APOE‐modulated Aβ‐induced neuroinflammation in Alzheimer's disease: current landscape, novel data, and future perspective

Tai, Leon M.; Ghura, Shivesh; Koster, Kevin P.; Liakaite, Vaiva; Maienschein‐Cline, Mark; Kanabar, Pinal; Collins, Nicole; Ben‐Aissa, Manel; Lei, Arden Zhengdeng; Bahroos, Neil; Green, Stefan J.; Hendrickson, Bill; Van Eldik, Linda J.; LaDu, Mary Jo

doi:10.1111/jnc.13072

Cited by 165Neuroinflammation and Neurodegeneration MechanismsAlzheimer's disease research and treatmentsInflammasome and immune disorders

APOE‐modulated Aβ‐induced neuroinflammation in Alzheimer's disease: current landscape, novel data, and future perspective

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Tai, Leon M., Ghura, Shivesh, Koster, Kevin P., Liakaite, Vaiva, Maienschein‐Cline, Mark, Kanabar, Pinal, Collins, Nicole, Ben‐Aissa, Manel +6 more·2015·Journal of Neurochemistry

DOI 10.1111/jnc.13072PMC PMC4400246

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Abstract

Chronic glial activation and neuroinflammation induced by the amyloid‐β peptide (Aβ) contribute to Alzheimer's disease (AD) pathology.APOE 4 is the greatest AD‐genetic risk factor; increasing risk up to 12‐fold compared toAPOE 3,withAPOE 4‐specific neuroinflammation an important component of this risk. This editorial review discusses the role ofAPOEin inflammation and AD, via a literature review, presentation of novel data on Aβ‐induced neuroinflammation, and discussion of future research directions. The complexity of chronic neuroinflammation, including multiple detrimental and beneficial effects occurring in a temporal and cell‐specific manner, has resulted in conflicting functional data for virtually every inflammatory mediator. Defining a neuroinflammatory phenotype (NIP) is one way to address this issue, focusing on profiling the changes in inflammatory mediator expression during disease progression. Although many studies have shown thatAPOE 4 induces a detrimental NIP in peripheral inflammation and Aβ‐independent neuroinflammation, data forAPOE‐modulated Aβ‐induced neuroinflammation are surprisingly limited. We present data supporting the hypothesis that impaired apoE4 function modulates Aβ‐induced effects on inflammatory receptor signaling, including amplification of detrimental (toll‐like receptor 4‐p38α) and suppression of beneficial (IL‐4R‐nuclear receptor) pathways. To ultimately developAPOEgenotype‐specific therapeutics, it is critical that future studies define the dynamic NIP profile and pathways that underlieAPOE‐modulated chronic neuroinflammation.imageIn this editorial review, we present data supporting the hypothesis that impaired apoE4 function modulates Aβ‐induced effects on inflammatory receptor signaling, including amplification of detrimental (TLR4‐p38α) and suppression of beneficial (IL‐4R‐nuclear receptor) pathways, resulting in an adverse NIP that causes neuronal dysfunction. NIP, Neuroinflammatory phenotype; P.I., pro‐inflammatory; A.I., anti‐inflammatory.

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ApoE may affect Alzheimer's disease pathogenesis through amyloid β-independent pathways.
“In addition, ApoE may directly affect neuroinflammation, cerebral vascular integrity, metabolism, synaptic plasticity, and transcription through amyloid β-independent mechanisms [23,35,50].”
From Apolipoprotein E metabolism and functions in brain and its role in Alzheimer's disease (2017) · cites this paper as [35]
The section “APOE modulation of Aβ-independent neuroinflammation” describes apoE effects on neuroinflammation and blood–brain barrier function without Aβ. The Introduction also lists metabolism and neuronal plasticity as functions modulated by neuroinflammation, but does not establish that apoE directly affects those functions or transcription through Aβ-independent mechanisms. The source supports the claim’s general possibility, not every pathway in the citing sentence. (LLM, conf=0.82)
Experimental — accuracy not yet measured
ApoE modulates neuroinflammation through several pathways, including alteration of cytokine levels in response to various stimulus, microglial migration, or microglia-mediated amyloid β phagocytosis.
“ApoE modulates neuroinflammation through several pathways, including the alteration of cytokine levels in response to various stimulus, microglial migration, or microglia-mediated amyloid β phagocytosis [35].”
From Apolipoprotein E metabolism and functions in brain and its role in Alzheimer's disease (2017) · cites this paper as [35]
The section on Aβ-independent neuroinflammation reports APOE-dependent cytokine responses to LPS and differences in a chemokine that may affect microglial migration. The sections on Aβ-dependent neuroinflammation and neuroinflammatory receptors discuss Aβ phagocytosis, but do not establish that apoE modulates microglia-mediated Aβ phagocytosis. No page numbers are available in our copy. (LLM, conf=0.85)
Experimental — accuracy not yet measured
Impaired APOE4 function is linked to modulation of Aβ-induced neuroinflammation.
“Impaired APOE4 function has also been linked to modulation of Aβ-induced neuroinflammation [67].”
From Analysis of early effects of human APOE isoforms on Alzheimer’s disease and type III hyperlipoproteinemia pathways using knock-in rat models with humanized APP and APOE (2024) · cites this paper as [67]

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Authors: Tai, L. M., Ghura, S., Koster, K. P., Liakaite, V., Maienschein‐Cline, M., Kanabar, P., Collins, N., Ben‐Aissa, M., Lei, A. Z., Bahroos, N., Green, S. J., Hendrickson, B., Van Eldik, L. J., & LaDu, M. J.
Affiliations: University of Illinois Chicago (US)
Sanders‐Brown Center on Aging University of Kentucky Lexington Kentucky USA
Corresponding author: LaDu, Mary Jo
ORCID: Tai, Leon M.
Ghura, Shivesh
Koster, Kevin P.
Maienschein‐Cline, Mark
Bahroos, Neil
Green, Stefan J.
LaDu, Mary Jo
Venue: Journal of Neurochemistry
Publisher: Wiley
Published: 2015-03-18
Volume: 133
Issue: 4
Pages: 465-488
ISSN: 0022-3042 (ISSN-L)
1471-4159
DOI: 10.1111/jnc.13072
PMC: PMC4400246
OpenAlex: W2019786269
Cited by: 165
References: 237
Citations by year: 2026: 11 · 2025: 16 · 2024: 14 · 2023: 11 · 2022: 17 · 2021: 11 · 2020: 15 · 2019: 10 · 2018: 15 · 2017: 15 · 2016: 22 · 2015: 8
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by-nc-nd
creativecommons.org/licenses/by-nc-nd/4.0/ (vor)
Locations: Journal of Neurochemistry (publishedVersion, cc-by-nc-nd)
Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-nd)
PubMed Central (publishedVersion, cc-by-nc-nd)
PubMed (publishedVersion)
Funders: NIH/NIA (P01AG030128, R21AG048498)
NIH/NINDS (R01NS064247)
University of Illinois at Chicago
Center for Clinical and Translational Science (UL1RR029879)
UIC OVCR
NIH (UL1TR000050)
Topics: Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
Keywords: Alzheimer's disease, APOE ε4, amyloid-beta, neuroinflammation, TLR4, p38 MAPK signaling, IL-4 receptor, nuclear receptor signaling, neuronal dysfunction
MeSH terms: Alzheimer Disease, Animals, Apolipoproteins E, Humans, Inflammation, Neuroglia, Signal Transduction, Amyloid beta-Peptides

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APOE‐modulated Aβ‐induced neuroinflammation in Alzheimer's disease: current landscape, novel data, and future perspective

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