Beneficial effects of miR-132/212 deficiency in the zQ175 mouse model of Huntington's disease.

Huntington's disease (HD) is a rare genetic neurodegenerative disorder caused by an expansion of CAG repeats in the Huntingtin (HTT) gene. One hypothesis suggests that the mutant HTT gene contributes to HD neuropathology through transcriptional dysregulation involving microRNAs (miRNAs). In particular, the miR-132/212 cluster is strongly diminished in the HD brain.

Study of The Correlation between miR-106a, miR-125b, and miR-330 on Multiple Sclerosis Patients by Targeting TNFSF4 and SP1 in NF-кb/TNF-α Pathway: A Case-Control Study.

Objective: Multiple sclerosis (MS) is a complex multifactorial neuro-inflammatory disorder. This complexity arises from the evidence suggesting that MS is developed by interacting with environmental and genetic factors. This study aimed to evaluate the miR-106a, miR-125b, and miR330- expression levels in relapsing-remitting multiple sclerosis (RRMS) patients.

miR-574, miR-499, miR-125b, miR-106a, and miR-9 potentially target TGFBR-1 and TGFBR-2 genes involving in inflammatory response pathway: Potential novel biomarkers for chronic lymphocytic leukemia.

MicroARNAs (miRNAs) are linked to a variety of cancers, which resulted in molecular pathway dysregulation in chronic lymphocytic leukemia (CLL). Using five dysregulated miRNAs identified by literature mining and in silico analysis, we were able to demonstrate the critical role that the TGFBR1 and TGFB receptor signaling pathways play in the state of CLL. Assays using real-time PCR were run on 30 patients and 30 healthy controls.

Widespread alterations in microRNA biogenesis in human Huntington's disease putamen.

Altered microRNA (miRNA) expression is a common feature of Huntington's disease (HD) and could participate in disease onset and progression. However, little is known about the underlying causes of miRNA disruption in HD. We and others have previously shown that mutant Huntingtin binds to Ago2, a central component of miRNA biogenesis, and disrupts mature miRNA levels.

Differential Regulation of Tau Exon 2 and 10 Isoforms in Huntington's Disease Brain.

Huntington's disease (HD) is an inherited neurodegenerative disorder caused by an expansion of CAG repeats in the Huntingtin (HTT) gene. Accumulating evidence suggests that the microtubule-associated tau protein participates in the pathogenesis of HD. Recently, we have identified changes in tau alternative splicing of exons 2, 3 and 10 in the putamen of HD patients (St-Amour et al, 2018).