International Journal of
eISSN: 2573-2889
Submit manuscript...
Short Communication Volume 7 Issue 1
The Role of MicroRNAs in regulating genes related to neurodegenerative diseases
Joao Vitor Carvalho Piasentim,
Verify Captcha
Regret for the inconvenience: we are taking measures to prevent fraudulent form submissions by extractors and page crawlers. Please type the correct Captcha word to see email ID.
Samya Nogueira Asseiss
Verify Captcha
Regret for the inconvenience: we are taking measures to prevent fraudulent form submissions by extractors and page crawlers. Please type the correct Captcha word to see email ID.
Faculty of Medicine, Union of Faculties of the Great Lakes -UNILAGO, Brazil
Correspondence: Joao Vitor Carvalho Piasentim, Faculty of Medicine, Union of Faculties of the Great Lakes-UNILAGO, Sao José do Rio Preto, SP, Brazil
Received: June 22, 2024 | Published: July 1, 2024
Citation: Piasentim JVC, Asseiss SN. The Role of MicroRNAs in regulating genes related to neurodegenerative diseases. Int J Mol Biol Open Access. 2024;7(1):81-82. DOI: 10.15406/ijmboa.2024.07.00174
Abstract
Neurodegenerative diseases pose significant challenges to public health worldwide. MicroRNAs (miRNAs) have emerged as critical regulators of gene expression and are implicated in the pathogenesis of various neurodegenerative disorders. This review comprehensively explores the current understanding of how miRNAs influence gene networks involved in Alzheimer disease, Parkinson disease and amyotrophic lateral sclerosis. We discuss the mechanisms by which miRNAs modulate disease associated genes, their potential as diagnostic biomarkers, and therapeutic targets in neurodegeneration.
Keywords: microRNA, neurodegenerative diseases, Alzheimer disease, parkinson disease, amyotrophic lateral sclerosis
Introduction
Neurodegenerative diseases, characterized by progressive loss of neuronal function and structure, represent a growing burden on healthcare systems globally. Understanding the molecular mechanisms underlying these disorders is crucial for developing effective treatments. MicroRNAs (miRNAs), small noncoding RNAs,1 have garnered significant attention for their regulatory roles in gene expression, influencing pathways implicated in neurodegeneration. This review aims to summarize the current literature on miRNA mediated gene regulation in Alzheimer disease (AD), Parkinson disease (PD), and amyotrophic lateral sclerosis (ALS),2 highlighting their potential implications for disease pathogenesis and therapeutic interventions.
Material and methods
A comprehensive literature search was conducted using electronic databases such as PubMed, Web of Science, and Scopus. Keywords included microRNA, neurodegenerative diseases, Alzheimer disease, Parkinson disease, amyotrophic lateral sclerosis, and gene regulation. Articles published within the last decade, including reviews, original research, and clinical studies, were selected for inclusion. Data were synthesized to elucidate the roles of specific miRNAs in modulating disease-related genes and pathways.
Results
MicroRNAs play diverse roles in neurodegenerative diseases by targeting key genes involved in neuronal survival, apoptosis, inflammation, and protein aggregation pathways. In AD, miRNAs such as miR-29, miR-124, and miR-132 regulate genes associated with amyloid-beta metabolism and tau protein phosphorylation. In PD, miRNAs including miR-133b, miR-7, and miR-34a modulate genes involved in alpha-synuclein aggregation and dopaminergic neuron function.3,4 ALS is influenced by miRNAs like miR206 and miR-155, which regulate genes related to neuro inflammation and oxidative stress. Dysregulation of these miRNAs contributes to disease pathogenesis, making them potential biomarkers and therapeutic targets.5
Discussion
The dysregulation of miRNAs in neurodegenerative diseases reflects their multifaceted roles in pathophysiology.6,7 Challenges include the complexity of miRNA target interactions, tissue-specific expression patterns, and variability in disease progression among patients. Advances in sequencing technologies and bioinformatics have enabled the identification of miRNA signatures associated with disease subtypes and progression stages. Therapeutic strategies targeting miRNAs, such as antisense oligonucleotides and viral vector-mediated delivery systems, hold promise for restoring miRNA homeostasis and ameliorating disease symptoms.
Conclusion
MicroRNAs represent integral components of gene regulatory networks implicated in neurodegenerative diseases.8 Understanding their roles in disease pathogenesis offers new avenues for developing biomarkers and therapeutic interventions. Future research should focus on elucidating miRNA-target interactions, validating biomarker utility in clinical settings, and advancing miRNA-based therapies towards clinical trials.
Acknowledgments
None.
Conflicts of interest
The authors declare that there are no conflicts of interest.
References
- Kumar S. Role of non-coding RNAs in neurodegenerative diseases. 2017.
- Jovicic A, Gitler AD. Distinct roles of ALS- associated proteins FUS/TLS and TDP-43 intersect in processing long pre-mRNAs. 2017.
- Salta E, De Strooper B. microRNA-132: a key noncoding RNA operating in the cellular phase of Alzheimer disease. FASEB J. 2017;31(2):424–433.
- Guo R. The regulatory roles of long noncoding RNAs in central nervous system disorders. 2018.
- Wei JY, Derek DY, Songqing N, et al. Dicer is required for embryonic angiogenesis during mouse development. J Biol chem. 2005;280(10):9330–9335.
- Lau P, De Strooper B. Dysregulated microRNAs in neurodegenerative disorders. Semin Cell Dev Biol. 2010;21(7):768–773.
- Schonrock N, Gotz J. Decoding the non-coding RNAs in Alzheimer disease. Cell Mol Life Sci. 2012;69(21):3543–3559.
- Delay C, Hebert SS. MicroRNAs and Alzheimer disease mouse models: current insights and future research avenues. Int J Alzheimers Dis. 2011;2011:894938
©2024 Piasentim, et al. This is an open access article distributed under the terms of the, which permits unrestricted use, distribution, and build upon your work non-commercially.