TY - JOUR
T1 - Association between Blood Pressure and Later-Life Cognition among Black and White Individuals
AU - Levine, Deborah A.
AU - Gross, Alden L.
AU - Briceño, Emily M.
AU - Tilton, Nicholas
AU - Kabeto, Mohammed U.
AU - Hingtgen, Stephanie M.
AU - Giordani, Bruno J.
AU - Sussman, Jeremy B.
AU - Hayward, Rodney A.
AU - Burke, James F.
AU - Elkind, Mitchell S.V.
AU - Manly, Jennifer J.
AU - Moran, Andrew E.
AU - Kulick, Erin R.
AU - Gottesman, Rebecca F.
AU - Walker, Keenan A.
AU - Yano, Yuichiro
AU - Gaskin, Darrell J.
AU - Sidney, Stephen
AU - Yaffe, Kristine
AU - Sacco, Ralph L.
AU - Wright, Clinton B.
AU - Roger, Veronique L.
AU - Allen, Norrina Bai
AU - Galecki, Andrzej T.
N1 - Funding Information:
grants from the National Institutes of Health (NIH) during the conduct of the study and outside the submitted work. Drs Tilton and Hingtgen report grants from the NIH/National Institute of Neurological Disorders and Stroke (NINDS) during the conduct of the study. Dr Sussman reports grants from US Department of Veterans Affairs during the conduct of the study. Dr Hayward reports grants from the NIH and US Department of Veterans Affairs during the conduct of the study. Dr Manly reports grants from NIH/National Institute on Aging during the conduct of the study. Dr Gottesman reports other support from the American Academy of Neurology outside the submitted work. Drs Gaskin and Galecki report grants from the NIH during the conduct of the study. Dr Sidney reports a contract from the National Heart, Lung, and Blood Institute outside the submitted work. Dr Yaffe reports grants from the National Heart, Lung, and Blood Institute during the conduct of the study. Dr Sacco reports grants from NINDS during the conduct of the study and grants from Boehringer Ingelheim, American Heart Association, and Florida Department of Health outside the submitted work. Dr Wright reports grants from NIH/NINDS during the conduct of the study and royalties from UpToDate for 2 chapters on vascular dementia. No other disclosures were reported.
Funding Information:
supported by the National Institute of Neurological Disorders and Stroke, National Institutes of Health, and US Department of Health and Human Services (grant R01 NS102715). Additional funding was provided by National Institute of Aging (grant R01 AG051827, Dr Levine; grant K01 AG050699, Dr Gross), National Institute of Aging Claude Pepper Center (grant P30 AG024824; Drs Galecki and Kabeto), and National Institute of Aging Michigan Alzheimer’s Disease Core Center (grant P30 AG053760, Dr Giordani).
Funding Information:
contributions. The ARIC Study is carried out as a collaborative study supported by the National Heart, Lung, and Blood Institute (NHLBI). Neurocognitive data were collected by grants supported by the National Institutes of Health (NIH) (NHLBI, National Institute of Neurological Disorders and Stroke [NINDS], National Institute on Aging [NIA], and National Institute on Deafness and Other Communication Disorders) and with previous brain magnetic resonance imaging examinations funded by the NHLBI. The Coronary Artery Risk Development in Young Adults Study (CARDIA) is conducted and supported by the NHLBI in collaboration with the University of Alabama at Birmingham, Northwestern University, University of Minnesota, and Kaiser Foundation Research Institute. This manuscript has been reviewed by CARDIA for scientific content. The Cardiovascular Health Study (CHS) was supported by contracts and grants from the NHLBI, with additional contribution from the NINDS. Additional support was provided by grants from the NIA. A full list of principal CHS investigators and institutions can be found at https://chs-nhlbi.org/. The Framingham Heart Study is a project of the NHLBI of the NIH and Boston University School of Medicine. This project has been funded in whole or in part with federal funds from the NHLBI, NIH, and US Department of Health and Human Services. The Northern Manhattan Stroke study has been funded at least in part with federal funds from the NIH and NINDS.
Publisher Copyright:
© 2020 American Medical Association. All rights reserved.
