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In concert, these findings highlight the therapeutic potential of Tα1 in MS as well as in other autoimmune conditions that show reduced differentiation of B reg subsets and chronic immune activation

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Collectively, these findings support a model in which neuronal α-syn pathology, particularly oligomeric species, acts as the upstream driver of astrocyte activation and pericyte alterations, with these secondary cellular responses serving as critical mediators of BBB disruption in synucleinopathies (Hourfar et al., 2023) Together, these findings outline a compelling model in which neuronal α-syn pathology, especially oligomeric species, initiates a cascade of non–cell-autonomous responses that ultimately destabilize the BBB through astrocytic, pericytic, and endothelial changes