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

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

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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Crossref · 10.1007/s12035-018-1237-z

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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
Venue
Molecular Neurobiology
Published
2018-07-21
Volume
56
Issue
4
Pages
2450-2465
ISSN
  • 0893-7648 (ISSN-L)
  • 1559-1182
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
Locations
  • Molecular Neurobiology (publishedVersion)
  • PubMed (publishedVersion)
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, 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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