PY - 2020/7
Y1 - 2020/7
N2 - Importance: Black individuals are more likely than white individuals to develop dementia. Whether higher blood pressure (BP) levels in black individuals explain differences between black and white individuals in dementia risk is uncertain. Objective: To determine whether cumulative BP levels explain racial differences in cognitive decline. Design, Setting, and Participants: Individual participant data from 5 cohorts (January 1971 to December 2017) were pooled from the Atherosclerosis Risk in Communities Study, Coronary Artery Risk Development in Young Adults Study, Cardiovascular Health Study, Framingham Offspring Study, and Northern Manhattan Study. Outcomes were standardized as t scores (mean [SD], 50 [10]); a 1-point difference represented a 0.1-SD difference in cognition. The median (interquartile range) follow-up was 12.4 (5.9-21.0) years. Analysis began September 2018. Main Outcomes and Measures: The primary outcome was change in global cognition, and secondary outcomes were change in memory and executive function. Exposures: Race (black vs white). Results: Among 34349 participants, 19378 individuals who were free of stroke and dementia and had longitudinal BP, cognitive, and covariate data were included in the analysis. The mean (SD) age at first cognitive assessment was 59.8 (10.4) years and ranged from 5 to 95 years. Of 19378 individuals, 10724 (55.3%) were female and 15526 (80.1%) were white. Compared with white individuals, black individuals had significantly faster declines in global cognition (-0.03 points per year faster [95% CI, -0.05 to -0.01]; P =.004) and memory (-0.08 points per year faster [95% CI, -0.11 to -0.06]; P <.001) but significantly slower declines in executive function (0.09 points per year slower [95% CI, 0.08-0.10]; P <.001). Time-dependent cumulative mean systolic BP level was associated with significantly faster declines in global cognition (-0.018 points per year faster per each 10-mm Hg increase [95% CI, -0.023 to -0.014]; P <.001), memory (-0.028 points per year faster per each 10-mm Hg increase [95% CI, -0.035 to -0.021]; P <.001), and executive function (-0.01 points per year faster per each 10-mm Hg increase [95% CI, -0.014 to -0.007]; P <.001). After adjusting for cumulative mean systolic BP, differences between black and white individuals in cognitive slopes were attenuated for global cognition (-0.01 points per year [95% CI, -0.03 to 0.01]; P =.56) and memory (-0.06 points per year [95% CI, -0.08 to -0.03]; P <.001) but not executive function (0.10 points per year [95% CI, 0.09-0.11]; P <.001). Conclusions and Relevance: These results suggest that black individuals' higher cumulative BP levels may contribute to racial differences in later-life cognitive decline.
AB - Importance: Black individuals are more likely than white individuals to develop dementia. Whether higher blood pressure (BP) levels in black individuals explain differences between black and white individuals in dementia risk is uncertain. Objective: To determine whether cumulative BP levels explain racial differences in cognitive decline. Design, Setting, and Participants: Individual participant data from 5 cohorts (January 1971 to December 2017) were pooled from the Atherosclerosis Risk in Communities Study, Coronary Artery Risk Development in Young Adults Study, Cardiovascular Health Study, Framingham Offspring Study, and Northern Manhattan Study. Outcomes were standardized as t scores (mean [SD], 50 [10]); a 1-point difference represented a 0.1-SD difference in cognition. The median (interquartile range) follow-up was 12.4 (5.9-21.0) years. Analysis began September 2018. Main Outcomes and Measures: The primary outcome was change in global cognition, and secondary outcomes were change in memory and executive function. Exposures: Race (black vs white). Results: Among 34349 participants, 19378 individuals who were free of stroke and dementia and had longitudinal BP, cognitive, and covariate data were included in the analysis. The mean (SD) age at first cognitive assessment was 59.8 (10.4) years and ranged from 5 to 95 years. Of 19378 individuals, 10724 (55.3%) were female and 15526 (80.1%) were white. Compared with white individuals, black individuals had significantly faster declines in global cognition (-0.03 points per year faster [95% CI, -0.05 to -0.01]; P =.004) and memory (-0.08 points per year faster [95% CI, -0.11 to -0.06]; P <.001) but significantly slower declines in executive function (0.09 points per year slower [95% CI, 0.08-0.10]; P <.001). Time-dependent cumulative mean systolic BP level was associated with significantly faster declines in global cognition (-0.018 points per year faster per each 10-mm Hg increase [95% CI, -0.023 to -0.014]; P <.001), memory (-0.028 points per year faster per each 10-mm Hg increase [95% CI, -0.035 to -0.021]; P <.001), and executive function (-0.01 points per year faster per each 10-mm Hg increase [95% CI, -0.014 to -0.007]; P <.001). After adjusting for cumulative mean systolic BP, differences between black and white individuals in cognitive slopes were attenuated for global cognition (-0.01 points per year [95% CI, -0.03 to 0.01]; P =.56) and memory (-0.06 points per year [95% CI, -0.08 to -0.03]; P <.001) but not executive function (0.10 points per year [95% CI, 0.09-0.11]; P <.001). Conclusions and Relevance: These results suggest that black individuals' higher cumulative BP levels may contribute to racial differences in later-life cognitive decline.
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U2 - 10.1001/jamaneurol.2020.0568
DO - 10.1001/jamaneurol.2020.0568
M3 - Article
C2 - 32282019
AN - SCOPUS:85083266633
SN - 2168-6149
VL - 77
SP - 810
EP - 819
JO - JAMA Neurology
JF - JAMA Neurology
IS - 7
ER -