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Project

Investigation of alpha-synuclein aggregation and propagation in preclinical models for Multiple System Atrophy

Multiple system atrophy (MSA) is a rare neurodegenerative disease characterized by a rapid and aggressive decline in motor and autonomic functions. Currently there are no symptomatic or disease-modifying treatment options for MSA patients. The major neuropathological hallmark are deposits of alpha-synuclein (αSYN) protein aggregates, mostly glial cytoplasmic inclusions (GCIs) in oligodendrocytes, and less frequently in neurons.
Most studies have focused on the central nervous system (CNS), but increasing evidence has shown aSYN aggregates in the periphery, which correlate with the earliest symptoms and affected regions. αSYN’s ability to propagate like a prion supports the hypothesis that the disease may start in the periphery and later advance to the brain when the motor deficits appear.
A major challenge to develop disease-modifying therapies for MSA relies on a better understanding of the disease aetiology and pathogenesis. In this project we aim to develop novel MSA models to study aSYN propagation from the periphery to the CNS as a potential contributor to disease pathogenesis. Additionally, we aim to elucidate the potential role of infections as triggers and MSA-linked genetic variants as facilitators of disease progression. This project will provide new insight into potential pathogenic mechanisms leading to MSA together with the development of tools that can be used for prospective therapeutic approaches

Date:1 Jan 2021 →  Today
Keywords:Multiple system atrophy (MSA), aSYN propagation
Disciplines:Neurological and neuromuscular diseases, Animal pathology