Seeking a Biological Cure
The SHINE Initiative provides funding for neurological research of the biological causes of and cures for mental illness, especially in children and young adults.
These are exciting times in neuroscience research as significant advances in brain scanning technologies coupled with a growing and vast body of genetic knowledge bring us ever closer to the Discovery of causes of mental illness in our children and young adults. Additionally, advanced treatment modalities, utilizing the latest information available, are emerging that hold great promise and Hope for Recovery for people living with mental illness as well as for their families and those working to provide direct services.
The SHINE Initiative is proud to play a role in the further development of neuroscience research by raising funds to support the work of extraordinary scientists who are dedicated to cutting edge research as a pathway to discovery of the root causes of mental illness. We are also proud to partner with NARSAD (The Brain and Behavior Research Fund), the world’s leading non- profit organization dedicated to scientific research in mental illness, in their Research Partners Program, to financially support the work of a scientist through the Young Investigator Award.
The SHINE Initiative is honored to introduce three of our Young Investigator Award recipients, working hard to make breakthroughs in their specific areas of research on behalf of children and young adults:
Magnetic Resonance Spectroscopy in Children At Risk for Bipolar Disorder
Aude Henin, Ph.D. – Massachusetts General Hospital – Boston, MA
Her Award supports a genetic imaging study (magnetic resonance spectroscopy) of children (ages 6-24) at risk for bipolar disorder. Dr. Henin examined whether there are associations between genes previously linked to bipolar disorder and neurochemical abnormalities in the anterior cingulate cortex, among youth at risk for bipolar disorder. Using data from an existing sample of 43 offspring of parents with bipolar disorder and 19 healthy control children of parents without mood disorders plus 8 new participants, she examined the genetic influence on brain chemistry in a population at risk for developing bipolar disorder. Preliminary results suggest that children at risk for bipolar disorder, even when they are asymptomatic, exhibit neurochemical abnormalities in cellular functioning and cellular health, and may point to specific risk factors for the development of bipolar disorder.
This study is of the highest public health importance because it may verify why some children at risk develop bipolar disorder whereas others do not. Additionally, identifying a population at extreme high risk for developing bipolar disorder is key to facilitating targeted early intervention and prevention efforts.
Misguided Development of Corticolimbic Circuitry after Early Life Stress
Heather Brenhouse, Ph.D. – McLean Hospital / Harvard University – Belmont, MA
Her Award build on her past research work and extends this work in two important ways. She proposed to further understand how early life stress changes the development of the prefrontal cortex of the brain..her study examines the time course of when stress effects first become apparent in the prefrontal cortex as it modulates /gates the activity in the nucleus accumbens. Her second piece of work aims to bring a novel look at how stress-induced inflammatory processes could alter development ( the long held hypothesis that the etiology of Schizophrenia is stress induce)y . Based on findings in the first aim of identifying the time course of vulnerability, she hypothesizes that COX-2 inhibition will reverse the aberrant development of the cortex set in motion by early life stress history.
The study shedï¿½s light on how early life experiences affect the Prefrontal Cortex of the brain specifically, which has been shown to mediate many of the behaviors involved in late onset disorders.
Anxiety and Stress in an Animal Model of Psychiatric Vulnerability
Alo C. Basu, Ph.D. – McLean Hospital – Belmont, MA
Dr. Basu examines anxiety and stress in an animal model of psychiatric vulnerability. A major issue in understanding what causes schizophrenia is understanding susceptibility to the effects of environmental stress. Dr Basu explores the behavioral, anatomical and physiological effects of stress in mutant mice that are genetically deficient in D-serine due to an absence of the enzyme serine racemase, which produces D-serine in the brain. The results of the behavioral experiments completed thus far indicate that brain D-serine levels do alter stress sensitivity in mice. Three genes that have been implicated in schizophrenia regulate levels of D-serine, an amino acid in the brain that functionally modulates a subclass of excitatory neurotransmitter receptors. Two of these genes have been implicated in bipolar disorder.