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This site is dedicated to scientific community working on ALS. Our aim is to optimize researchers time and efforts by providing updated, well organized information on novel findings, available resources and research support.
AriSLA - The Foundation for research on ALS - has been set up to make ALS research investments more effective and efficient, to speed up the clinical research impact e and to provide patients with better care, improved conditions and life expectancy. Its aim is to boost Italian excellencies in basic, clinical and technological research. The Foundation founders are Fondazione Cariplo, Fondazione Telethon, Fondazione Vialli and Mauro and AISLA.

 

 

New article published on Cell Death & Differentiation by AriSLA Funded Projects MAMMALS "Mir-125b as Microglia Modifier for ALS"

MicroRNA-125b regulates microglia activation and motor neuron death in ALS

C Parisi, G Napoli, S Amadio, A Spalloni, S Apolloni, P Longone and C Volonté

Understanding the means by which microglia self-regulate the neuroinflammatory response helps modulating their reaction during neurodegeneration. In amyotrophic lateral sclerosis (ALS), classical NF-κB pathway is related to persistent microglia activation and motor neuron injury; however, mechanisms of negative control of NF-κB activity remain unexplored. One of the major players in the termination of classical NF-κB pathway is the ubiquitin-editing enzyme A20, which has recognized anti-inflammatory functions. Lately, microRNAs are emerging as potent fine-tuners of neuroinflammation and reported to be regulated in ALS, for instance, by purinergic P2X7 receptor activation. In this work, we uncover an interplay between miR-125b and A20 protein in the modulation of classical NF-κB signaling in microglia. In particular, we establish the existence of a pathological circuit in which termination of A20 function by miR-125b strengthens and prolongs the noxious P2X7 receptor-dependent activation of NF-κB in microglia, with deleterious consequences on motor neurons. We prove that, by restoring A20 levels, miR-125b inhibition then sustains motor neuron survival. These results introduce miR-125b as a key mediator of microglia dynamics in ALS. 

 

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