Topic: SOD1G93A mice

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by selective death of motoneurons (MNs). Our previous results revealed that intravenous administration of mesenchymal stem cells (MSCs) improved different pathological features in SOD1G93A ALS mice. We hypothesised that the beneficial effect could be mediated by paracrine activity of extracellular vesicles (EVs) secreted by MSCs shuttling microRNAs . Subsequently, we studied in-vitro the activity of MSCs-derived EVs on spinal cord astrocytes of symptomatic SOD1G93A mice. The results demonstrated that 24h in-

Amyotrophic lateral sclerosis (ALS) is a fatal and non-curable neurodegenerative disease for which the etiology remains poorly understood. However, among the pathophysiological hallmarks observed both in patients and in animal models, mitochondrial dysfunctions appear to be one of the earliest events and thus might be causative for the progressive loss of motor neurons (Le Masson et al, 2014). Therefore, restoring mitochondrial functions could be a therapeutic area of interest in the development of new therapies in the context of ALS.For this purpose, we are interested in the Bornavirus X prot

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease, involving the selective degeneration of cortical upper synapses in the primary motor cortex (M1). Excitotoxicity in ALS occurs due to an imbalance between excitation and inhibition, closely linked to the loss/gain of astrocytic function. Using the ALS SOD1G93A mice, we investigated the astrocytic contribution for the electrophysiological alterations observed in the M1 (layer 2/3) of SOD1G93A mice, throughout disease progression. Astrocytic metabolism was selectively reduced using fluorocitrate (FC). Synaptic plasticity/transmi