The involvement of microRNAs in neurodegenerative diseases

Maciotta, Simona; Meregalli, Mirella; Torrente, Yvan

doi:10.3389/fncel.2013.00265

Cited by 212 publications

(165 citation statements)

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“…Alzheimer's disease (AD) is the most common cause of dementia worldwide and is characterized by pathological β-amyloid (Aβ) deposition and neurodegeneration (1). Although the precise mechanisms underlying neurodegeneration in AD remain to be elucidated, the role of the complex interaction between genetic and environmental factors has been supported in previous studies (2)(3)(4).…”

Section: Introductionmentioning

confidence: 99%

MicroRNA-29c targets β-site amyloid precursor protein-cleaving enzyme 1 and has a neuroprotective role in vitro and in vivo

Yang

Song

Zhou

et al. 2015

Molecular Medicine Reports

103

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Abstract. Alzheimer's disease (AD), characterized by β-amyloid deposition and neurodegeneration, is the most common cause of dementia worldwide. Emerging evidence suggests that ectopic expression of micro (mi)RNAs is involved in the pathogenesis of AD. There is increasing evidence that miRNAs expressed in the brain are involved in neuronal development, survival and apoptosis. The expression of β-site amyloid precursor protein-cleaving enzyme 1 (BACE1) is regulated by dysregulated miRNAs in the brain. The present study determined the expression levels of the miRNA-29 (miR-29) family in peripheral blood samples of patients with AD and demonstrated a marked decrease in the expression of miR-29c compared with age-matched controls. In addition, a significant increase in the exprssion of BACE1 was observed in the peripheral blood of patients with AD. Correlation analysis revealed that the expression of miR-29c was negatively correlated with the protein expression of BACE1 in the peripheral blood samples from patients with AD. The present study also investigated the role of miR-29 on hippocampal neurons in vitro and in vivo. The results demonstrated that the upregulation of miR-29c promoted learning and memory behaviors in SAMP8 mice, at least partially, by increasing the activity of protein kinase A/cAMP response element-binding protein, involved in neuroprotection. This evidence suggested that miR-29c may be a promising potential therapeutic target against AD.

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Section: Introductionmentioning

confidence: 99%

MicroRNA-29c targets β-site amyloid precursor protein-cleaving enzyme 1 and has a neuroprotective role in vitro and in vivo

Yang

Song

Zhou

et al. 2015

Molecular Medicine Reports

103

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“…The biological pathways associated with the mRNA modules include long-term potentiation and depression, glutamate and neuroimmune signaling, RNA processing, etc., suggesting the regulation of microRNAs in multiple processes. As for many other diseases (Maciotta et al, 2013), the neuroadaptations associated with alcohol dependence likely rely on many mRNAs. A subset of the mRNA changes may be driven by only a small number of microRNAs, each with the ability to target multiple mRNAs, thereby impacting alcohol-mediated responses and therapeutic strategies.…”

Section: Most Et Almentioning

confidence: 99%

Synaptic microRNAs Coordinately Regulate Synaptic mRNAs: Perturbation by Chronic Alcohol Consumption

Most

Leiter

Blednov

et al. 2015

Neuropsychopharmacol

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Local translation of mRNAs in the synapse has a major role in synaptic structure and function. Chronic alcohol use causes persistent changes in synaptic mRNA expression, possibly mediated by microRNAs localized in the synapse. We profiled the transcriptome of synaptoneurosomes (SN) obtained from the amygdala of mice that consumed 20% ethanol (alcohol) in a 30-day continuous two-bottle choice test to identify the microRNAs that target alcohol-induced mRNAs. SN are membrane vesicles containing pre-and post-synaptic compartments of neurons and astroglia and are a unique model for studying the synaptic transcriptome. We previously showed that chronic alcohol regulates mRNA expression in a coordinated manner. Here, we examine microRNAs and mRNAs from the same samples to define alcohol-responsive synaptic microRNAs and their predicted interactions with targeted mRNAs. The aim of the study was to identify the microRNA-mRNA synaptic interactions that are altered by alcohol. This was accomplished by comparing the effect of alcohol in SN and total homogenate preparations from the same samples. We used a combination of unbiased bioinformatic methods (differential expression, correlation, co-expression, microRNA-mRNA target prediction, co-targeting, and cell type-specific analyses) to identify key alcohol-sensitive microRNAs. Prediction analysis showed that a subset of alcohol-responsive microRNAs was predicted to target many alcohol-responsive mRNAs, providing a bidirectional analysis for identifying microRNA-mRNA interactions. We found microRNAs and mRNAs with overlapping patterns of expression that correlated with alcohol consumption. Cell type-specific analysis revealed that a significant number of alcohol-responsive mRNAs and microRNAs were unique to glutamate neurons and were predicted to target each other. Chronic alcohol consumption appears to perturb the coordinated microRNA regulation of mRNAs in SN, a mechanism that may explain the aberrations in synaptic plasticity affecting the alcoholic brain.

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“…miRNAs have emerged as key regulators of various aspects of neuronal development and dysfunction. Deregulated small RNA signatures, especially miRNAs, have been observed in the brain of a broad range of neurodegenerative diseases such as AD, PD, HD or ALS [171,172] and experimental evidences ascribe a functional role to miRNAs in the pathogenic molecular mechanisms leading to neurodegeneration [173][174][175]. With the advent of high-throughput technologies, full transcriptomic signatures can be provided not only from tissues, but also from samples with small amounts of starting material such as biological fluids and associated exosomes [176][177][178].…”

Section: Micrornasmentioning

confidence: 99%