MicroRNAs and MAPKs: Evidence of These Molecular Interactions in Alzheimer's Disease

• Published in: International journal of molecular sciences Vol. 24; no. 5; p. 4736
• Main Authors: Raffaele, Ivana, Silvestro, Serena, Mazzon, Emanuela
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 01.03.2023; MDPI
• Subjects: Advertising executives; Alzheimer Disease - metabolism; Alzheimer's disease; Amyloid beta-Peptides - metabolism; Animal models; Animals; Brain - metabolism; Cell death; Dementia disorders; Deregulation; Development and progression; Inflammation; Kinases; MAP kinase; MAPK; MicroRNA; MicroRNAs; MicroRNAs - genetics; miRNA; Mitogen-Activated Protein Kinases - metabolism; Molecular interactions; Neurodegeneration; Neuroprotection; Oxidative stress; Pathogenesis; Pathology; Protein kinases; Review; Signal Transduction; Tau protein; microRNAs; neurodegeneration; Alzheimer’s disease; MAPK
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms24054736

Alzheimer's disease (AD) is a neurodegenerative disorder known to be the leading cause of dementia worldwide. Many microRNAs (miRNAs) were found deregulated in the brain or blood of AD patients, suggesting a possible key role in different stages of neurodegeneration. In particular, mitogen-activated protein kinases (MAPK) signaling can be impaired by miRNA dysregulation during AD. Indeed, the aberrant MAPK pathway may facilitate the development of amyloid-beta (Aβ) and Tau pathology, oxidative stress, neuroinflammation, and brain cell death. The aim of this review was to describe the molecular interactions between miRNAs and MAPKs during AD pathogenesis by selecting evidence from experimental AD models. Publications ranging from 2010 to 2023 were considered, based on PubMed and Web of Science databases. According to obtained data, several miRNA deregulations may regulate MAPK signaling in different stages of AD and conversely. Moreover, overexpressing or silencing miRNAs involved in MAPK regulation was seen to improve cognitive deficits in AD animal models. In particular, miR-132 is of particular interest due to its neuroprotective functions by inhibiting Aβ and Tau depositions, as well as oxidative stress, through ERK/MAPK1 signaling modulation. However, further investigations are required to confirm and implement these promising results.