Role of APOE ϵ4 Allele and Incident Stroke on Cognitive Decline and Mortality

Kumar B. Rajan; Neelum T. Aggarwal; Julie A. Schneider; Robert S. Wilson; Susan A. Everson-Rose; Denis A. Evans

doi:10.1097/WAD.0000000000000173

Role of APOE ϵ4 Allele and Incident Stroke on Cognitive Decline and Mortality

Kumar B. Rajan, Neelum T. Aggarwal, Julie A. Schneider, Robert S. Wilson, Susan A. Everson-Rose, Denis A. Evans

Medicine - Geriatrics, Palliative and Primary Care (GPPC)

Research output: Contribution to journal › Article › peer-review

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Abstract

Background: The apolipoprotein E (APOE) ϵ4 allele and stroke increase the risk of cognitive decline. However, the association of the APOE ϵ4 allele before and after stroke is not well understood. Methods: Using a prospective sample of 3444 (66% African Americans, 61% females, mean age=71.9 y) participants, we examined cognitive decline relative to stroke among those with and without the APOE ϵ4 allele. Results: In our sample, 505 (15%) had incident stroke. Among participants without stroke, the ϵ4 allele was associated with increased cognitive decline compared to noncarriers (0.080 vs. 0.036 units/year; P<0.0001). Among participants without the ϵ4 allele, cognitive decline increased significantly after stroke compared to before stroke (0.115 vs. 0.039 units/year; P<0.0001). Interestingly, cognitive decline before and after stroke was not significantly different among those with the ϵ4 allele (0.091 vs. 0.102 units/year; P=0.32). Poor cognitive function was associated with higher risk of stroke (hazard ratio=1.41, 95% confidence interval, 1.25-1.58), but the APOE ϵ4 allele was not (P=0.66). The APOE ϵ4 allele, cognitive function, and incident stroke were associated with mortality. Conclusions: The association of stroke with cognitive decline appears to differ by the presence of the APOE ϵ4 allele, but no such interaction was observed for mortality.

Original language	English (US)
Pages (from-to)	318-323
Number of pages	6
Journal	Alzheimer disease and associated disorders
Volume	30
Issue number	4
DOIs	https://doi.org/10.1097/WAD.0000000000000173
State	Published - 2016

Bibliographical note

Funding Information:
Supported by grants from the National Institutes for Health (R01- AG051635, R01-AG09966 and R01-AG030146). S.A.E.-R. was supported in part by grant (1P60MD003422) from the National Institute on Minority Health and Health Disparities (NIMHD) and by the Program in Health Disparities Research and the Applied Clinical Research Program at the University of Minnesota. Contents of this paper are solely the responsibility of the authors and do not necessarily represent the official views of the NIH, NIA, or NIMHD.

Publisher Copyright:
Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved.

Keywords

APOE
cognitive decline
mortality
stroke

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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http://europepmc.org/articles/pmc5117953

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@article{f172937a1b2b44d5abf8e3ecaa1824cd,

title = "Role of APOE ϵ4 Allele and Incident Stroke on Cognitive Decline and Mortality",

abstract = "Background: The apolipoprotein E (APOE) ϵ4 allele and stroke increase the risk of cognitive decline. However, the association of the APOE ϵ4 allele before and after stroke is not well understood. Methods: Using a prospective sample of 3444 (66% African Americans, 61% females, mean age=71.9 y) participants, we examined cognitive decline relative to stroke among those with and without the APOE ϵ4 allele. Results: In our sample, 505 (15%) had incident stroke. Among participants without stroke, the ϵ4 allele was associated with increased cognitive decline compared to noncarriers (0.080 vs. 0.036 units/year; P<0.0001). Among participants without the ϵ4 allele, cognitive decline increased significantly after stroke compared to before stroke (0.115 vs. 0.039 units/year; P<0.0001). Interestingly, cognitive decline before and after stroke was not significantly different among those with the ϵ4 allele (0.091 vs. 0.102 units/year; P=0.32). Poor cognitive function was associated with higher risk of stroke (hazard ratio=1.41, 95% confidence interval, 1.25-1.58), but the APOE ϵ4 allele was not (P=0.66). The APOE ϵ4 allele, cognitive function, and incident stroke were associated with mortality. Conclusions: The association of stroke with cognitive decline appears to differ by the presence of the APOE ϵ4 allele, but no such interaction was observed for mortality.",

