Topic: microglia/macrophages

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by a selective loss of motor neurons (MN). During ALS, ATP released by neurons and glial cells modulates the neuroglial interplay via activation of P2X receptors. Among these, P2X4 receptor, which is a non-selective cationic channel, has been recently involved in ALS pathogenesis. We found that both the absence of P2X4 or the increase of surface P2X4 using P2X4KO or non-internalized P2X4KI mice respectively, have a beneficial outcome in the SOD1 mice. This paradoxical output suggests a complex cell-role of P2X4 in

Traumatic brain injury (TBI) can cause life-changing neurological deficits. There are currently no neuroprotective treatments in TBI. The high content of oxidation-sensitive polyunsaturated fatty acids (PUFAs) in the brain generates an environment vulnerable to TBI-related oxidative damage. We hypothesised that partial replacement of tissue PUFAs with deuterium - enriched PUFAs (D-PUFAs), could act as a brake against oxidation and improve outcome.A moderately severe TBI was induced using a controlled cortical impact (CCI) in adult male and female CD1 mice. Animals received a control or a D-PUF