Topic: a-synuclein

Parkinson’s disease (PD) is the second most common neurodegenerative disorder worldwide. One of the hallmarks of PD is the alteration in the expression and function of NMDA receptor (NMDAR) and cannabinoid receptor 1 (CB1R). The presence of CB1R-NMDAR complexes has been described in neuronal primary cultures, where the activation of CB1R was suggested to counteract the detrimental NMDAR overactivation in an AD mice model. Thus, we aimed to explore the role of this receptor complex in PD. By using BRET assay, it was demonstrated that a-synuclein induces a reorganization of CB1R-NMDAR complex in

Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterised by midbrain dopaminergic neuron degeneration and intracellular a-synuclein (aSyn) accumulation. Here we show that AAV-shRNA-mediated inhibition of HDAC5 protected against aSyn-induced neurodegeneration in vitro and in vivo. We also show that AAV-mediated overexpression of aSyn induces HDAC5 nuclear accumulation in dopaminergic neurons in the rat substantia nigra in vivo, and in SH-SY5Y cells in vitro. To investigate the nuclear HDAC5 complex induced by aSyn, we used a co-immunoprecipitation proteomics approach t