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Cited by 41Alzheimer's disease research and treatmentsMicroRNA in disease regulationNeuroinflammation and Neurodegeneration Mechanisms

Potential microRNA-related targets in clearance pathways of amyloid-β: novel therapeutic approach for the treatment of Alzheimer’s disease

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Madadi, Soheil, Schwarzenbach, Heidi, Saidijam, Massoud, Mahjub, Reza, Soleimani, Meysam·2019·Cell & Bioscience
DOI 10.1186/s13578-019-0354-3PMC PMC6852943
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Abstract

Imbalance between amyloid-beta (Aβ) peptide synthesis and clearance results in Aβ deregulation. Failure to clear these peptides appears to cause the development of Alzheimer’s disease (AD). In recent years, microRNAs have become established key regulators of biological processes that relate among others to the development and progression of neurodegenerative diseases, such as AD. This review article gives an overview on microRNAs that are involved in the Aβ cascade and discusses their inhibitory impact on their target mRNAs whose products participate in Aβ clearance. Understanding of the mechanism of microRNA in the associated signal pathways could identify novel therapeutic targets for the treatment of AD.

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  • Some microRNAs (including miR-19, -27a, -96, -143, -146a, -155, -185, -203, -223, and -590) modulate TLR activity.

    “Some microRNAs have been identified as modulators of TLRs activity e.g., miR-19, -27a, -96, -143, -146a, -155, -185, -203, -223, -590 [204].”

    From MicroRNAs as Regulators of Phagocytosis (2022) · cites this paper as [204]

    The Toll-like receptors section says that miRNAs inhibit TLR2 and TLR4 expression, and the References identify miR-19, miR-27a, and miR-203 as targeting or regulating those receptors. The passages available from our copy do not establish the claimed TLR-modulating role for every other miRNA in the cited list, although the section points to Table 5 for additional miRNAs. (LLM, conf=0.79)

    Experimental — accuracy not yet measured

  • These microRNAs modulate expression of TLR2, TLR4, and scavenger receptors SR-A, SR-BI, and CD36.

    “They modulate expression of TLR2 and TLR4, as well as scavenger receptors (SR-A, SR-BI, CD36).”

    From MicroRNAs as Regulators of Phagocytosis (2022) · cites this paper as [204]

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References 300 · Cited by 41

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Authors
Madadi, S., Schwarzenbach, H., Saidijam, M., Mahjub, R., & Soleimani, M.
Affiliations
  • Hamedan University of Medical Sciences (IR)
  • University Medical Center Hamburg-Eppendorf (DE)
Corresponding author
Soleimani, Meysam
ORCID
Venue
Cell & Bioscience
Publisher
Springer Science and Business Media LLC
Published
2019-11-12
Volume
9
Issue
1
Pages
91-91
ISSN
2045-3701 (ISSN-L)
DOI
10.1186/s13578-019-0354-3
PMC
PMC6852943
OpenAlex
W2983989986
Cited by
41
References
300
Citations by year
2026: 1 · 2025: 4 · 2024: 6 · 2023: 1 · 2022: 13 · 2021: 6 · 2020: 8 · 2018: 1
FWCI
0.88
Type
journal article
Language
en
Open access
Licence
Locations
  • Cell & Bioscience (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
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, amyloid-beta, amyloid-beta clearance, Alzheimer's disease, microRNA target mRNAs, amyloid hypothesis, therapeutic target, neurodegeneration

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