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The forgotten APOE allele: A review of the evidence and suggested mechanisms for the protective effect of APOE ɛ2
Abstract
Ongoing efforts to improve survival, and enhance quality of life have led biomedical research to focus on disease and the mechanisms that increase risk for disease. The other side of that coin may be as important, i.e. examining the protective factors that allow some individuals to enjoy long, healthy lives. One of the best examples of a gene that positively influences cognitive health is the apolipoprotein (APOE) ɛ2 allele. The APOE ɛ4 allele is a well-established risk factor for Alzheimer's disease (AD) and has thus dominated the APOE literature, with the putative protective role of ɛ2 receiving little attention. This review describes the effects of APOE ɛ2 on the structure and function of the brain. With a focus on neurodegeneration, we discuss evidence for APOE ɛ2's protective effects, explore some key mechanisms through which this protection may be conferred, and address a few inconsistencies in the literature. Understanding the mechanisms that underlie the association between APOE ɛ2, cognition and longevity may provide new targets for research on promoting life-long health.
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“This finding is consistent with recent research,62 and suggests that PSEN1 and APOE may interact to modify ADAOO in these patients.”
From APOE*E2 allele delays age of onset in PSEN1 E280A Alzheimer’s disease (2016) · cites this paper as [62]
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Metadata
- Authors
- Suri, S., Heise, V., Trachtenberg, A. J., & Mackay, C. E.
- Affiliations
- John Radcliffe Hospital (GB)
- Corresponding author
- Mackay, Clare E.
- Venue
- Neuroscience & Biobehavioral Reviews
- Publisher
- Elsevier BV
- Published
- 2013-12
- Volume
- 37
- Issue
- 10
- Pages
- 2878-2886
- ISSN
- 0149-7634 (ISSN-L)
- OpenAlex
- W2067079625
- Cited by
- 183
- References
- 126
- Citations by year
- 2026: 6 · 2025: 9 · 2024: 14 · 2023: 15 · 2022: 15 · 2021: 24 · 2020: 26 · 2019: 14 · 2018: 11 · 2017: 14 · 2016: 18 · 2015: 14 · 2014: 3
- FWCI
- 1.29
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience & Biobehavioral Reviews (publishedVersion)
- PubMed (publishedVersion)
- Funders
- University of Oxford Clarendon scholarship
- Alzheimer's Research UK studentship
- Rhodes scholarship
- National Institute for Health Research (NIHR), UK
- 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 ε2 allele, APOE ε4, apolipoprotein E, Alzheimer's disease, neuroprotection, cognitive health, longevity, neurodegeneration, brain structure and function, protective genetic factor
- MeSH terms
- Alleles, Cognition Disorders, Genotype, Humans, Longevity, Risk Factors, Neurodegenerative Diseases, Apolipoprotein E2
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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