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Apolipoprotein E in Alzheimer's Disease: An Update
Open accessAbstract
The vast majority of Alzheimer's disease (AD) cases are late onset (LOAD), which is genetically complex with heritability estimates up to 80%. Apolipoprotein E (APOE) has been irrefutably recognized as the major genetic risk factor, with semidominant inheritance, for LOAD. Although the mechanisms that underlie the pathogenic nature of APOE in AD are still not completely understood, emerging data suggest that APOE contributes to AD pathogenesis through both amyloid-β (Aβ)-dependent and Aβ-independent pathways. Given the central role for APOE in the modulation of AD pathogenesis, many therapeutic strategies have emerged, including converting APOE conformation, regulating APOE expression, mimicking APOE peptides, blocking the APOE/Aβ interaction, modulating APOE lipidation state, and gene therapy. Accumulating evidence also suggests the utility of APOE genotyping in AD diagnosis, risk assessment, prevention, and treatment response.
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“ApoE isoforms encoded by various APOE alleles differentially influence the rate of soluble Aβ clearance from the brain interstitial space and formation of Aβ parenchymal plaques and VAβ [32, 33].”
From APOE Genotype Differentially Modulates Effects of Anti-Aβ, Passive Immunization in APP Transgenic Mice (2017) · cites this paper as [33]
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“The ɛ4 allele has detrimental effects on production, deposition, and clearance of amyloid-β, in phosphorylation of tau, in neurotoxicity, mitochondrial dysfunction, and in blood–brain barrier permeability.57,59,60”
From Plasma levels of apolipoprotein E, APOE genotype, and all-cause and cause-specific mortality in 105 949 individuals from a white general population cohort (2019) · cites this paper as [57]
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“Plausible mechanisms underlying the association between low apoE levels and dementia-associated mortality are not explained by peripheral lipid metabolism, but likely by the role of apoE in β-amyloid handling and in neurodegenerative processes.57,58”
From Plasma levels of apolipoprotein E, APOE genotype, and all-cause and cause-specific mortality in 105 949 individuals from a white general population cohort (2019) · cites this paper as [57]
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“APOE genotype critically affects the burden of Aβ pathology in sporadic AD.”
From APOE Genotype Differentially Modulates Effects of Anti-Aβ, Passive Immunization in APP Transgenic Mice (2017) · cites this paper as [33]
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“Several studies have reported human APOE isoform-dependent differences in Aβ deposition (APOE4 APOE3>APOE2) (Figure 2b) (Bales et al. 2009, Castellano et al. 2011, Youmans et al. 2012).”
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NSAID use and dementia risk in the Cardiovascular Health Study*: Role of APOE and NSAID type
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Rosiglitazone Induces Mitochondrial Biogenesis in Mouse Brain
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Anti-apoE immunotherapy inhibits amyloid accumulation in a transgenic mouse model of Aβ amyloidosis
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“3, inhibits amyloid accumulation in APPswe/PS1 E9 mice, suggesting antiapoE immunotherapy may represent a novel AD therapeutic strategy (Kim et al. 2012).”
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Cholesterol, APOE genotype, and Alzheimer disease: An epidemiologic study of Nigerian Yoruba
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Accumulation of intraneuronal Aβ correlates with ApoE4 genotype
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Differential effect of APOE genotype on amyloid load and glucose metabolism in AD dementia
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Low‐density lipoprotein receptors regulate microglial inflammation through c‐Jun N‐terminal kinase
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“Loci identified by GWAS have much smaller effect sizes than that of APOE, typically with odds ratios between 1.1 and 1.3 in contrast to a ratio of ∼4 for APOE4 (Lambert et al. 2013).”
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Apolipoprotein E modulates γ‐secretase cleavage of the amyloid precursor protein
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Distortion of Allelic Expression of Apolipoprotein E in Alzheimer's Disease
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Self-citationAPOE ε4 worsens hippocampal CA1 apical neuropil atrophy and episodic memory
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Omega-3 fatty acids and cognitive decline: modulation by ApoEε4 allele and depression
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Apolipoprotein mimetic peptides: Mechanisms of action as anti-atherogenic agents
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The role of inflammatory processes in Alzheimer’s disease
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Familial Alzheimer's disease: Site of mutation influences clinical phenotype
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Plasma Signaling Proteins in Persons at Genetic Risk for Alzheimer Disease
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Genomics of Dementia:APOE- andCYP2D6-Related Pharmacogenetics
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A Multifaceted Role for apoE in the Clearance of Beta-Amyloid across the Blood-Brain Barrier
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Proteomic Analysis of Mitochondria in APOE Transgenic Mice and in Response to an Ischemic Challenge
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Apolipoprotein E decreases tau kinases and phospho-tau levels in primary neurons.
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Impact of genetic factors on outcome from brain injury
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ApoE mimetic peptide decreases Aβ production in vitro and in vivo
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Mapping ApoE/Aβ binding regions to guide inhibitor discovery
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Presymptomatic apolipoprotein E genotyping for Alzheimer's disease risk assessment and prevention
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Altering Mitochondrial Dysfunction as an Approach to Treating Alzheimer’s Disease
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“APOE isoforms may differentially affect synaptic plasticity and dendritic spine integrity via the modulation of spine elimination (Basak & Kim 2010); as a result of isoformdependent levels of APOE (Basak & Kim 2010, Dumanis et al. 2009); and by acting as signaling molecules through interactions…”
Background
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Metadata
- Authors
- Yu, J.-T., Tan, L., & Hardy, J.
- Affiliations
- Qingdao University (CN)
- UCL Queen Square Institute of Neurology (GB)
- Venue
- Annual Review of Neuroscience
- Publisher
- Annual Reviews
- Published
- 2014-07-08
- Volume
- 37
- Issue
- 1
- Pages
- 79-100
- ISSN
- 0147-006X (ISSN-L)
- 1545-4126
- OpenAlex
- W2097112082
- Cited by
- 394
- References
- 152
- Citations by year
- 2026: 7 · 2025: 15 · 2024: 27 · 2023: 20 · 2022: 26 · 2021: 32 · 2020: 39 · 2019: 46 · 2018: 47 · 2017: 46 · 2016: 46 · 2015: 27 · 2014: 14
- FWCI
- 5.19
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Annual Review of Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- National Natural Science Foundation of China (81000544, 81171209)
- 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
- apolipoprotein E, Alzheimer's disease, late-onset Alzheimer's disease, genetic risk factors, amyloid-beta, gene therapy, APOE genotyping, treatment options
- MeSH terms
- Alzheimer Disease, Apolipoproteins E, Brain, Genotype, Humans, Models, Biological, Signal Transduction, Amyloid beta-Peptides, tau Proteins, Genetic Predisposition to Disease, Molecular Targeted Therapy
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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