Adekunle Bademosi

A key pathological feature of frontotemporal dementia (FTD) diagnosis is the mislocalisation and clumping of proteins leading to neurodegeneration. In most cases, the cause of FTD is unknown. However, recent genome wide studies have identified variances in different genes that increase the risk for sporadic FTD. One such gene is UNC13A, which produces a key neuronal protein essential for neuronal communication across all eighty-six billion neurons of the brain. Interestingly, the expression of this UNC13A is also reduced in people living with FTD. It is therefore vital to understand the role UNC13A risk variants play in sporadic FTD. In this work, Dr Bademosi and the team at the University of Queensland will generate new fruit fly and roundworm animal models expressing key UNC13A genetic risk variants that increases the likelihood of sporadic FTD. The team will then investigate disease changes that occur in these models, including - locomotion, life span, and neuronal communication. 

Finally, the team will identify whether the beneficial effect of lithium treatment on people living with FTD who have this UNC13 risk variants is due to a direct effect of the drug on UNC13A function. Overall, Dr Bademosi aims to create sporadic FTD model organisms that can better help us understand disease onset, progression, and possible treatment. 

Dr Adekunle Bademosi is a Research Fellow at Walker Neurodegeneration pathobiology lab, The Queensland Brain Institute at The University of Queensland.