It is abundantly clear that mental illnesses are not due to a single gene, neurotransmitter or cell type, but are complex, whole organism disorders modulated by many genes, environmental factors, and their interactions. This makes many traditional research approaches limited: in vitro assays cannot account for metabolic or immunological interactions between organs; human, clinical studies do not have the genetic or environmental control of lab studies, and we cannot perform invasive assays; traditional in vivo assays often only use a single genome of organism, and are therefore effectively an n of 1 – a single genome in a single environment repeatedly sampled – and do not reflect the genetic diversity of the human population. We require models that mirror the complexity of human patients.

My approach, experimental precision medicine, makes use of genetically diverse organisms, particularly mice, to produce models that allow whole organism identification of gene-gene and gene-environment interactions, across all organ systems, throughout the lifespan. This allows us to investigate the interactive effects of metabolism and severe mental illness – how interventions to alter one may have a feedback effect on the other. This provides an interventional mirror to Mendelian randomization and causal inference studies carried out on human populations.

We have seen repeatedly that findings in one strain of mouse often do not replicates across other strains, leading to both false positives and false negatives. If findings do not generalize within a species, how do we expect them to generalize across species to humans? By using a number of different strains, we can firstly identify effects that are generalizable (and therefore more likely to translate to humans), and secondly, identify outlier strains that can be further investigated to give insight into mechanisms of action (why might an intervention work for some people, but not others?).

Health and disease are controlled by interactions between all of our genes and the world we live in. In my lab, we try to understand these complex interactions, and to create better preclinical models.

I am currently an Baszucki Foundation Chancellor’s Fellow in the Hub for Metabolic Psychiatry and Centre for Clinical Brain Sciences at the University of Edinburgh, and Associate Professor in the Department of Genetics, Genomics and Informatics, at the University of Tennessee Health Science Center, Memphis.

I graduated in 2011 from the University of Leeds with a BSc in Neuroscience, which included a year spent on industrial placement at AstraZeneca. I completed my PhD in Systems Biology at the University of Manchester's doctoral teaching centre in December 2015, where I had been supervised by Dr Reinmar Hager. I completed my first Postdoctoral Fellowship in the McGowan lab at the University of Toronto Scarborough, where I investigated the epigenetics of Gulf War Illness. I completed my second Postdoctoral Fellowship with Dr. Rob Williams at UTHSC, working on integrating multiple levels of sequencing data and a deep phenome in the BXD recombinant inbred mouse population.

My primary research interest is the brain, and its resultant behavioural phenotypes. I am intrigued by how genetic and cellular changes can be traced through a biological system to result in changes at the whole organism level, such as neuropsychiatric and neurodegenerative disorders, both of which are becoming an increasing health burden. The ability to produce and share massive datasets is one of the most exciting advancements in modern science because it enables a comprehensive systems approach to fundamental biological questions.

Other aspects of my work include the examination of indirect genetic effects and parent-of-origin effects on early life behaviour and developmental disorders, and the joint-analysis of phenotypes collected across species.