APOE predicts amyloid‐beta but not tau Alzheimer pathology in cognitively normal aging

Morris, John C.; Roe, Catherine M.; Xiong, Chengjie; Fagan, Anne M.; Goate, Alison M.; Holtzman, David M.; Mintun, Mark A.

doi:10.1002/ana.21843

Cited by 835Dementia and Cognitive Impairment ResearchAlzheimer's disease research and treatmentsCancer-related cognitive impairment studies

APOE predicts amyloid‐beta but not tau Alzheimer pathology in cognitively normal aging

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Morris, John C., Roe, Catherine M., Xiong, Chengjie, Fagan, Anne M., Goate, Alison M., Holtzman, David M., Mintun, Mark A.·2010·Annals of Neurology

DOI 10.1002/ana.21843PMC PMC2830375

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Abstract

Objective: To examine interactions of apolipoprotein E ( APOE) genotype with age and with in vivo measures of preclinical Alzheimer disease (AD) in cognitively normal aging. Methods: Two hundred forty‐one cognitively normal individuals, aged 45–88 years, had cerebral amyloid imaging studies with Pittsburgh Compound‐B (PIB). Of the 241 individuals, 168 (70%) also had cerebrospinal fluid (CSF) assays of amyloid‐beta 42 (Aβ 42 ), tau, and phosphorylated tau (ptau 181 ). All individuals were genotyped for APOE . Results: The frequency of individuals with elevated mean cortical binding potential (MCBP) for PIB rose in an age‐dependent manner from 0% at ages 45–49 years to 30.3% at 80–88 years. Reduced levels of CSF Aβ 42 appeared to begin earlier (18.2% of those aged 45–49 years) and increase with age in higher frequencies (50% at age 80–88 years) than elevations of MCBP. There was a gene dose effect for the APOE4 genotype, with greater MCBP increases and greater reductions in CSF Aβ 42 with increased numbers of APOE4 alleles. Individuals with an APOE2 allele had no increase in MCBP with age and had higher CSF Aβ 42 levels than individuals without an APOE2 allele. There was no APOE4 or APOE2 effect on CSF tau or ptau 181 . Interpretation: Increasing cerebral Aβ deposition with age is the pathobiological phenotype of APOE4 . The biomarker sequence that detects Aβ deposition may first be lowered CSF Aβ 42 , followed by elevated MCBP for PIB. A substantial proportion of cognitively normal individuals have presumptive preclinical AD. ANN NEUROL 2010;67:122–131

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The association of the APOE4 isoform with amyloid deposition has been well established in human studies, where APOE4 carriers exhibit higher Aβ plaque burden and earlier onset of amyloid positivity compared with non-carriers.
“The association of the APOE4 isoform with amyloid deposition has been well established in human studies, where APOE4 carriers exhibit higher A β plaque burden and earlier onset of amyloid positivity compared with non-carriers 35 -37 .”
From APOE2 attenuates APOE4-associated amyloid pathology and related toxicity in a mouse model of Alzheimer’s disease (2026) · cites this paper as [36]
The Results (Adjusted analyses; page unavailable) show greater amyloid-imaging binding in APOE4 carriers and a faster increase with age than in non-carriers, supporting higher Aβ burden. The paper does not establish that carriers become amyloid-positive at an earlier age: its references to earlier onset concern clinical dementia, while its earlier biomarker finding compares CSF Aβ42 with PET binding rather than carriers with non-carriers. (LLM, conf=0.84)
Experimental — accuracy not yet measured
APOE status modulates the onset of extracellular amyloid plaque deposition.
“APOE status has been found to modulate the onset of extracellular amyloid plaque deposition, one of the key pathognomonic features of the disease (6, 7).”
From Human ApoE isoforms differentially regulate brain amyloid-β peptide clearance (2011) · cites this paper as [7]
The Discussion reports that age and APOE genotype interact to affect the frequency of cerebral amyloid-β deposition in cognitively normal older adults, and the Results show genotype-dependent differences in deposition markers. This supports an effect on deposition with age, but the paper does not directly establish when extracellular plaques first appear in individuals of each genotype. (LLM, conf=0.82)
Experimental — accuracy not yet measured
Individuals with mean cortical binding potential (MCBP) for PIB >0.18 were considered PIB-positive.
“On the basis of previous studies (7, 27), individuals with mean cortical binding potential (MCBP) for PIB >0.18 were considered PIB-positive (PIB+).”
From Human ApoE isoforms differentially regulate brain amyloid-β peptide clearance (2011) · cites this paper as [7]
A CSF Aβ42 concentration lower than 500 pg/mL has been utilized as a reliable threshold for the presence of cerebral Aβ deposition in humans.
“Given that a CSF Aβ42 concentration lower than 500 pg/mL has been utilized as a reliable threshold for the presence of cerebral Aβ deposition in humans (7, 19, 22, 26)”
From Human ApoE isoforms differentially regulate brain amyloid-β peptide clearance (2011) · cites this paper as [7]
Increasing age and ApoE genetic background are the strongest known risk factors for AD and plaque load.
“Increasing age and ApoE genetic background are the strongest known risk factors for AD and plaque load (33, 48); thus it was critical that these parameters were controlled.”
From Serotonin signaling is associated with lower amyloid-β levels and plaques in transgenic mice and humans (2011) · cites this paper as [33]

