Wed. May 19, 2021 9:50 AM - 11:50 AM Room 06 (ICC Kyoto 2F Room B-2)

Chair：Surmeier D. James(Department of Physiology, Feinberg School of Medicine, Northwestern University, IL),Uchihara Toshiki(Nitobe Memorial Nakano General Hospital, Neurology Clinic with Neuromorphomics Laboratory)

Misfolded alpha-synuclein (αS) is, a major component constituent of Lewy bodybodies – a common pathological feature , is tightly related to pathogenesis of Parkinson Ddisease (PD). However, Current disease-modification therapties for PD are largely focused on using antibodies to block the spread of aS pathology. But the success of this approach, which has failed in other neurodegenerative diseases, remains uncertain. One key question that is relevant to the success of this strategy is how the peculiar pattern of aS pathology seen in the PD brain arises. it is not yet clear how αS interplays with other molecules to spread itself in selected structures or neuronal groups to template PD-specific patterns of neurodegeneration. In this session, the molecule-oriented mechanisms are expandedunderlying this pattern will be explored using in the context of different systems, ranging from cellular models, novel animal models and human from human brains brains to cellular and animal models. The dDiscussion will identify what are the relevantkey molecular players in aS pathogenesis that could become future therapeutic targets to establish PD-specific strategies to tackle PDto modify PD progression