Multiple system atrophy (MSA) is characterized pathologically by glial cytoplasmic inclusion (GCI) of the oligodendrocyte. Multiple system atrophy (MSA) is, which is associated with the degeneration of multiple regions (cerebellum, basal ganglion (pyramidal tract), autonomic nervous system), one of the degenerative neurological disorders. alpha-synuclein is major protein of alpha-synucleinopathy and is abundant in the glial cytoplasmic inclusion (GCI), but the molecular mechanism remains unclear. Recently, it has been reported that alpha-synuclein is included in the neuronal exosome, which is a small vesicle and is transmitted among several cells due to signal transduction, and seems to be transferred to several glia cells. To investigate whether neuronal exosome involves neuron-glia cell communication, we performed analysis of glia response regulator via neuronal exosome.
In the present study, a recruitment of alpha-synuclein into neuronal exosome was promoted in an IP3 stimulation-dependent manner by using mouse primary neuron culture. Some IP3-stimulated candidate proteins that were recruited to neuronal exosome were identified in mouse primary neuron culture by using shotgun MS. We are trying to examine a transmission from neuron to oligodendrocyte cells via neuronal exosome including alpha-synuclein.