Abstract

Parkinson's disease (PD) is an extremely heterogeneous disorder with varying symptomatology among patients. The majority of cases display asymmetric motor symptoms and most cases eventually develop dementia. The underlying causes for this motor asymmetry, non-motor subtypes and differing progression rates towards dementia have never been satisfactorily explained.

This lecture covers the new alpha-synuclein origin and connectome (SOC) model of PD, recently proposed as a unifying theory to resolve those hitherto unexplained phenomena of PD. The model suggests that the initial misfolding and aggregation of alpha-synuclein occurs in a single location within the central or peripheral nervous system - leading to body-first PD if the first pathology arises in the peripheral nervous system and brain-first if the first pathology occurs in the CNS. The subsequent spreading of pathology is then dependent on the connectome, especially the predominantly ipsilateral connectivity of mammalian brains. Together, these details can explain why PD is often but not always an asymmetric disease, and why the temporal sequence of symptom development varies from patient to patient.  

Recent open access paper on the SOC model: https://content.iospress.com/articles/journal-of-parkinsons-disease/jpd202481 

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https://aarhusuniversity.zoom.us/j/63590142121