Cited by 282Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

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Apolipoprotein E ε4 allele, AD pathology, and the clinical expression of Alzheimer’s disease

Bennett, D.A., Wilson, R.S., Schneider, J.A., Evans, D.A., Aggarwal, N.T., Arnold, S.E., Cochran, E.J., Berry-Kravis, E., Bienias, J.L.·2003·Neurology

DOI 10.1212/01.wnl.0000042478.08543.f7

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Abstract

Objective To test the hypothesis that the APOE epsilon4 allele is associated with the clinical manifestations of AD through an association with the pathologic hallmarks of disease. Methods Participants were older Catholic nuns, priests, and brothers who agreed to annual neurologic and neuropsychological evaluation for AD and other common neurologic conditions and brain autopsy at the time of death. There were 77 persons without dementia and 51 with probable AD; 38 participants had one or more epsilon4 alleles. Results In logistic regression analyses, controlling for age, sex, and education, the epsilon4 allele was strongly associated with the likelihood of clinical AD (odds = 3.46, 95% CI = 1.44 to 8.33). However, controlling for the effect of AD pathology, the association of the epsilon allele with clinical AD was reduced by >50% and was no longer significant (odds = 1.58, 95% CI = 0.56 to 4.43). Similarly, in linear regression analyses, controlling for age, sex, and education, the epsilon4 allele was strongly associated with level of cognitive function proximate to death (regression coefficient = -0.477, p = 0.005). However, after controlling for the effect of AD pathology, the association of the epsilon4 allele with level of cognition was reduced by >80% and was no longer significant (regression coefficient = -0.093). Similar results were found in analyses using separate measures of neuritic plaques, diffuse plaques, and neurofibrillary tangles, and in analyses of five dif…

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Authors: Bennett, D. A., Wilson, R. S., Schneider, J. A., Evans, D. A., Aggarwal, N. T., Arnold, S. E., Cochran, E. J., Berry-Kravis, E., & Bienias, J. L.
Affiliations: From the Rush Alzheimer’s Disease Center and Rush Institute for Healthy Aging (Drs. Bennett, Wilson, Schneider, Evans, Aggarwal, and Bienias); Department of Neurological Sciences (Drs. Bennett, Wilson, Schneider, Evans, Aggarwal, Cochran, and Berry-Kravis); Department of Psychology (Dr. Wilson); Department of Pathology (Drs. Schneider and Cochran); Department of Internal Medicine (Drs. Evans and Bienias), Department of Pediatrics (Dr. Berry-Kravis), Rush Presbyterian-St. Luke’s Medical Center,...
ORCID: Bennett, D.A.
Schneider, J.A.
Evans, D.A.
Aggarwal, N.T.
Arnold, S.E.
Cochran, E.J.
Venue: Neurology
Publisher: Ovid Technologies (Wolters Kluwer Health)
Published: 2003-01-28
Volume: 60
Issue: 2
Pages: 246-252
ISSN: 0028-3878 (ISSN-L)
1526-632X
DOI: 10.1212/01.wnl.0000042478.08543.f7
OpenAlex: W2005578478
Cited by: 282
References: 64
Citations by year: 2026: 10 · 2025: 13 · 2024: 11 · 2023: 10 · 2022: 9 · 2021: 15 · 2020: 9 · 2019: 11 · 2018: 10 · 2017: 13 · 2016: 10 · 2015: 10 · 2014: 8 · 2013: 9 · 2012: 15
FWCI: 12.10
Type: journal article
Language: en
Open access: closed
Locations: Neurology (publishedVersion)
PubMed (publishedVersion)
Funders: National Institute on Aging (AG-15819, AG 10161, P30AG010161)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords: APOE ε4, Alzheimer's disease, neuropathology, neuritic plaques, neurofibrillary tangles, cognitive function, episodic memory, semantic memory, working memory, perceptual speed, visuospatial ability, women religious, brain autopsy
MeSH terms: Age Factors, Aged, Aged, 80 and over, Alleles, Alzheimer Disease, Apolipoproteins E, Brain, Cognition Disorders, Educational Status, Female, Humans, Longitudinal Studies, Male, Memory Disorders, Neuropsychological Tests, Risk Factors, Linear Models, Logistic Models, Odds Ratio, Disease Progression, Genetic Predisposition to Disease, Apolipoprotein E4

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Apolipoprotein E ε4 allele, AD pathology, and the clinical expression of Alzheimer’s disease

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