Releasing the tiger from the cage – fibrillisation of a peptide model of the aggregation prone segement of α-Synuclein leads to novel structures
The misfolding of the α-synuclein protein into insoluble amyloid fibril structures is a process known to cause neurodegenerative disease such as Parkinson’s Disease (PD) and Lewy Bodies with Dementia (LBD). To date, our understanding about the molecular origin of PD and LBD is not complete and many questions e.g. how and why the misfolding process starts and how misfolded α-synuclein is transported from one nerve cell to another, still need an answer. Hence much effort is nowadays directed towards increasing the knowledge on what atomic-level factors that are important to control and ultimately stop the origin to disease.
In this talk Associate professor Björn C.G. Karlsson will present the results from their on-going research on an amino acid sequence of α-synuclein that has been shown to dictate the misfolding process of the full-length protein and whose early aggregated pre-fibrillar structures would provide interesting target motifs for sensor-based applications and therapeutic strategies.
Date: October 18 Time: 14:30-15:30 Location: Room Magenta (Vi2144), Vita, Norra Kajplan 6 The seminar is in English