Topic: diet-induced obesity

AIMS: The activation of CB1 receptor (CB1R) is reported to favor energy accumulation and promote resiliency against stress. The aim of this study is to elucidate whether CB1R expression in CaMKII+ neurons is sufficient to restore its role in the regulation of energy metabolism and contingent behaviors.METHODS: To this end, we applied a genetic strategy to reconstitute CB1R expression at endogenous levels in CaMKII+ neurons (CaMKII-CB1-RS).RESULTS: The rescue of CB1R expression in these neurons promotes feeding behavior causing fasting-induced hyperphagia, increased motivation and impulsivity t

A combination of genetic and environmental factors likely underlies most neurodegenerative diseases. Among environmental factors, metabolic disease is an emerging risk factor, but the mechanisms that confer risk are still poorly understood. We hypothesise that diet-induced obesity dysregulates lipid metabolism and promotes glial activation in a mouse model of Amyotrophic Lateral Sclerosis (ALS) and Frontotemporal Dementia (FTD). In particular, we aim to study the role of altered lipid metabolism and neuroinflammation in response to short (12 weeks) and prolonged (14-16 months) high-fat diet (H