Cited by 33Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchRedox biology and oxidative stress

Redox signaling and Alzheimer’s disease: from pathomechanism insights to biomarker discovery and therapy strategy

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Chen, Yuan-Yuan, Wang, Min-Chang, Wang, Yan-Ni, Hu, He-He, Liu, Qing-Quan, Liu, Hai-Jing, Zhao, Ying-Yong·2020·Biomarker Research

Abstract

Aging and average life expectancy have been increasing at a rapid rate, while there is an exponential risk to suffer from brain-related frailties and neurodegenerative diseases as the population ages. Alzheimer’s disease (AD) is the most common neurodegenerative disease worldwide with a projected expectation to blossom into the major challenge in elders and the cases are forecasted to increase about 3-fold in the next 40 years. Considering the etiological factors of AD are too complex to be completely understood, there is almost no effective cure to date, suggesting deeper pathomechanism insights are urgently needed. Metabolites are able to reflect the dynamic processes that are in progress or have happened, and metabolomic may therefore provide a more cost-effective and productive route to disease intervention, especially in the arena for pathomechanism exploration and new biomarker identification. In this review, we primarily focused on how redox signaling was involved in AD-related pathologies and the association between redox signaling and altered metabolic pathways. Moreover, we also expatiated the main redox signaling-associated mechanisms and their cross-talk that may be amenable to mechanism-based therapies. Five natural products with promising efficacy on AD inhibition and the benefit of AD intervention on its complications were highlighted as well. Graphical Abstract:

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  • For males, no significant GO terms were identified at 25% FDR; the strongest enrichment with nominal P<0.001 involved immune responses to accumulation of amyloid-β in the brain, such as regulation of T cell activation via T cell receptor contact with antigen bound to MHC molecule on antigen presenting cell, and other biological processes recently implicated in AD such as response to angiotensin [

    “For males, we did not identify any significant GO terms at 25% FDR; the strongest enrichment with nominal P-value less than 0.001 involved immune responses to the accumulation of amyloid-β (Aβ) in the brain, such as regulation of T cell activation via T cell receptor contact with antigen bound to MHC molecule on antigen presenting cell, and other biological processes recently implicated in AD such”

    From Sex-specific DNA methylation differences in Alzheimer’s disease pathology (2021) · cites this paper as [60]

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Authors
Chen, Y.-Y., Wang, M.-C., Wang, Y.-N., Hu, H.-H., Liu, Q.-Q., Liu, H.-J., & Zhao, Y.-Y.
Affiliations
Northwest University (CN)
Corresponding author
Zhao, Ying-Yong
Venue
Biomarker Research
Published
2020-09-11
Volume
8
Issue
1
Pages
42-42
ISSN
2050-7771 (ISSN-L)
OpenAlex
W3085682383
Cited by
33
References
12
Citations by year
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0.67
Type
journal article
Language
en
Open access
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  • Biomarker Research (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • National Key Research and Development Project of China (2019YFC1709405)
  • National Natural Science Foundation of China (81603271, 81872985, 81673578)
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 › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Redox biology and oxidative stress
Keywords
Alzheimer's disease, redox signaling, oxidative stress, metabolomics, biomarker discovery, metabolic pathways, neurodegeneration, natural products, treatment options, aging

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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