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Project

Extracellular Vesicles and InfLammation: the EVIL two in alpha- synuclein propagation?

For 20 years, researchers and clinicians are unraveling the critical role of α-synuclein (aSYN) in protein aggregation and neuronal death in Parkinson’s disease (PD). Recently, they discovered that aSYN facilitates propagation of PD pathology across distinct brain areas, thereby inducing progressive worsening of the disease. This research project is centered on the so-called ‘prion-like hypothesis’ of aSYN propagation and I aim to investigate how toxic aSYN species propagate between neurons/brain areas, focusing on the role of innate immune cells and extracellular vesicles (EVs). EVs have emerged as important mediators of intercellular communication, that – by transporting their cargo from the donor to the acceptor cell – can modify the behavior of the acceptor cell. EVs appear to be the major vehicles for shuttling toxic proteins, such as aSYN, out of the cell and seeding protein aggregation in acceptor cells. In addition, they also play an important role in the propagation of the inflammatory response – which is believed to have a profound impact on disease progression – by facilitating communication between immune cells. In this project, I will focus on disentangling the role of EVs and neuroinflammation in aSYN propagation and design a unifying theory that reconciles the role of these two disease processes. Thus, the central research question is: “Do EVs add to the creation of an inflammatory micro-environment that modulates aSYN propagation?”

Date:1 Jan 2021 →  Today
Keywords:Neurophysiology, Protein spreading, Parkinson's disease
Disciplines:Neurophysiology
Project type:PhD project