This webinar takes place on Tuesday May 19 between 16.00 and 16.30 CEST / 15.00-15.30 GMT / 10.00-10.30 AM EDT / 7.00-7.30 AM PDT.

Follow the link to register for the webinar. Please note that the presentation will be given during the live event only and on demand viewing at a later date will not be possible. Contact us for any questions.

 

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THIS WEBINAR IS ARRANGED BY CELLECTRICON AB. FOR MORE INFORMATION ON THE HANDLING OF YOUR PERSONAL INFORMATION, SEE OUR PRIVACY POLICY.

Abstract:

Insoluble aggregates (Lewy bodies) consisting of misfolded alpha-synuclein accumulate in the nervous system of most Parkinson’s disease patients. This process can affect multiple cellular functions and eventually leads to neuronal death. From a drug discovery perspective, preventing protein aggregation or promoting protein clearance provide interesting opportunities as pharmacological intervention points.

In this webinar, we will present a high-capacity in vitro platform for studying alpha-synuclein aggregation and how it can be utilized for evaluation of modulation of alpha-synuclein aggregation and cell health. The process of inducing alpha-synuclein aggregation will be outlined, as well as image analysis pipelines, and examples of validation against human genetic targets.

Presented by:

Linnea Strid Orrhult, External Collaborations Manager

Linnea joined the company in 2019 as an External Collaborations Manager. In her role, she designs and drives drug discovery projects for clients, mainly in the areas of neurodegeneration and neuroinflammation. Before joining Cellectricon, Linnea was a postdoctoral researcher at the University of Gothenburg studying the role of innate immunity after infection and hypoxia-ischemia in the neonatal brain and its barriers. She also worked as lab manager and research scientist leading projects focused on 3D printing of primary cells. Linnea received a PhD in Medicine from the University of Gothenburg in 2011, where she investigated the role of Toll like receptors for inflammation in the immature brain.