Biosketch
Bankole Molakun is currently a PhD student in the department of Neuroscience, Biomedicine and Movement sciences at the University of Verona. Prior to this, she had her bachelor’s degrees in Human Biology and graduated with a first-class honour in 2013 from Afe Babalola University, Nigeria where she also commenced her master’s degree in Biology, graduated in 2016 and began her early lecturing career as a graduate assistant. She is currently a member of the Italian Society of Neuroscience (SINS), Federation of European Neuroscience Societies (FENS), Society of Neuroscientists in Africa (SONA) as well as the Neuroscience Society of Nigeria (NSN).
Project
PhD candidate: Bankole Molakun
Supervisor: Raffaella Mariotti
Title: Epigenetic modulations in ALS murine models
PhD Programme: Neuroscience, Psychology and Psychiatric Sciences
I am interested in understanding the processes involved in the pathogenesis of certain neurodegenerative diseases such as Parkinson’s disease and Amyotrophic lateral Sclerosis (ALS). In my pre-doctoral investigations, I have especially focused on themes related to perturbations of the dopaminergic system, including dopamine receptor regulation, and torodent models of Parkinson’s disease. My current research involves studying epigenetic modulations in ALS murine models, specifically focusing on histone deacetylases (HDACs), a group of enzymes which are known to be involved in several cellular processes such as cell death and stress responses, and have recently been implicated in the pathogenesis of ALS. Several studies have indicated that pharmacological inhibition of HDACs improves cell survival by promoting acetylation of histone, gene transcription and protein synthesis. My research focuses on exploring for the first time in ALS models, the effect of a combination of two epigenetic drugs, Valproate an inhibitor of HDACs, and Resveratrol, and activator of sirtuins (SIRT) , to modulate histone homeostasis and determine the capability of these epigenetic drugs to directly protect motor neurons from neurodegeneration, improve motor performance and prolong the lifespan in SOD1(G93A) ALS mice.