MicroRNAs in Alzheimer's disease: differential expression in hippocampus and cell-free cerebrospinal fluid

Müller, Maria; Kuiperij, H. Bea; Claassen, Jurgen A.H.R.; Küsters, Benno; Verbeek, Marcel M.

doi:10.1016/j.neurobiolaging.2013.07.005

Cited by 218 publications

(214 citation statements)

References 38 publications

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“…[67][68][69] Upregulation of miR-146a/b is also associated with several pathological alterations. 70,71 Consistent with the anti-inflammatory effect proposed for miR-146a/b, transfection of HTM cells with miR-146a agomirs resulted in downregulation of multiple genes associated with inflammation, including IRAK1, IL6, IL8, and SERP1. Further, miR-146a inhibited senescence-associated b-galactosidase activity and production of intracellular reactive oxygen species (iROS), and increased cell proliferation.…”

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confidence: 53%

Role of MicroRNAs in the Trabecular Meshwork

González

Qiu

et al. 2014

Journal of Ocular Pharmacology and Therapeutics

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MicroRNAs (miRNAs) are now recognized as important post-transcriptional regulators of gene expression. MiRNAs are known to modulate cellular functions relevant to the normal and pathological physiology of the trabecular meshwork (TM) such as cell contraction and extracellular matrix turnover. There is also increasing evidence supporting the role of miRNAs in the pathogenesis of multiple diseases, and their potential value as both biomarkers of disease and therapeutic targets. However, compared with other tissues, our current knowledge regarding the roles played by miRNAs in the TM is still very limited. Here, we review the information currently available about miRNAs in the TM and discuss the main challenges and opportunities to incorporate the rapid progress in miRNA biology to the understanding of the normal and pathological physiology of the TM, and to develop novel clinical applications for diagnosis and therapy of high intraocular pressure.

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mentioning

confidence: 53%

Role of MicroRNAs in the Trabecular Meshwork

González

Qiu

et al. 2014

Journal of Ocular Pharmacology and Therapeutics

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“…Hébert et al also identified that miR-29a/b-1 was significantly downregulated in the brains of patients with sporadic AD and correlated with increased BACE1 expression (19). In addition, Müller et al revealed that miR-16, miR-34c, miR-107, miR-128a and miR-146a were differentially regulated in the hippocampi of patients with AD and age-matched normal controls, while only miR-16 and miR-146a were reliably detected in the cerebrospinal fluid of patients with AD (20).…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-135b has a neuroprotective role via targeting of β-site APP-cleaving enzyme 1

Zhang

Xing

Guo

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. MicroRNAs (miRs) are a class of endogenous small non-coding RNAs that have been revealed to negatively mediate the expression of their target genes at the post-transcriptional level. Recently, particular miRs have demonstrated an involvement in the pathogenesis of Alzheimer's disease (AD). However, the specific role of miR-135b in AD has yet to be elucidated. The present study aimed to investigate the neuroprotective role of miR-135b, in addition to its underlying mechanism. Herein, reverse transcription-quantitative polymerase chain reaction was conducted to determine miR-135b expression levels in the peripheral blood samples of patients with AD and age-matched normal controls. The data of the present study revealed that the expression levels of miR-135b were significantly reduced in the peripheral blood of AD patients compared with normal controls (P<0.01). In vitro MTT analyses identified that the overexpression of miR-135b significantly enhanced the proliferation of hippocampal cells (P<0.01). Furthermore, in vivo analysis using a Y-maze test indicated that injection with miR-135b mimics into the third ventricle of anesthetized SAMP8 mice significantly enhanced their learning and memory capacities (P<0.01). Molecular mechanism investigations identified β-site APP-cleaving enzyme 1 (BACE1) as a direct target gene of miR-135b, and the latter was identified to negatively mediate the protein expression levels of BACE1 in hippocampal cells, in addition to hippocampal tissues, of SAMP8 mice. Based on the aforementioned findings, we propose that miR-135b has a neuroprotective role via direct targeting of BACE1 and, thus, may be used for the treatment of AD.

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“…Previous studies have focused on the involvement of miRNAs in AD. In a previous study, miRNAs with a differential expression in either the hippocampus or CSF from patients with AD and age-matched healthy control individuals were identified, the results of which suggested that low levels of miR-146a in the CSF were associated with AD (16). In the present study, miR-29c was significantly decreased in the peripheral blood of patients with AD compared with the age-matched control individuals, and was negatively correlated with an increased expression of BACE1.…”

Section: Discussionmentioning

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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MicroRNAs in Alzheimer's disease: differential expression in hippocampus and cell-free cerebrospinal fluid

Cited by 218 publications

References 38 publications

Role of MicroRNAs in the Trabecular Meshwork

Role of MicroRNAs in the Trabecular Meshwork

MicroRNA-135b has a neuroprotective role via targeting of β-site APP-cleaving enzyme 1

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

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