Children's Memorial Research Center scientist receives McKnight grant to explore causes of brain disorders
FOR IMMEDIATE RELEASE (Minneapolis, MN, January 3, 2006)—The McKnight Endowment Fund for Neuroscience has committed $1.5 million over three years to investigate the root causes of neurological and psychiatric disorders.
The 2006 Neuroscience of Brain Disorders Awards will support U.S. scientists for research aimed at diagnosing, preventing, and treating injuries or diseases of the brain or spinal cord. The five projects selected this year are studying mechanisms involved in stroke, obsessive-compulsive disorder, schizophrenia, autism, and sleep disorders. Each will receive $300,000 over the three-year period.
“To achieve our long-term goal of developing effective preventions and treatments for neurological disorders, we need a deeper understanding of how the brain works,” said Larry R. Squire, Ph.D., chair of the awards committee. Dr. Squire is a professor of psychiatry, neurosciences, and psychology at the University of California, San Diego School of Medicine, and research career scientist at the Veterans Affairs Medical Center, San Diego. “These scientists are focused on moving us closer to that goal by probing for the mechanisms that underlie brain injury and disease.”
The McKnight Endowment Fund created the Neuroscience of Brain Disorders Awards to support innovative efforts aimed at translating basic laboratory discoveries in neuroscience into clinical benefits for patients. The awards are highly competitive; 205 letters of intent were received this year.
Recipients and their projects are:
- C. Michael Crowder, M.D., Ph.D., Washington University School of Medicine, Identification of Genes Regulating Survival Following Hypoxic Insult in Caenorhabditis elegans
- Guoping Feng, Ph.D., Duke University Medical Center, Understanding the Molecular and Cellular Basis of Obsessive-Compulsive Disorder Using a Novel Mouse Model
- Jill Morris, Ph.D., Northwestern University Children’s Memorial Research Center, The Role of DISC1 in Neuronal Migration
- Jeffrey Noebels, M.D., Ph.D., and Richard Gibbs, Ph.D., Baylor College of Medicine, Profiling Ion Channel Genes in Autism
- Alexander Schier, Ph.D., Harvard University, Genetic Analysis of Sleep Disorders in Zebrafish
Letters of intent for next year’s awards are due by April 3, 2006. For more information, see www.mcknight.org/neuroscience/.
ABOUT THE McKNIGHT ENDOWMENT FUND FOR NEUROSCIENCE
The McKnight Endowment Fund for Neuroscience is an independent organization funded solely by The McKnight Foundation of Minneapolis, Minnesota, and led by a board of prominent neuroscientists from around the country. The McKnight Foundation has supported neuroscience research since 1977. The foundation established the Endowment Fund in 1986 to carry out one of the intentions of founder William L. McKnight (1887–1978). One of the early leaders of the 3M Company, he had a personal interest in memory and its diseases and wanted part of his legacy used to help find cures.
The Endowment Fund makes three types of awards each year. In addition to the Neuroscience of Brain Disorders Awards, they are the McKnight Technological Innovations in Neuroscience Awards, providing seed money to develop technical inventions to advance brain research; and the McKnight Scholar Awards, supporting neuroscientists in the early stages of their research careers.
Attached: Project Descriptions
2006 McKnight Neuroscience of Brain Disorders Awards
C. Michael Crowder, M.D., Ph.D., Washington University School of Medicine
Identification of Genes Regulating Survival Following Hypoxic Insult in Caenorhabditis elegans
Stroke is the leading cause of long-term disability and the third leading cause of death in the United States. Stroke can cause lasting damage or death by depriving cells of oxygen, a condition called hypoxic injury. Yet nature seems to have developed ways to protect some cells from oxygen deprivation (anoxia). For example, certain hibernating fish, frogs and turtles undergo months of near-complete anoxia yet return to normal. Working with the nematode C. elegans, which has a well-developed nervous system, Crowder will search for genes that control the susceptibility of an organism and its nerve cells to hypoxic injury. He will use a high-throughput reverse genetic screening approach to identify the responsible genes. Those genes will be potential therapeutic targets for prevention and treatment of stroke.
Guoping Feng, Ph.D., Duke University Medical Center
Understanding the Molecular and Cellular Basis of Obsessive-Compulsive Disorder Using a Novel Mouse Model
People with obsessive-compulsive disorder suffer from anxiety and often perform repetitive or ritualistic actions to relieve the anxiety. The neurobiological basis of this disorder is not well understood. Evidence suggests that OCD has a genetic basis, but no genes have yet been directly linked to it, and it is believed that multiple genes may be involved. Furthermore, the molecular mechanisms of OCD are completely unknown. Feng will use genetic approaches in mice to explore the pathogenic mechanisms of OCD and to identify potential new molecular targets for drug development. He is focusing on the possibility that OCD is related to synaptic defects, an avenue that has not been widely investigated. In previous work, Feng has been able to develop mice that exhibit OCD-like behavior and therefore provide an opportunity to study the molecular and cellular basis of such behavior.
Jill Morris, Ph.D., Northwestern University and Children’s Memorial Research Center
The Role of DISC1 in Neuronal Migration
People with mutations or changes in the gene called DISC1 (Disrupted in Schizophrenia 1) have an increased risk of developing schizophrenia, a debilitating neurodevelopmental illness characterized by such symptoms as hallucinations, delusions, and social withdrawal. The gene was identified in a Scottish family with members who suffered from schizophrenia, bipolar disorder, and depression. In people with schizophrenia, the DISC1 gene is mutated, and this mutation may cause neurons to grow abnormally during brain development. With a mouse model, Morris will seek to determine the role DISC1 plays in brain development and how mutations or changes in the gene alter that development to cause schizophrenia and related neurodevelopmental disorders.
Jeffrey Noebels, M.D., Ph.D., and Richard Gibbs, Ph.D., Baylor College of Medicine
Profiling Ion Channel Genes in Autism
Ion channels allow cells to generate electrical signals in neurons and govern the precise patterns of signaling in brain networks. These patterns sharpen our ability for perception, cognition, and behavioral responses to the external world. Noebels, Gibbs, and co-investigator Dan Burgess, Ph.D., hope to learn whether variation in genes encoding ion channels may give rise to autism, a poorly understood neurodevelopmental syndrome in children. Autism is also frequently associated with seizure disorders, suggesting that the excitability of neurons is altered in these individuals. The project will examine the exact gene sequence of all 250 human ion channels in groups of children with autism, and in those with autism and epilepsy. This is the first large-scale translational neurogenomics project in autism and will be performed in partnership between Baylor’s Department of Neurology and Human Genome Sequencing Center.
Alexander Schier, Ph.D., Harvard University
Genetic Analysis of Sleep Disorders in Zebrafish
As many as 10 percent of Americans sleep poorly, but the genetic mechanisms that control sleeping and waking remain largely unknown. Narcolepsy has been related to the hormone hypocretin, but there’s no effective treatment for narcolepsy, and numerous other sleep disorders remain to be studied. Schier proposes to study sleep disorders using zebrafish, because they have hypocretin as well as brain structures similar to those that regulate sleep in humans. During the grant period, Schier will use forward genetic screening to look for the genes that regulate sleep and wakefulness. Once the relevant mutations are identified, it will become possible to clone those genes and translate the findings to mammals.
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