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William Thomas Booth Scholars in Pharmacology

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Dr. Falvia Carreno and Jennifer Parrot received a travel award made possible by the William Thomas Booth Endowment Fund.

Posted by: Evelyn Head | Category: Around Campus | October 22, 2014

Dr. Falvia Carreno
William Thomas Booth Scholar 2014 

Dr. Carreno’s studies focus on the circuits in the brain by which the drug ketamine exerts its antidepressant effects and also explores the cellular mechanisms that might be responsible for such effects. There is currently great interest in ketamine as it has been found to improve the symptoms of depression rapidly, within a day, in treatment-resistant depressed patients. Perhaps not surprisingly, it has also been shown to reduce suicide rates in such patients. However, there are problems with the drug as its effects are not long-lasting, rarely lasting for more than two weeks after a single intravenous infusion (which is how the drug is given). One problem with ketamine is having to give it by intravenous infusion (as opposed to orally) with the other being that it can produce psychotic-like symptoms (visual-type hallucinations, distortion of perception) such that there is concern about giving injections of the drug more than several times. So clearly if we can find out how ketamine works, we might be able to develop drugs that have its beneficial effects without its deleterious ones.

Jennifer Parrot 
William Thomas Booth Scholar 2014 

Ms. Parrott’s research is focused on understanding how inflammation disrupts brain function and alters behavior. Inflammation, which increases in response to chronic disease, psychological stress and even normal aging, is a significant risk factor for the development of neuropsychiatric disorders, particularly depression. Recent research in Dr. O’Connor’s laboratory has identified disruptions in the metabolism of tryptophan (an essential amino acid and precursor to the important neurotransmitter serotonin) as critical in mediating the effects of inflammation within the brain. In fact, apparent disruptions in the balance of tryptophan metabolism were identified in post-mortem analysis of the brains of suicide victims. However, tryptophan metabolism is complex, and there are many potential mechanisms by which disrupted tryptophan metabolism in the brain could impair normal brain function. Ms. Parrott is using new genetic tools to tease apart the precise metabolic steps required for inflammation-induced behavioral changes in a mouse model of depression. More complete understanding of the neuropathology underlying depression during periods of inflammation will permit the development of more effective treatments (aimed at the cause rather than the symptoms) for suffering individuals.

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