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Cited by 112Alzheimer's disease research and treatmentsMicroRNA in disease regulationNeuroinflammation and Neurodegeneration Mechanisms

The Regulation of microRNAs in Alzheimer's Disease

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Kou, Xianjuan, Chen, Dandan, Chen, Ning·2020·Frontiers in Neurology
DOI 10.3389/fneur.2020.00288PMC PMC7180504
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Abstract

MicroRNAs are small non-coding nucleic acids that are responsible for regulating the gene expression by binding to the coding region and 3' and 5' un-translated region of target messenger RNA. Approximately 70% of known microRNAs are expressed in the brain and increasing evidences demonstrate the possible involvement of microRNAs in Alzheimer's disease (AD) according to the statistics. The characteristic symptoms of AD are the progressive loss of memory and cognitive functions due to the deposition of amyloid β (Aβ) peptide, intracellular aggregation of hyperphosphorylated Tau protein, the loss of synapses, and neuroinflammation, as well as dysfunctional autophagy. Therefore, microRNA-mediated regulation for above-mentioned changes may be the potential therapeutic strategies for AD. In this review, the role of specific microRNAs involved in AD and corresponding applications are systematically discussed, including positive effects associated with the reduction of Aβ or Tau protein, the protection of synapses, the inhibition of neuroinflammation, the mitigation of aging, and the induction of autophagy in AD. It will be beneficial to develop effective targets for establishing a cross link between pharmacological intervention and AD in the near future.

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  • Neu-AD cells showed upregulated miR-21, miR-124 and miR-125b.

    “However, Neu-AD showed upregulated miR-21, miR-124 and miR-125b, which are all found to be dysregulated in AD models [25,39,76].”

    From Emerging Role of miR-21-5p in Neuron–Glia Dysregulation and Exosome Transfer Using Multiple Models of Alzheimer’s Disease (2022) · cites this paper as [76]

    The sections on synaptic dysfunction and tau hyperphosphorylation report elevated miR-124 in Tg2576 mice and elevated miR-125b in AD animal models. The cited paper does not establish dysregulation of miR-21 or report the Neu-AD cell result; the citation therefore supports only part of the statement about dysregulation in AD models. (LLM, conf=0.86)

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Cited by

Sorted by citations

Authors
Kou, X., Chen, D., & Chen, N.
Affiliations
Wuhan Sports University (CN)
Corresponding author
Chen, Ning
ORCID
Venue
Frontiers in Neurology
Publisher
Frontiers Media SA
Published
2020-04-17
Volume
11
Pages
288-288
ISSN
1664-2295 (ISSN-L)
DOI
10.3389/fneur.2020.00288
PMC
PMC7180504
OpenAlex
W3016444570
Cited by
112
References
9
Citations by year
2026: 5 · 2025: 14 · 2024: 19 · 2023: 22 · 2022: 26 · 2021: 21 · 2020: 5
FWCI
2.36
Type
journal article
Language
en
Open access
Licence
Locations
  • Frontiers in Neurology (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • National Natural Science Foundation of China
  • Natural Science Foundation of Hubei Province
  • Hubei Provincial Department of Education
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
microRNA, Alzheimer's disease, amyloid-beta, tau protein, neuroinflammation, autophagy, aging, gene expression regulation, therapeutic target

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