Frequency of the apolipoprotein E ε2 allele is diminished in sporadic Alzheimer disease
Abstract
Recent data have demonstrated genetic disequilibrium between inheritance of the apolipoprotein E (apoE) epsilon 4 allele and increased risk of Alzheimer disease. We tested the idea that inheritance of other allelic variations of apoE might also increase or decrease the risk of developing Alzheimer disease. We studied apoE genotypes in a large clinic based population of Alzheimer disease patients and age-compatible, tested control individuals. We confirm the genetic disequilibrium between apoE epsilon 4 and Alzheimer disease and now report that inheritance of apoE epsilon 2, another common variant of the apolipoprotein E gene, is negatively associated with risk of developing Alzheimer disease.
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APOE is genetically linked to late-onset sporadic Alzheimer's disease (LOAD), with APOE4 being a significant risk factor, APOE3 considered the "neutral" allele, and APOE2 exerting a protective role against LOAD.
“APOE is genetically linked to late-onset sporadic Alzheimer’s disease (LOAD), with APOE4 being a significant risk factor, APOE3 considered the “neutral” allele, and APOE2 exerting a protective role against LOAD [6, 7].”
APOE2 is a protective factor for LOAD.
“whereas APOE2 is a protective factor [6, 72].”
APOE4 is the most prominent genetic risk factor for LOAD, increasing the risk up to 12-fold.
“while APOE4 is the most prominent genetic risk factor for LOAD, increasing the risk up to 12-fold”
APOE ε2 allele carriers show reduced Alzheimer's disease risk, later age of disease onset, and lesser Aβ accumulation.
“In contrast, APOE ε2 allele carries show reduced AD risk, later age of disease onset, and lesser Aβ accumulation.”
From Blocking the apoE/Aβ interaction ameliorates Aβ-related pathology in APOE ε2 and ε4 targeted replacement Alzheimer model mice (2014) · cites this paper as [10]
apoE2 exerts a protective effect against Aβ pathology and AD morbidity.
“Epidemiological evidence and evidence from neuropathological assessment of the impact of apoE isoforms on the brain Aβ load, have suggested that apoE2 exerts a protective effect against Aβ pathology and AD morbidity [3,9,10], while apoE4, in contrast, markedly enhances the disease process [7,8,30].”
From Blocking the apoE/Aβ interaction ameliorates Aβ-related pathology in APOE ε2 and ε4 targeted replacement Alzheimer model mice (2014) · cites this paper as [10]
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References 19 · Cited by 125
- Authors
- West, H. L., William Rebeck, G., & Hyman, B. T.
- Affiliations
- Massachusetts General Hospital (US)
- Corresponding author
- Hyman, Bradley T.
- ORCID
- Hyman, Bradley T.
- Venue
- Neuroscience Letters
- Publisher
- Elsevier BV
- Published
- 1994-07
- Volume
- 175
- Issue
- 1-2
- Pages
- 46-48
- ISSN
- 0304-3940 (ISSN-L)
- OpenAlex
- W2084687969
- Cited by
- 125
- References
- 19
- Citations by year
- 2025: 2 · 2024: 3 · 2023: 1 · 2022: 2 · 2021: 4 · 2020: 3 · 2019: 2 · 2018: 1 · 2017: 4 · 2016: 1 · 2015: 3 · 2014: 11 · 2013: 3 · 2012: 2
- FWCI
- 9.73
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Neuroscience Letters (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (AG-08487, 2P50 AG05134, P50AG005134)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Keywords
- apolipoprotein E, APOE ε4, sporadic Alzheimer's disease, genetic risk, genetic disequilibrium, allele frequency, Alzheimer's disease risk
- MeSH terms
- Alleles, Alzheimer Disease, Apolipoproteins E, Gene Frequency, Genotype, Humans, Middle Aged, Reference Values, Risk Factors, Biomarkers
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