects
OLDER people, MIDDLE age, PHYSICAL mobility, SYSTOLIC blood pressure, BLOOD pressure
Abstract

Background Physical function and its decline in older age may be connected to treatable vascular risk factors in mid-life. This study aimed to evaluate whether these factors affect the underlying rate of decline. Methods This prospective cohort included 5 481 older adults aged 67–91 in the Atherosclerosis Risk in Communities Study (mean [standard deviation { SD }] age = 75.8 [5.0], 58% women, 21% Black race) without a history of stroke. The main outcome was the rate of Short Physical Performance Battery (SPPB) decline over a median late-life follow-up of 4.8 years. Primary mid-life (aged 45–64) exposures were Visit 1 hypertension (>140/90 mm Hg or treatment), diabetes (>126 mg/dL or treatment), high cholesterol (>240 mg/dL or treatment), and smoking, and number of decades of vascular risk exposure across Visits 1–4. Results The average adjusted rate of SPPB decline (points per 5 years) for older adults was −0.79 (confidence interval [CI]: −0.87, 0.71) and was accelerated by mid-life hypertension (+57% decline vs normotension: additional decline of −0.47, 95% CI: −0.64, −0.30), diabetes (+73% decline vs no diabetes: additional decline of −0.67, 95% CI: −1.09, −0.24), elevated systolic blood pressure (+17% decline per SD : −0.16, 95% CI: −0.23, −0.10), and elevated fasting blood glucose (+16% decline per SD : −0.015, 95% CI: −0.24, −0.06). Each decade greater mid-life exposure to hypertension (+32% decline: −0.93, 95% CI: −1.25, −0.61) and diabetes (+35% decline: −1.03, 95% CI: −1.68, −0.38) was associated with faster SPPB decline. Conclusions Mid-life control of blood pressure and diabetes may offset aging-related functional decline. [ABSTRACT FROM AUTHOR]

Published
2024
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33. Correction: Dysregulation of multiple metabolic networks related to brain transmethylation and polyamine pathways in Alzheimer disease: A targeted metabolomic and transcriptomic study

Author

Mahajan, Uma V., Varma, Vijay R., Griswold, Michael E., Blackshear, Chad T., An, Yang, Oommen, Anup M., Varma, Sudhir, Troncoso, Juan C., Pletnikova, Olga, O'Brien, Richard, Hohman, Timothy J., Legido-Quigley, Cristina, and Thambisetty, Madhav

Subjects
Biological sciences
Abstract

Author(s): Uma V. Mahajan, Vijay R. Varma, Michael E. Griswold, Chad T. Blackshear, Yang An, Anup M. Oommen, Sudhir Varma, Juan C. Troncoso, Olga Pletnikova, Richard O'Brien, Timothy J. Hohman, [...]

Published
2020
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44. Relationships of Cerebral Perfusion With Gait Speed Across Systolic Blood Pressure Levels and Age: A Cohort Study.

Author

Windham, B Gwen, Griswold, Michael E, Ranadive, Radhikesh, Sullivan, Kevin J, Mosley, Thomas H, Mielke, Michelle M, Jack, Clifford R, Knopman, Dave, Petersen, Ron, and Vemuri, Prashanthi

Subjects
*WALKING speed, *SYSTOLIC blood pressure, *AGE differences, *PERFUSION, *SPIN labels
Abstract

Background This study aimed to examine if the association of cerebral perfusion with gait speed differs across systolic blood pressure (SBP) and age. Methods Cerebral perfusion was measured via arterial spin labeled (ASL)-MRI among community-dwelling adults aged 31–94 years in the population-based Mayo Clinic Study of Aging. Usual gait speed was assessed over 5.6 meters on an electronic mat. Sex- and body mass index (BMI)-adjusted linear regression models estimated cross-sectional gait speed associations with ASL and modifying effects of age and SBP using 3-way and 2-way interaction terms between continuous age, SBP, and ASL. Results report estimated differences in gait speed per standard deviation (SD) lower ASL for exemplar SBPs and ages. Results Among 479 participants (mean age 67.6 years; 44% women; mean gait speed 1.17 m/s), ASL relations to gait speed varied by age (ASL-x–age interaction: p =.001) and SBP (ASL-x–SBP interaction: p =.009). At an SBP of 120 mmHg, each SD lower ASL was associated with a 0.04 m/s (95% confidence interval [CI]: 0.01, 0.07) slower gait speed at 65 years, 0.07 m/s (0.04, 0.10) at 75 years, and 0.09 m/s (0.05, 0.13) at 85 years. At an SBP of 140 mmHg, ASL associations with gait speed were attenuated to 0.01 (−0.01, 0.04), 0.04 (0.02, 0.06), and 0.06 (0.04, 0.09) m/s slower gait speed at ages 65, 75, and 85, respectively. Conclusion Poorer cerebral perfusion is associated with clinically meaningful slower gait speeds, particularly with older age, while higher perfusion markedly attenuates age differences in gait speed. [ABSTRACT FROM AUTHOR]

Published
2023
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