Cited by 212Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

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APOE and Alzheimer’s Disease: Evidence Mounts that Targeting APOE4 may Combat Alzheimer’s Pathogenesis

Uddin, Md. Sahab, Kabir, Md. Tanvir, Al Mamun, Abdullah, Abdel-Daim, Mohamed M., Barreto, George E., Ashraf, Ghulam Md·2019·Molecular Neurobiology

DOI 10.1007/s12035-018-1237-z

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Abstract

Alzheimer's disease (AD) is an immutable neurodegenerative disease featured by the two hallmark brain pathologies that are the extracellular amyloid ß (Aß) and intraneuronal tau protein. People carrying the APOE4 allele are at high risk of AD concerning the ones carrying the ε3 allele, while the ε2 allele abates risk. ApoE isoforms exert a central role in controlling the transport of brain lipid, neuronal signaling, mitochondrial function, glucose metabolism, and neuroinflammation. Regardless of widespread indispensable studies, the appropriate function of APOE in AD etiology stays ambiguous. Existing proof recommends that the disparate outcomes of ApoE isoforms on Aβ accretion and clearance have a distinct function in AD pathogenesis. ApoE-lipoproteins combine diverse cell-surface receptors to transport lipids and moreover to lipophilic Aβ peptide, that is believed to begin deadly events that generate neurodegeneration in the AD. ApoE has great influence in tau pathogenesis, tau-mediated neurodegeneration, and neuroinflammation, as well as α-synucleinopathy, lipid metabolism, and synaptic plasticity despite the presence of Aβ pathology. ApoE4 shows the deleterious effect for AD while the lack of ApoE4 is defensive. Therapeutic strategies primarily depend on APOE suggest to lessen the noxious effects of ApoE4 and reestablish the protective aptitudes of ApoE. This appraisal represents the critical interactions of APOE and AD pathology, existing facts on ApoE levels in the central nervous system (CNS), and the credible active stratagems for AD therapy by aiming ApoE. This review also highlighted utmost ApoE targeting therapeutic tactics that are crucial for controlling Alzheimer's pathogenesis.

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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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Neuronal heparan sulfates promote amyloid pathology by modulating brain amyloid-β clearance and aggregation in Alzheimer’s disease
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Reducing Human Apolipoprotein E Levels Attenuates Age-Dependent Aβ Accumulation in Mutant Human Amyloid Precursor Protein Transgenic Mice
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Small Molecule Structure Correctors Abolish Detrimental Effects of Apolipoprotein E4 in Cultured Neurons
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Genetic studies of human apolipoproteins
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Liver X receptor activation restores memory in aged AD mice without reducing amyloid
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A Synthetic Peptide Blocking the Apolipoprotein E/β-Amyloid Binding Mitigates β-Amyloid Toxicity and Fibril Formation in Vitro and Reduces β-Amyloid Plaques in Transgenic Mice
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Increased tau Phosphorylation in Apolipoprotein E4 Transgenic Mice Is Associated with Activation of Extracellular Signal-regulated Kinase
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Familial Alzheimer’s Disease Mutations within the Amyloid Precursor Protein Alter the Aggregation and Conformation of the Amyloid-β Peptide
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α-Synuclein Expression Modulates Microglial Activation Phenotype
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Reversal of apoE4-driven brain pathology and behavioral deficits by bexarotene
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Absence of α-synuclein affects dopamine metabolism and synaptic markers in the striatum of aging mice
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Implication of apoE isoforms in cholesterol metabolism by primary rat hippocampal neurons and astrocytes.
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Anti-ApoE Antibody Given after Plaque Onset Decreases Aβ Accumulation and Improves Brain Function in a Mouse Model of Aβ Amyloidosis
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Effects of Age, Sex, and Ethnicity on the Association Between Apolipoprotein E Genotype and Alzheimer Disease: A Meta-analysis
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Reduction of Brain β-Amyloid (Aβ) by Fluvastatin, a Hydroxymethylglutaryl-CoA Reductase Inhibitor, through Increase in Degradation of Amyloid Precursor Protein C-terminal Fragments (APP-CTFs) and Aβ Clearance
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Apolipoprotein E and apolipoprotein E receptors modulate Aβ-induced glial neuroinflammatory responses
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α-Synuclein Membrane Association Is Regulated by the Rab3a Recycling Machinery and Presynaptic Activity*
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Multiple pathways of apolipoprotein E signaling in primary neurons
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Exploring the Effect of Phyllanthus emblica L. on Cognitive Performance, Brain Antioxidant Markers and Acetylcholinesterase Activity in Rats: Promising Natural Gift for the Mitigation of Alzheimer's Disease
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Apolipoprotein Receptor 2 and X11α/β Mediate Apolipoprotein E-Induced Endocytosis of Amyloid-β Precursor Protein and β-Secretase, Leading to Amyloid-β Production
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Amino-terminal domain stability mediates apolipoprotein E aggregation into neurotoxic fibrils
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Impact of Apolipoprotein E on Alzheimer’s Disease
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Blocking the Interaction between Apolipoprotein E and Aβ Reduces Intraneuronal Accumulation of Aβ and Inhibits Synaptic Degeneration
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Amyloid β40/42 clearance across the blood-brain barrier following intra-ventricular injections in wild-type, apoE knock-out and human apoE3 or E4 expressing transgenic mice
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Multiple SNPs within and surrounding the apolipoprotein E gene influence cerebrospinal fluid apolipoprotein E protein levels
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Obesity Accelerates Alzheimer-Related Pathology inAPOE4but notAPOE3Mice
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γ-Secretase Catalyzes Sequential Cleavages of the AβPP Transmembrane Domain
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Authors: Uddin, M. S., Kabir, M. T., Al Mamun, A., Abdel-Daim, M. M., Barreto, G. E., & Ashraf, G. M.
Affiliations: Southeast University (BD)
BRAC University (BD)
Pontificia Universidad Javeriana (CO)
King Abdulaziz University (SA)
Corresponding author: Uddin, Md. Sahab
Ashraf, Ghulam Md
ORCID: Uddin, Md. Sahab
Kabir, Md. Tanvir
Barreto, George E.
Ashraf, Ghulam Md
Venue: Molecular Neurobiology
Publisher: Springer Science and Business Media LLC
Published: 2018-07-21
Volume: 56
Issue: 4
Pages: 2450-2465
ISSN: 0893-7648 (ISSN-L)
1559-1182
DOI: 10.1007/s12035-018-1237-z
OpenAlex: W2883974615
Cited by: 212
References: 175
Citations by year: 2026: 9 · 2025: 25 · 2024: 15 · 2023: 34 · 2022: 34 · 2021: 23 · 2020: 49 · 2019: 20 · 2018: 3
FWCI: 3.12
Type: journal article
Language: en
Open access: closed
Licence: www.springer.com/tdm (tdm)
Locations: Molecular Neurobiology (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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, APOE isoforms, neuroinflammation, lipid metabolism, synaptic plasticity, synucleinopathies, neurodegeneration
MeSH terms: Alzheimer Disease, Amyloid, Animals, Apolipoproteins E, Humans, Risk Factors, Genetic Predisposition to Disease, Apolipoprotein E4

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APOE and Alzheimer’s Disease: Evidence Mounts that Targeting APOE4 may Combat Alzheimer’s Pathogenesis

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