Apolipoprotein E isoforms and regulation of the innate immune response in brain of patients with Alzheimer's disease
Open accessAbstract
The largest genetic risk for late-onset Alzheimer's disease (AD) resides at the apolipoprotein E gene (APOE) locus, which has three common alleles (ɛ2, ɛ3, ɛ4) that encode three isoforms (apoE2, apoE3, apoE4). The very strong association of the APOE ɛ4 allele with AD risk and its role in the accumulation of amyloid β in brains of people and animal models solidify the biological relevance of apoE isoforms but do not provide mechanistic insight. The innate immune response is consistently observed in AD and is a likely contributor to neuronal injury and response to injury. Here we review emerging data showing that apoE isoform regulation of multiple facets of the innate immune response in the brain may alter AD not only through amyloid β-dependent mechanisms, but also through other, amyloid β-independent mechanisms.
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APOE isoforms differentially influence the innate immune response.
“APOE isoforms are known to differentially influence the innate immune response [65].”
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Self-citationChen, H.-F., Huang, C.-Q., You, C., Wang, Z.-R., & Si-qing, H. (2013) · Archives of Medical Research · doi:10.1016/j.arcmed.2013.01.002 · Cited by 48 · see citing works
Jones, N. S., Watson, K. Q., & Rebeck, G. W. (2021) · Journal of Neuroinflammation · doi:10.1186/s12974-021-02256-2 · Cited by 26 · see citing works
Yesiltepe, M., Yin, T., Tambini, M., Bao, H., Pan, M., d’Abramo, C., Giliberto, L., Han, X., & D’Adamio, L. (2024) · Cell Communication and Signaling · doi:10.1186/s12964-024-01832-2 · Cited by 10 · see citing works
“APOE isoforms are known to differentially influence the innate immune response [65].”
Background
- Authors
- Keene, C. D., Cudaback, E., Li, X., Montine, K. S., & Montine, T. J.
- Affiliations
- University of Washington (US)
- Corresponding author
- Montine, Thomas J
- Venue
- Current Opinion in Neurobiology
- Publisher
- Elsevier BV
- Published
- 2011-12
- Volume
- 21
- Issue
- 6
- Pages
- 920-928
- ISSN
- 0959-4388 (ISSN-L)
- PMC
- PMC3237894
- OpenAlex
- W1985814840
- Cited by
- 103
- References
- 78
- Citations by year
- 2026: 7 · 2025: 4 · 2024: 3 · 2023: 7 · 2022: 14 · 2021: 9 · 2020: 9 · 2019: 4 · 2018: 3 · 2017: 4 · 2016: 9 · 2015: 6 · 2014: 9 · 2013: 7 · 2012: 8
- FWCI
- 0.83
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Current Opinion in Neurobiology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Nancy and Buster Alvord Endowment
- National Institutes of Health (1z01ag000258-03, Z01 AG000258)
- National Institute on Aging (AG 05136, T32AG000258, P50AG005136)
- National Institute of Environmental Health Sciences (ES16754, R01ES016754)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- apolipoprotein E, APOE isoforms, Alzheimer's disease, innate immunity, brain, APOE ε4, amyloid-beta, neuroinflammation, neuronal injury
- MeSH terms
- Alzheimer Disease, Animals, Apolipoproteins E, Humans, Immunity, Innate, Genetic Predisposition to Disease, Protein Isoforms
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.
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