June 19, 2009

Grants boost mental health research

Grants boost mental health research

Five Vanderbilt Medical Center scientists have received 2009 Young Investigator Awards from NARSAD, the world’s leading mental health research charity.

The Young Investigator grants allow promising new researchers, typically assistant professors or postdoctoral fellows, to generate the pilot data necessary to secure additional research funding. Each of the scientists will receive $30,000 per year in support of one or two years of research.

NARSAD named 200 Young Investigators from a pool of more than 800 proposals from researchers worldwide.

Herbert Meltzer, M.D., director of the Division of Psychopharmacology at Vanderbilt, chaired NARSAD’s Young Investigator selection committee.

“The 200 selected Young Investigator applicants represent a new generation of researchers ready and able to make major advances in the understanding and treatment of mental illness,” Meltzer said. “The sophistication of their science – in basic and clinical research, at the molecular and cellular levels, in genetics and brain imaging, in characterizing the course of illnesses from the prenatal stage across the lifespan – is truly astonishing compared to the science of only a decade ago.

“These proposals are proof positive that NARSAD has had a major impact on shaping the research agenda of neuroscience laboratories everywhere. This is another year in which Vanderbilt applicants have been successful in this highly competitive program.”

Vanderbilt’s 2009 NARSAD Young Investigators and their research aims:

Kevin Erreger, Ph.D., research fellow in Molecular Physiology & Biophysics, will test the hypothesis that aberrant dopamine receptor signaling increases levels of the neurotransmitter dopamine in individuals with schizophrenia.

Kevin Erreger, Ph.D.

Kevin Erreger, Ph.D.

An increase in signaling by dopamine – hyperdopaminergia – is believed to be instrumental in the pathophysiology of schizophrenia. Erreger is examining whether aberrant dopamine receptor signaling leads to altered dopamine release by reversing the flow of dopamine through the dopamine transporter, contributing to the hyperdopaminergia implicated in schizophrenia.

Maureen Hahn, Ph.D., assistant professor of Medicine and Pharmacology, will examine genetic variation in the regulation of the norepinephrine system and its impact on normal and abnormal behavior.

Maureen Hahn, Ph.D.

Maureen Hahn, Ph.D.

The neurotransmitter norepinephrine has been implicated in stress-related disorders (depression, post-traumatic stress disorder) and in disorders of altered cognitive function (schizophrenia, ADHD). It is removed from the synapse by the norepinephrine transporter (NET), which is a target for antidepressants and psychostimulants (cocaine, amphetamine). Hahn will examine how two proteins called Slug and Scratch regulate the NET gene, which may suggest new targets for treating cognitive and affective disorders.

Shikha Snigdha, Ph.D., research fellow in Psychiatry, will use rodent models to study various aspects of cognitive deficits in schizophrenia.

Shikha Snigdha, Ph.D.

Shikha Snigdha, Ph.D.

Using an animal model of the long-term memory deficit in schizophrenia, in which the drug phencyclidine (Angel Dust) is given to rats for a week, Snigdha will study how to reverse the deficit with currently available antipsychotic drugs and identify the pharmacology that is critical for this reversal. Understanding how cognitive deficits emerge could lead to treatments during the prodromal (early) period of schizophrenia to prevent the development of cognitive impairments.

Gregg Stanwood, Ph.D., assistant professor of Pharmacology and Vanderbilt Kennedy Center member, will study interactions between serotonin and dopamine receptors with a view to developing new therapies for mood disorders.

Gregg Stanwood, Ph.D.

Gregg Stanwood, Ph.D.

Stanwood recently discovered that certain serotonin and dopamine receptors interact with each other in specific protein complexes within the brain. The interactions appear to be regulated during normal brain development and may serve as a molecular substrate for the integration of mood, emotion, learning and reward systems. He will pursue the functional consequences of these interactions on the distribution and signaling properties of the receptors.

Neil Woodward, Ph.D., assistant professor of Psychiatry, will investigate the neural and genetic basis of processing speed deficits in schizophrenia.

Neil Woodward, Ph.D.

Neil Woodward, Ph.D.

Processing speed impairments in schizophrenia contribute to deficits in higher cognitive functions, such as intellectual ability, and are a robust predictor of functional outcome. Woodward will use multi-modal magnetic resonance imaging methods to elucidate the neural basis of performance deficits in choice reaction and inspection time (two simple tasks of processing speed) in people with schizophrenia. In a separate study, Woodward will examine candidate gene effects on behavioral performance in patients and controls.