keywords = "APOE, cognitive decline, mortality, stroke",

author = "Rajan, {Kumar B.} and Aggarwal, {Neelum T.} and Schneider, {Julie A.} and Wilson, {Robert S.} and Everson-Rose, {Susan A.} and Evans, {Denis A.}",

note = "Funding Information: Supported by grants from the National Institutes for Health (R01- AG051635, R01-AG09966 and R01-AG030146). S.A.E.-R. was supported in part by grant (1P60MD003422) from the National Institute on Minority Health and Health Disparities (NIMHD) and by the Program in Health Disparities Research and the Applied Clinical Research Program at the University of Minnesota. Contents of this paper are solely the responsibility of the authors and do not necessarily represent the official views of the NIH, NIA, or NIMHD. Publisher Copyright: Copyright {\textcopyright} 2016 Wolters Kluwer Health, Inc. All rights reserved.",

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doi = "10.1097/WAD.0000000000000173",

language = "English (US)",

volume = "30",

pages = "318--323",

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T1 - Role of APOE ϵ4 Allele and Incident Stroke on Cognitive Decline and Mortality

AU - Rajan, Kumar B.

AU - Aggarwal, Neelum T.

AU - Schneider, Julie A.

AU - Wilson, Robert S.

AU - Everson-Rose, Susan A.

AU - Evans, Denis A.

N1 - Funding Information: Supported by grants from the National Institutes for Health (R01- AG051635, R01-AG09966 and R01-AG030146). S.A.E.-R. was supported in part by grant (1P60MD003422) from the National Institute on Minority Health and Health Disparities (NIMHD) and by the Program in Health Disparities Research and the Applied Clinical Research Program at the University of Minnesota. Contents of this paper are solely the responsibility of the authors and do not necessarily represent the official views of the NIH, NIA, or NIMHD. Publisher Copyright: Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved.

PY - 2016

Y1 - 2016

N2 - Background: The apolipoprotein E (APOE) ϵ4 allele and stroke increase the risk of cognitive decline. However, the association of the APOE ϵ4 allele before and after stroke is not well understood. Methods: Using a prospective sample of 3444 (66% African Americans, 61% females, mean age=71.9 y) participants, we examined cognitive decline relative to stroke among those with and without the APOE ϵ4 allele. Results: In our sample, 505 (15%) had incident stroke. Among participants without stroke, the ϵ4 allele was associated with increased cognitive decline compared to noncarriers (0.080 vs. 0.036 units/year; P<0.0001). Among participants without the ϵ4 allele, cognitive decline increased significantly after stroke compared to before stroke (0.115 vs. 0.039 units/year; P<0.0001). Interestingly, cognitive decline before and after stroke was not significantly different among those with the ϵ4 allele (0.091 vs. 0.102 units/year; P=0.32). Poor cognitive function was associated with higher risk of stroke (hazard ratio=1.41, 95% confidence interval, 1.25-1.58), but the APOE ϵ4 allele was not (P=0.66). The APOE ϵ4 allele, cognitive function, and incident stroke were associated with mortality. Conclusions: The association of stroke with cognitive decline appears to differ by the presence of the APOE ϵ4 allele, but no such interaction was observed for mortality.

AB - Background: The apolipoprotein E (APOE) ϵ4 allele and stroke increase the risk of cognitive decline. However, the association of the APOE ϵ4 allele before and after stroke is not well understood. Methods: Using a prospective sample of 3444 (66% African Americans, 61% females, mean age=71.9 y) participants, we examined cognitive decline relative to stroke among those with and without the APOE ϵ4 allele. Results: In our sample, 505 (15%) had incident stroke. Among participants without stroke, the ϵ4 allele was associated with increased cognitive decline compared to noncarriers (0.080 vs. 0.036 units/year; P<0.0001). Among participants without the ϵ4 allele, cognitive decline increased significantly after stroke compared to before stroke (0.115 vs. 0.039 units/year; P<0.0001). Interestingly, cognitive decline before and after stroke was not significantly different among those with the ϵ4 allele (0.091 vs. 0.102 units/year; P=0.32). Poor cognitive function was associated with higher risk of stroke (hazard ratio=1.41, 95% confidence interval, 1.25-1.58), but the APOE ϵ4 allele was not (P=0.66). The APOE ϵ4 allele, cognitive function, and incident stroke were associated with mortality. Conclusions: The association of stroke with cognitive decline appears to differ by the presence of the APOE ϵ4 allele, but no such interaction was observed for mortality.

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Role of APOE ϵ4 Allele and Incident Stroke on Cognitive Decline and Mortality

Abstract

Bibliographical note

Keywords

UN SDGs

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