Frank Mobilio
Frank Mobilio

Frank Mobilio

‘Post-Traumatic Stress Disorder and Traumatic Brain Injury: role of neuroinflammation.’

University of Melbourne, VIC
Awarded 2021
Co-funded by Rotary District 9790 & Victorian RSL

“I have always had a keen interest in the complexity of the brain and how its dysfunction leads to disease.”

Post Traumatic Stress Disorder PhD Scholarship

Researcher Profile

In 2018 I completed my Bachelor of Science (Hons) at The University of Melbourne, were I developed key skills that allowed me to explore the role of neuroinflammation in the Central Nervous System. From here, I commenced the position of a Research Assistant at The University of Melbourne, in the Neuropharmacology Laboratory.

During my time as a Research Assistant, I have participated in a number of different projects, exploring the role of neuroinflammation in many neuropathologies including Alzheimer’s Disease, Parkinson’s Disease and Traumatic Brain Injury.

Project Summary

Traumatic brain injury (TBI) is a major cause of mortality and morbidity in those that have served in modern theatres of war. Whilst most attention has focussed on moderate-severe TBIs, the long-term residual effects in those that sustained a mild TBI during service are now only being recognised, with Post Traumatic Stress Disorder (PTSD) or depression increasingly reported. It now appears that gaining a greater understanding of the underlying causes of TBI/PTSD co-morbidity is crucial if we are to address the increasing concerns surrounding the mental health of our servicemen.

Over the past decade it has become clear that the brain exhibits features of inflammation, known as “neuroinflammation” in response to TBI. We have demonstrated that this neuroinflammatory response contributes to cell damage caused by TBI. Our studies are now focussed on the long-term implications of this chronic neuroinflammation on brain structure and function and its contribution to further complications and symptoms associated with PTSD such as depression.

This project will characterise the role of a key facilitator of neuroinflammation, the type-I interferons, in driving long-term brain dysfunction caused by TBI. The significance of this pathway in TBI and its links to PTSD will be further characterised through a bioinformatic analysis of publicly available TBI genetic databases with subsequent characterisation of novel, target genes. The identified genes will be compared to the genomic profile of individuals with PTSD through publicly available genetic databases.

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