Apolipoprotein E and Alzheimer’s disease: Findings, hypotheses, and potential mechanisms

Koutsodendris, Nicole; Nelson, Maxine R.; Rao, Antara; Huang, Yadong

doi:10.1146/annurev-pathmechdis-030421-112756

Cited by 231Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Apolipoprotein E and Alzheimer’s disease: Findings, hypotheses, and potential mechanisms

Koutsodendris, Nicole, Nelson, Maxine R., Rao, Antara, Huang, Yadong·2022·Annual Review of Pathology Mechanisms of Disease

DOI 10.1146/annurev-pathmechdis-030421-112756

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Abstract

Alzheimer's disease (AD) is a multifactorial neurodegenerative disorder that involves dysregulation of many cellular and molecular processes. It is notoriously difficult to develop therapeutics for AD due to its complex nature. Nevertheless, recent advancements in imaging technology and the development of innovative experimental techniques have allowed researchers to perform in-depth analyses to uncover the pathogenic mechanisms of AD. An important consideration when studying late-onset AD is its major genetic risk factor, apolipoprotein E4 (apoE4). Although the exact mechanisms underlying apoE4 effects on AD initiation and progression are not fully understood, recent studies have revealed critical insights into the apoE4-induced deficits that occur in AD. In this review, we highlight notable studies that detail apoE4 effects on prominent AD pathologies, including amyloid-β, tau pathology, neuroinflammation, and neural network dysfunction. We also discuss evidence that defines the physiological functions of apoE and outlines how these functions are disrupted in apoE4-related AD.

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Neuroinflammation is a common feature of Alzheimer's disease and may be a potential treatment target.
“Widespread neuroinflammation is a common feature of AD and may present a potential treatment target (Koutsodendris et al., 2021).”
From A novel molecular class that recruits HDAC/MECP2 complexes to PU.1 motifs reduces neuroinflammation (2023) · cites this paper as Koutsodendris et al., 2021
APOE4 exacerbates AD-related pathologies, including amyloid-beta plaques, Tau tangles, neurodegeneration and neuroinflammation.
“It exacerbates AD-related pathologies, including amyloid-beta (Aβ) plaques, Tau tangles, neurodegeneration and neuroinflammation4–16.”
From The APOE-R136S mutation protects against APOE4-driven tau pathology, neurodegeneration, and neuroinflammation (2023) · cites this paper as [4]
ApoE4 exacerbates amyloid pathology by promoting Aβ production and aggregation, and inhibiting Aβ clearance and degradation.
“apoE4 exacerbates amyloid pathology by promoting Aβ production and aggregation, and inhibiting Aβ clearance and degradation”
From ApoE4 reduction: An emerging and promising therapeutic strategy for Alzheimer's disease (2022) · cites this paper as Koutsodendris et al 2021
ApoE4 aggravates tau pathology via promoting tau phosphorylation, aggregation, propagation, and tau-mediated neurodegeneration.
“apoE4 aggravates the tau pathology via promoting tau phosphorylation, aggregation, propagation, and tau-mediated neurodegeneration”
From ApoE4 reduction: An emerging and promising therapeutic strategy for Alzheimer's disease (2022) · cites this paper as Koutsodendris et al 2021
ApoE4 exacerbates amyloid pathology.
“apoE4 exerts its detrimental effects mainly via a ‘toxic’ gain of function mechanism to provoke neuroinflammation, impair cerebrovasculature, and exacerbate amyloid and tau pathologies”
From ApoE4 reduction: An emerging and promising therapeutic strategy for Alzheimer's disease (2022) · cites this paper as Koutsodendris et al 2021

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Apolipoprotein E fragments present in Alzheimer's disease brains induce neurofibrillary tangle-like intracellular inclusions in neurons
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APOE4 exacerbates synapse loss and neurodegeneration in Alzheimer’s disease patient iPSC-derived cerebral organoids
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Phases of Hyperconnectivity and Hypoconnectivity in the Default Mode and Salience Networks Track with Amyloid and Tau in Clinically Normal Individuals
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Association of Factors With Elevated Amyloid Burden in Clinically Normal Older Individuals
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Apolipoprotein E4, inhibitory network dysfunction, and Alzheimer’s disease
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Neuronal hyperactivity due to loss of inhibitory tone in APOE4 mice lacking Alzheimer’s disease-like pathology
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Microglial Activation in Alzheimer Disease: Association with APOE Genotype
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Longitudinal brain imaging in preclinical Alzheimer disease: impact of APOE ε4 genotype
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Authors: Koutsodendris, N., Nelson, M. R., Rao, A., & Huang, Y.
Affiliations: Gladstone Institutes (US)
Corresponding author: Koutsodendris, Nicole
Nelson, Maxine R.
ORCID: Koutsodendris, Nicole
Nelson, Maxine R.
Rao, Antara
Huang, Yadong
Venue: Annual Review of Pathology Mechanisms of Disease
Publisher: Annual Reviews
Published: 2022-01-24
Volume: 17
Issue: 1
Pages: 73-99
ISSN: 1553-4006 (ISSN-L)
1553-4014
DOI: 10.1146/annurev-pathmechdis-030421-112756
OpenAlex: W3198271209
Cited by: 231
References: 182
Citations by year: 2026: 33 · 2025: 54 · 2024: 69 · 2023: 50 · 2022: 22 · 2021: 3
FWCI: 4.80
Type: journal article
Language: en
Open access: closed
Locations: Annual Review of Pathology Mechanisms of Disease (publishedVersion)
PubMed (publishedVersion)
Funders: Eunice Kennedy Shriver National Institute of Child Health and Human Development (T32HD007470)
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 › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords: apolipoprotein E, APOE ε4, Alzheimer's disease, amyloid-beta, tau pathology, neuroinflammation, neural network dysfunction, late-onset Alzheimer's disease, pathogenesis
MeSH terms: Alzheimer Disease, Apolipoproteins E, Humans, Amyloid beta-Peptides, Apolipoprotein E4

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Apolipoprotein E and Alzheimer’s disease: Findings, hypotheses, and potential mechanisms

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