Robert Andrew

Post-doctoral Fellow

Born: Milton Keynes, UK

B.Sc. Biology (2011)
Newcastle University, Newcastle-upon-Tyne, UK

M.Sc. Bioscience (Human Disease and Therapy) (2012)
University of Leeds, Leeds, UK

Ph.D. Cellular and molecular biology (2015)
University of Manchester, Manchester, UK

As a graduate student, I investigated the causes of differential proteolysis of two major amyloid precursor protein (APP) isoforms for my PhD thesis. Amyloid-β (Aβ), produced through proteolytic cleavage of APP is thought to be the causative molecule in a cascade of downstream events leading to neuronal loss and Alzheimer’s disease (AD), and inhibiting its production remains a major target in the development of AD therapeutics.  Strong evidence suggests a shift in the expression profile of the APP within the brains of AD patients, but the causes and consequences of this shift in expression remain enigmatic.  Having observed differences in the production of Aβ from differences in isoforms, I investigated how subcellular distribution and protein-protein interactions differentially affected proteolysis in these isoforms, with the hope of elucidating novel molecular targets for intervention in AD.  In the Thinakaran I participate in research on neuronal trafficking of BACE1 as well as on the characterization of disease mechanisms and pathways associated with recently identified GWAS risk factors.

Contact Rob by email email_icon.jpg