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Cited by 19Autophagy in Disease and TherapyAlzheimer's disease research and treatmentsMitochondrial Function and Pathology

A Review of ApoE4 Interference Targeting Mitophagy Molecular Pathways for Alzheimer's Disease

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Chen, Huiyi, Chen, Feng, Jiang, Ying, Zhang, Lu, Hu, Guizhen, Sun, Furong, Zhang, Miaoping, Ji, Yao +4 more·2022·Frontiers in Aging Neuroscience
DOI 10.3389/fnagi.2022.881239PMC PMC9166238
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Abstract

Alzheimer's disease (AD) is one of the major worldwide causes of dementia that is characterized by irreversible decline in learning, memory loss, and behavioral impairments. Mitophagy is selective autophagy through the clearance of aberrant mitochondria, specifically for degradation to maintain energy generation and neuronal and synaptic function in the brain. Accumulating evidence shows that defective mitophagy is believed to be as one of the early and prominent features in AD pathogenesis and has drawn attention in the recent few years. APOE ε4 allele is the greatest genetic determinant for AD and is widely reported to mediate detrimental effects on mitochondria function and mitophagic process. Given the continuity of the physiological process, this review takes the mitochondrial dynamic and mitophagic core events into consideration, which highlights the current knowledge about the molecular alterations from an APOE-genotype perspective, synthesizes ApoE4-associated regulations, and the cross-talk between these signaling, along with the focuses on general autophagic process and several pivotal processes of mitophagy, including mitochondrial dynamic (DRP1, MFN-1), mitophagic induction (PINK1, Parkin). These may shed new light on the link between ApoE4 and AD and provide novel insights for promising mitophagy-targeted therapeutic strategies for AD.

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  • In ApoE4 mutant mice, mitochondrial phenotypes include increased fusion, disrupted mitophagy, and calcium overload.

    “In ApoE4 mutant mice, mitochondrial phenotypes include increased fusion, disrupted mitophagy, and calcium overload [45–47].”

    From Dyslipidemia-Induced Mitochondrial Dysfunctions in the Brains Does Not Reach Pathological Levels in the ApoE-Knockout Mice (2026) · cites this paper as [46]

    The ‘ApoE4 and Mitochondrial Fusion in AD’ section reports hyperfusion in ApoE4 astrocytes and elevated MFN-1 in brain tissue from young ApoE4 mice. ‘ApoE4 and Mitophagy Induction in AD’ describes altered mitophagy-related proteins in ApoE4 mice, but frames impaired mitophagy as an inference. The fusion section mentions excess calcium in the cytoplasm, not mitochondrial calcium overload in ApoE4 mice; the sentence therefore presents all three as established mouse mitochondrial phenotypes more strongly than this review supports. (LLM, conf=0.86)

    Experimental — accuracy not yet measured

  • Sirt1 is involved in normal aging and has neuroprotective effects, such as promoting autophagy.

    “Sirt1 is involved in normal aging and has neuroprotective effects, such as promoting autophagy [4,43]”

    From Apoe4 and Alzheimer’s Disease Pathogenesis—Mitochondrial Deregulation and Targeted Therapeutic Strategies (2023) · cites this paper as [4]

    The “ApoE4 and Mitophagy Induction in AD” section says SIRT1 regulates autophagy and mitophagy and has neuroprotective implications in Alzheimer’s disease; it also describes SIRT1 activation facilitating mitophagy. The paper does not explicitly address SIRT1’s involvement in normal aging, so that part of the claim is not supported by our copy. (LLM, conf=0.85)

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Cited by

Sorted by citations

Authors
Chen, H., Chen, F., Jiang, Y., Zhang, L., Hu, G., Sun, F., Zhang, M., Ji, Y., Chen, Y., Che, G., Zhou, X., & Zhang, Y.
Affiliations
  • Yue Bei People's Hospital (CN)
  • Guangdong Medical College (CN)
Corresponding author
Che, Gang
ORCID
Venue
Frontiers in Aging Neuroscience
Publisher
Frontiers Media SA
Published
2022-05-20
Volume
14
Pages
881239-881239
ISSN
1663-4365 (ISSN-L)
DOI
10.3389/fnagi.2022.881239
PMC
PMC9166238
OpenAlex
W4280591287
Cited by
19
References
23
Citations by year
2026: 6 · 2025: 2 · 2024: 4 · 2023: 6 · 2022: 1
FWCI
0.51
Type
journal article
Language
en
Open access
Licence
Locations
  • Frontiers in Aging Neuroscience (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
Topics
  • Health Sciences › Medicine › Epidemiology › Autophagy in Disease and Therapy
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
Keywords
Alzheimer's disease, APOE ε4, mitophagy, mitochondrial dynamics, Drp1, Mfn1, PINK1, Parkin, autophagy, mitochondrial dysfunction, therapeutic target

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