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APOE predicts amyloid‐beta but not tau Alzheimer pathology in cognitively normal aging
Open accessAbstract
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 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]
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“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]
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“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]
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“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]
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“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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“Sex differences in Aβ burden alone have not been reported in older adults,11–13”
From Sex Differences in the Association of Global Amyloid and Regional Tau Deposition Measured by Positron Emission Tomography in Clinically Normal Older Adults (2019) · cites this paper as [13]
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“Previous cross-sectional studies indicate that Aβ42 levels decrease in the CSF as Aβ starts to accumulate, before fibrillar plaques can be detected with PET7–11.”
From Earliest accumulation of β-amyloid occurs within the default-mode network and concurrently affects brain connectivity (2017) · cites this paper as [11]
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Metadata
- 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
- Venue
- Annals of Neurology
- Publisher
- Wiley
- Published
- 2010-01
- Volume
- 67
- Issue
- 1
- Pages
- 122-131
- ISSN
- 0364-5134 (ISSN-L)
- 1531-8249
- 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
- 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
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Oncology › 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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