Sandor Szunyogh

I joined the Wade-Martins group in 2020 to study the formation of the HDAC4/N-CoR/HDAC3 protein complex and its functional consequences in epigenetic gene repression, to gain insights into the underlying mechanisms of Parkinson’s disease; ultimately, to find a way to therapeutically intervene and stop the progression of the disease in an early stage.

Later on, my research turned to the epigenetic regulation of another neurodegenerative disease, Friedreich’s ataxia, where I screened potential drug candidates to increase frataxin levels and reduce pathological phenotypes in fibroblasts, PBMCs and iPSC-derived cardiomyocytes and sensory neurons, which are the most affected cell types in the disease. 

Most recently I started to work on correcting a few key mutations in Parkinson’s disease by gene therapy via the Herpes simplex virus. These complex neurotropic molecular machines have the ability to deliver entire genomic segments containing the correct versions of genes which lost their functions in the disease to restore their original functions. 

I gained my scientific background in Biochemistry and Molecular Cell Biology at the Eötvös Loránd Science University in Budapest, where I obtained both my B.Sc. and M.Sc. degrees. I completed my PhD in collaboration with the Hungarian Academy of Sciences, Institute of Enzymology, where I studied the interactions of the protein TPPP/p25 (p25a). Particularly, I identified the interfaces of TPPP/p25 which bind its physiological partner tubulin and its pathological partner alpha-synuclein, in order to selectively inhibit the regions affected in neurodegenerative diseases.