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PhD defence: Malene Overby

New research contributes to a better understanding of the role of the sortilin receptor in dementia

Info about event

Time

Wednesday 12 October 2022,  at 14:00 - 16:00

Location

Building 1324, auditorium 011 ("Tvillingeauditorierne") Aarhus University

On Wednesday 12 October at 14.00, Malene Overby defends her PhD dissertation entitled "Discovery of novel interacting proteins of the sortilin receptor - mechanistic insights into the regulation of a key protein involved in neurological and psychiatric disorders".

Alzheimer's disease is the most frequent cause of dementia. The disease is strongly associated with age; consequently, as we grow older, a larger proportion of us will be affected by Alzheimer's. The disease is highly incapacitating for the people who are affected by it as well as for their relatives. Alzheimer's disease cannot yet be cured, in spite of more than 200 potential drugs having been tested over the years. There is therefore a great need for a better understanding of the basic mechanisms that trigger the disease. This is where this study comes into play as we explore new mechanisms involved in Alzheimer's and other types of dementia. Sortilin has been demonstrated to be a key protein in many of the important mechanisms of the brain, but our understanding of how sortilin is regulated in our brain cells is insufficient. Therefore, mechanisms centered around the regulation of sortilin can help us increase our understanding of the disease. This study has found new mechanisms in which sortilin is involved and provided a new perspective on how the expression of sortilin in our brain cells can be changed by cooperating with other proteins that are specific to our brain cells.

The summary is written by the PhD student.

The defence is public and takes in Building 1324, auditorium 011 ("Tvillingeauditorierne") Aarhus University. Please read the attached press release for more information.

Contact

PhD student Malene Overby
Mail: maleneoverby@clin.au.dk 
Phone: (+45) 20959539

Read full press release