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Price (1999) · doi:10.1002/1531-8249(199903)45:3
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P2–134: Age and apolipoprotein E*4 effects on cerebrospinal fluid Aβ42 in cognitively normal adults
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Authors: Morris, J. C., Roe, C. M., Xiong, C., Fagan, A. M., Goate, A. M., Holtzman, D. M., & Mintun, M. A.
Affiliations: Washington University in St. Louis (US)
Corresponding author: Morris, John C.
ORCID: Morris, John C.
Roe, Catherine M.
Xiong, Chengjie
Fagan, Anne M.
Goate, Alison M.
Holtzman, David M.
Venue: Annals of Neurology
Publisher: Wiley
Published: 2010-01
Volume: 67
Issue: 1
Pages: 122-131
ISSN: 0364-5134 (ISSN-L)
1531-8249
DOI: 10.1002/ana.21843
PMC: PMC2830375
OpenAlex: W2014897304
Cited by: 830
References: 80
Citations by year: 2026: 21 · 2025: 23 · 2024: 38 · 2023: 39 · 2022: 54 · 2021: 40 · 2020: 53 · 2019: 53 · 2018: 49 · 2017: 58 · 2016: 54 · 2015: 48 · 2014: 65 · 2013: 76 · 2012: 63
FWCI: 32.20
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: onlinelibrary.wiley.com/termsAndConditions#vor (vor)
Locations: Annals of Neurology (publishedVersion)
PubMed (publishedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health (UL1TR000448)
National Institute on Aging (P50AG005681, P01AG003991, P01AG026276)
National Center for Research Resources (UL1RR024992)
National Center for Advancing Translational Sciences
Topics: Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Health Sciences › Medicine › Pulmonary and Respiratory Medicine › Cancer-related cognitive impairment studies
Keywords: apolipoprotein E, APOE ε4, APOE2, amyloid-beta, tau protein, preclinical Alzheimer's disease, Pittsburgh compound B, cerebrospinal fluid biomarkers, gene dosage effect, phosphorylated tau
MeSH terms: Aged, Aged, 80 and over, Aging, Alzheimer Disease, Aniline Compounds, Apolipoproteins E, Brain, Female, Follow-Up Studies, Genotype, Humans, Longitudinal Studies, Male, Middle Aged, Peptide Fragments, Phosphorylation, Thiazoles, Amyloid beta-Peptides, tau Proteins, Apolipoprotein E4, Apolipoprotein E2, Plaque, Amyloid

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APOE predicts amyloid‐beta but not tau Alzheimer pathology in cognitively normal aging

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