tram-34 and Amyotrophic-Lateral-Sclerosis

Amyotrophic lateral sclerosis (ALS) patients exhibit dysfunctional energy metabolism and weight loss, which is negatively correlated with survival, together with neuroinflammation. However, the possible contribution of neuroinflammation to deregulations of feeding behaviour in ALS has not been studied in detail. We here investigated if microglial K. hSOD1. We found that treatment of hSOD1. Using ALS mouse models, we describe defects in the hypothalamic melanocortin system that affect appetite control. These results reveal a new regulatory role for K

Topics: Amyotrophic Lateral Sclerosis; Animals; Disease Models, Animal; Energy Metabolism; Feeding Behavior; Homeostasis; Melanocortins; Mice; Mice, Transgenic; Microglia; Potassium Channels, Calcium-Activated; Pyrazoles; Receptors, Cannabinoid; Spinal Cord; Superoxide Dismutase-1; Weight Gain

Recent studies described a critical role for microglia in amyotrophic lateral sclerosis (ALS), where these CNS-resident immune cells participate in the establishment of an inflammatory microenvironment that contributes to motor neuron degeneration. Understanding the mechanisms leading to microglia activation in ALS could help to identify specific molecular pathways which could be targeted to reduce or delay motor neuron degeneration and muscle paralysis in patients. The intermediate-conductance calcium-activated potassium channel KCa3.1 has been reported to modulate the "pro-inflammatory" phenotype of microglia in different pathological conditions. We here investigated the effects of blocking KCa3.1 activity in the hSOD1

Topics: Amyotrophic Lateral Sclerosis; Animals; Cell Death; Disease Models, Animal; Disease Progression; Humans; Mice; Mice, Inbred C57BL; Mice, Transgenic; Microglia; Motor Neurons; Phenotype; Potassium Channels, Calcium-Activated; Pyrazoles; Spinal Cord; Superoxide Dismutase