Advances with microRNAs in Parkinson&amp;rsquo;s disease research

Ma, Liuqing; Wei, Liangming; Wu, Fei; Hu, Zhenhua; Liu, Zhenguo; Yuan, Weien

doi:10.2147/dddt.s48500

Cited by 33 publications

(16 citation statements)

References 105 publications

(126 reference statements)

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“…As an example, the list of miRNAs that target other PD-related genes such as LRKK2, Parkin and Pink becomes longer every year. Several reviews are available that illustrate the complex interplay of miRNAs in PD (Salta and De Strooper, 2012; Ma et al, 2013; Majidinia et al, 2016; Xie and Chen, 2016). …”

Section: Discussionmentioning

confidence: 99%

Role of microRNAs in the Regulation of α-Synuclein Expression: A Systematic Review

Recasens

Perier

Sue

2016

Front. Mol. Neurosci.

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Growing evidence suggests that increased levels of α-synuclein might contribute to the pathogenesis of Parkinson’s disease (PD) and therefore, it is crucial to understand the mechanisms underlying α-synuclein expression. Recently, microRNAs (miRNAs) have emerged as key regulators of gene expression involved in several diseases such as PD and other neurodegenerative disorders. A systematic literature search was performed here to identify microRNAs that directly or indirectly impact in α-synuclein expression/accumulation and describe its mechanism of action. A total of 27 studies were incorporated in the review article showing evidences that six microRNAs directly bind and regulate α-synuclein expression while several miRNAs impact on α-synuclein expression indirectly by targeting other genes. In turn, α-synuclein overexpression also impacts miRNAs expression, indicating the complex network between miRNAs and α-synuclein. From the current knowledge on the central role of α-synuclein in PD pathogenesis/progression, miRNAs are likely to play a crucial role at different stages of PD and might potentially be considered as new PD therapeutic approaches.

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Section: Discussionmentioning

confidence: 99%

Role of microRNAs in the Regulation of α-Synuclein Expression: A Systematic Review

Recasens

Perier

Sue

2016

Front. Mol. Neurosci.

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“…Mutated leucine-rich repeat kinase2 (LRRK2) counteract let-7 miRNA due to which overexpressed E2F1 transcription factor leads to death of dopaminergic neuron. PD model of C. elegans also has low level of let-7 miRNA which was studied via microarray as well as qPCR techniques [17,36,37].…”

Section: Let-7 In Parkinson's Diseasementioning

confidence: 99%

Role of MicroRNA Let-7 in Modulating Multifactorial Aspect of Neurodegenerative Diseases: an Overview

et al. 2015

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The multifactorial aspect of neurodegenerative diseases has posed challenges in terms of understanding various mechanistic cues behind these ailments. The fact that single microRNA (miRNA) molecules can regulate multiple genes and associated pathways makes these molecules interesting for studies within the area of age-associated neurodegenerative diseases. miRNAs are endogenous, evolutionarily conserved, 20-23 nucleotide non-coding RNAs, which were first discovered in Caenorhabditis elegans. They play a key role in gene regulation and are known to be deregulated in many disease conditions. Steady regulations of miRNAs are required for normal biological processes. One of the crucial miRNA molecules let-7 is highly conserved and is known to be required for development and viability. It acts as a regulator for oncogenes and insulin-PI3K-mTOR pathway genes. Upregulation of let-7 impairs glucose homeostasis and results in degeneration of neurons, while its downregulation leads to cancer. Maturation of let-7 in cancer subjects is inhibited by lin-28, an RNA-binding protein inhibitor. This highlights the importance of let-7 miRNAs in various diseases and developmental processes. This article provides an overview on the functions of let-7 and its probable association with various neurodegenerative diseases.

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“…Interestingly, the expression of SNCA mRNA is negatively regulated by at least two microRNAs, miR-7 and miR-153 (Doxakis, 2010;Junn et al, 2009) and DJ1 and Parkin expression has also been suggested to be connected to reduced miR-34b/c expression in late stage PD brain samples (Miñones-Moyano et al, 2011). While much more work is needed to elucidate which and how miRNAs are controlling PD-gene expression, the discovery that LRRK2 may more directly affect the expression and function of miRNAs themselves may suggest a more direct connection between PD and miRNA function (Ma et al, 2013;Mouradian, 2012).…”

Section: Misregulation Of Micrornasmentioning

confidence: 99%