As a neuroscientist, I’ve had a long-standing interest in the mechanisms of learning and memory. We know cellular metabolism changes have profound effects on brain function, but we are still learning how it influences behavioral outputs.
When I joined Cincinnati Children’s in 2006 after completing my PhD in molecular and developmental biology, I was excited for the opportunity to help study the metabolic effects of creatine transporter deficiency (CTD) — which was discovered right here at Cincinnati Children’s — and bipolar disorder.
Most people with creatine deficiency, which causes moderate to severe intellectual disability, epilepsy and a lack of language development, have CTD. Although there are no treatments for this devastating disorder, my colleagues and I hope to change that.
Our lab developed a novel, high-fidelity mouse model of CTD that shows severe learning and memory deficits while demonstrating that creatine is necessary for proper brain development. We are using this model to better understand the mechanisms that underlie CTD and to test potential treatments.
One of the most important takeaways from our CTD research is that creatine is more than just a dietary supplement for athletes. It is one of the most abundant molecules in the brain and plays an important role in cellular health.
Our team is also interested in creating mental health disorders models to see if there are metabolic differences that underlie these changes. For example, we’ve achieved a mouse model of increased dopamine activation by slowing the termination of dopamine signals. We are using this model to better understand aspects of human affective disorders and to see how changes in neuronal signaling affect metabolism.
Outside of my research and teaching activities, I’m a member of the Scientific and Medical Advisory Board for the Association of Creatine Deficiencies.
Assistant Professor, UC Department of Pediatrics