4.6 Review

The Regulation of microRNAs in Alzheimer's Disease

Journal

FRONTIERS IN NEUROLOGY
Volume 11, Issue -, Pages -

Publisher

FRONTIERS MEDIA SA
DOI: 10.3389/fneur.2020.00288

Keywords

Alzheimer's disease; A beta; microRNA; biomarker; autophagy

Funding

  1. National Natural Science Foundation of China [81601228]
  2. Natural Science Foundation of Hubei province [2019CFB761]
  3. Scientific Research Project of Hubei Ministry of Education [B2019200]
  4. Donghu Scholar Program from Wuhan Sports University
  5. Outstanding Youth Scientific and Research Team from Hubei Provincial Department of Education [T201624]
  6. Hubei Superior Discipline Group of Physical Education and Health Promotion
  7. Chutian Scholar Program from Wuhan Sports University
  8. Innovative Start-Up Foundation from Wuhan Sports University

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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 beta (A beta) 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 A beta 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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