Fig. 2
From: Multiple system atrophy: α-Synuclein strains at the neuron-oligodendrocyte crossroad
Strain pathology is dependent on strain and host characteristics. The ability of α-Synuclein strains to seed and spread is dictated by the properties of the strain itself in combination with the characteristics of the host. When tested in the same cell lines, Multiple system atrophy (MSA) and Parkinson’s Disease (PD) patient extracts display differing abilities to seed aggregation, with PD extracts only seeding new aggregation via insoluble fractions. In comparison, both insoluble and soluble fractions of MSA extracts were successful in seeding aggregation. Inclusions formed in cells differed in both size and morphology. Injections of MSA extracts into different transgenic mice models highlighted the effects of host characteristics on pathology. In TgM83+/− mice, inclusion pathology was localized to neurons in the hindbrain, while in Tg(SNCA*A53T+/+)Nbm (mice expressing A53T human α-Syn on a mouse α-Syn knockout background), the limbic system was affected with neuronal and astrocytic inclusions. Therefore, in synucleinopathies such as MSA, strain characteristics may dictate the propagation of pathology, while host characteristics determine the cell types and brain regions affected