Cited by 103Alzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration MechanismsDementia and Cognitive Impairment Research

Apolipoprotein E isoforms and regulation of the innate immune response in brain of patients with Alzheimer's disease

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Keene, C Dirk, Cudaback, Eiron, Li, Xianwu, Montine, Kathleen S, Montine, Thomas J·2011·Current Opinion in Neurobiology

Abstract

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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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)
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
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

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