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

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-acti...

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Published inInternational journal of molecular sciences Vol. 24; no. 5; p. 4736
Main Authors Raffaele, Ivana, Silvestro, Serena, Mazzon, Emanuela
Format Journal Article
LanguageEnglish
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
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Abstract 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.
AbstractList 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.
Audience Academic
Author Raffaele, Ivana
Silvestro, Serena
Mazzon, Emanuela
AuthorAffiliation IRCCS Centro Neurolesi Bonino Pulejo, Via Provinciale Palermo, Contrada Casazza, 98124 Messina, Italy
AuthorAffiliation_xml – name: IRCCS Centro Neurolesi Bonino Pulejo, Via Provinciale Palermo, Contrada Casazza, 98124 Messina, Italy
Author_xml – sequence: 1
  givenname: Ivana
  surname: Raffaele
  fullname: Raffaele, Ivana
  organization: IRCCS Centro Neurolesi Bonino Pulejo, Via Provinciale Palermo, Contrada Casazza, 98124 Messina, Italy
– sequence: 2
  givenname: Serena
  orcidid: 0000-0003-3846-0785
  surname: Silvestro
  fullname: Silvestro, Serena
  organization: IRCCS Centro Neurolesi Bonino Pulejo, Via Provinciale Palermo, Contrada Casazza, 98124 Messina, Italy
– sequence: 3
  givenname: Emanuela
  surname: Mazzon
  fullname: Mazzon, Emanuela
  organization: IRCCS Centro Neurolesi Bonino Pulejo, Via Provinciale Palermo, Contrada Casazza, 98124 Messina, Italy
BackLink https://www.ncbi.nlm.nih.gov/pubmed/36902178$$D View this record in MEDLINE/PubMed
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Issue 5
Keywords microRNAs
neurodegeneration
Alzheimer’s disease
MAPK
Language English
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Snippet Alzheimer's disease (AD) is a neurodegenerative disorder known to be the leading cause of dementia worldwide. Many microRNAs (miRNAs) were found deregulated in...
Alzheimer’s disease (AD) is a neurodegenerative disorder known to be the leading cause of dementia worldwide. Many microRNAs (miRNAs) were found deregulated in...
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pubmedcentral
proquest
gale
crossref
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SourceType Open Website
Open Access Repository
Aggregation Database
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StartPage 4736
SubjectTerms 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
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Title MicroRNAs and MAPKs: Evidence of These Molecular Interactions in Alzheimer's Disease
URI https://www.ncbi.nlm.nih.gov/pubmed/36902178
https://www.proquest.com/docview/2785219184
https://search.proquest.com/docview/2786094896
https://pubmed.ncbi.nlm.nih.gov/PMC10003111
https://doaj.org/article/ecc5474123674267833b06fb3419e7ce
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