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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]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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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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
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