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Cited by 115Ferroptosis and cancer prognosisAlzheimer's disease research and treatmentsNeurological diseases and metabolism

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The mechanisms of ferroptosis and its role in alzheimer’s disease

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Ma, Hongyue, Dong, Yan, Chu, Yanhui, Guo, Yanqin, Li, Luxin·2022·Frontiers in Molecular Biosciences
DOI 10.3389/fmolb.2022.965064PMC PMC9459389
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Abstract

Alzheimer’s disease (AD) accounts for two-thirds of all dementia cases, affecting 50 million people worldwide. Only four of the more than 100 AD drugs developed thus far have successfully improved AD symptoms. Furthermore, these improvements are only temporary, as no treatment can stop or reverse AD progression. A growing number of recent studies have demonstrated that iron-dependent programmed cell death, known as ferroptosis, contributes to AD-mediated nerve cell death. The ferroptosis pathways within nerve cells include iron homeostasis regulation, cystine/glutamate (Glu) reverse transporter (system xc − ), glutathione (GSH)/glutathione peroxidase 4 (GPX4), and lipid peroxidation. In the regulation pathway of AD iron homeostasis, abnormal iron uptake, excretion and storage in nerve cells lead to increased intracellular free iron and Fenton reactions. Furthermore, decreased Glu transporter expression leads to Glu accumulation outside nerve cells, resulting in the inhibition of the system xc − pathway. GSH depletion causes abnormalities in GPX4, leading to excessive accumulation of lipid peroxides. Alterations in these specific pathways and amino acid metabolism eventually lead to ferroptosis. This review explores the connection between AD and the ferroptosis signaling pathways and amino acid metabolism, potentially informing future AD diagnosis and treatment methodologies.

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Metadata

Authors
Ma, H., Dong, Y., Chu, Y., Guo, Y., & Li, L.
Affiliations
Mudanjiang Medical University (CN)
Corresponding author
  • Guo, Yanqin
  • Li, Luxin
ORCID
Venue
Frontiers in Molecular Biosciences
Publisher
Frontiers Media SA
Published
2022-08-26
Volume
9
Pages
965064-965064
ISSN
2296-889X (ISSN-L)
DOI
10.3389/fmolb.2022.965064
PMC
PMC9459389
OpenAlex
W4293109399
Cited by
115
References
14
Citations by year
2026: 37 · 2025: 30 · 2024: 29 · 2023: 16 · 2022: 3
FWCI
2.11
Type
journal article
Language
en
Open access
Licence
Locations
  • Frontiers in Molecular Biosciences (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
  • Greater South Information System
Funders
Natural Science Foundation of Heilongjiang Province (H2017077, 2020GSP09)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Ferroptosis and cancer prognosis
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neurological diseases and metabolism
Keywords
ferroptosis, Alzheimer's disease, iron homeostasis, system xc-, cystine-glutamate exchange, glutathione, GPX4, lipid peroxidation, Fenton reaction, glutamate accumulation, amino acid metabolism, neuronal cell death, neurodegeneration

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

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