I Want To...
I Want To...
Find Research Faculty
Enter the last name, specialty or keyword for your search below.
School of Medicine
I Want to...
10 Johns Hopkins Scientists Awarded NARSAD Research Grants - 08/27/2013
10 Johns Hopkins Scientists Awarded NARSAD Research Grants
Release Date: August 27, 2013
The Brain & Behavior Research Foundation (formerly known as NARSAD, or the National Alliance for Research on Schizophrenia and Depression) has announced 10 new grants totaling $600,000 to Johns Hopkins University researchers Ashley M. Blouin, Solange P. Brown, Jennifer M. Coughlin, Yongjun Gao, Jia-Hua Hu, Pan Li, Keri Martinowich, Rashelle J. Musci, Frederick C. Nucifora and Juan Song. The 10 are among this year’s 200 total recipients.
The NARSAD grants program, begun in 1987, invests in early-career scientists’ bold and original research ideas. One hundred Johns Hopkins researchers have received approximately $9 million in NARSAD grants over the years.
“The Johns Hopkins University is at the forefront of research into the molecular mechanisms of neurological and psychiatric diseases, including schizophrenia, depression, bipolar disorder and autism,” says Jeffrey Borenstein, M.D., Brain & Behavior Research Foundation president and CEO. “We are very happy to be able to support these brilliant scientists pursuing cutting-edge research ideas to improve the lives of those with mental illness."
Borenstein notes that the NARSAD Young Investigator Grants enable early-career scientists to garner pilot data for innovative ideas before they have “proof of concept” for their work. “After our initial funding, they usually go on to receive sustained grant support from other sources that has proven to equal as much as 50 times the original NARSAD Grant amount. Our grants offer the first critical backing of their work,” he says.
The 2013 Johns Hopkins grant recipients are:
Ashley M. Blouin, Ph.D., will explore whether a gene called Narp (neuronal activity-regulated pentraxin) is acting in the brain to mediate the antidepressant effect of electroconvulsive therapy, research that could aid the development of new treatments for resistant depression with fewer side effects.
Solange P. Brown, M.D., Ph.D., seeks to clarify, using mouse models, the role of particular neurons located below the cerebral cortex, which are known to be abnormally distributed in schizophrenia.
Jennifer M. Coughlin, M.D., will investigate the hypothesis that oxidative stress (an excess of free radicals) and the associated neuroinflammatory response may play a role in schizophrenia in high-risk people.
Yongjun Gao, Ph.D., aims to develop more effective radioligands –– that is, radioactive molecules that bind to receptor molecules –– for use in PET imaging to examine the distribution of the ?7 nicotinic acetylcholine receptors, which are implicated in schizophrenia, Alzheimer’s disease, anxiety, depression and drug addiction.
Jia-Hua Hu, Ph.D., will examine aspects of how cocaine addiction works by elucidating the mechanisms of a protein he identified as regulating dopamine signaling.
Pan Li, Ph.D., will explore a possible regulatory mechanism affecting a protein called DISC (Disrupted-in-Schizophrenia), building on his earlier research suggesting that DISC2 regulates DISC1, with implications for schizophrenia and bipolar disorder.
Keri Martinowich, Ph.D., will focus on the role of brain-derived neurotrophic factor (BDNF), a nerve growth factor protein, in mediating behavioral response to antidepressant therapy.
Rashelle J. Musci, Ph.D., will explore the relationship between aggressive and impulsive suicidal behavior and genes associated with serotonin neurotransmission.
Frederick C. Nucifora, Ph.D., D.O., M.H.S., will investigate whether mutant NPAS3, a protein associated with schizophrenia, bipolar disorder and antipsychotic treatment efficacy, leads to abnormal neuronal structure and function.
Juan Song, Ph.D., seeks to discover the cause of disturbances in gamma-frequency oscillation — rhythms that emerge during performance of cognitive tasks –– which are thought to be a source of brain dysfunction in schizophrenia.