•   grumbaug@scripps.edu
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    SynGAP1, a synaptic RasGAP that mediates NMDA-dependent G-protein signaling , is critical for proper development and subsequent functioning of memory circuits. SYNGAP1 haploinsufficiency causes non-syndromic intellectual disability and comorbid autism spectrum disorder and epilepsy in humans as evidenced in clinical cases. We have generated a conditional SYNGAP1 heterozygous flox mouse line as well as a SYNGAP1 rescue mouse line for behavioral, biochemical, cellular and molecular characterizations that can be manipulated at various time points during development for the purpose of discovering specific time-restricted windows of impaired synaptic phenotypes to detect vulnerable periods of development when the brain may be more amenable to potential therapeutic intervention.
    Alterations in synaptic connections are implicated in nearly all brain disorders. In particular, synapse loss is a particularly profound problem in brain disorders that attack cognitive function, such as schizophrenia and Alzheimer’s disease.  Our lab has initiated a research program aimed at discovering novel mechanisms that trigger increases in neural connectivity as a strategy to combat these illnesses. We believe that increasing connectivity among neurons in networks that mediate critical cognitive processes, such as memory and executive function, will lead to significant improvements in patients with these types of mental disorders. Our approach is to combine the vast chemical resources at TSRI with a novel neuron-based screening platform that was created in the Department of Neuroscience at Scripps Florida. We expect that this combined technology will facilitate the discovery novel chemical probes that trigger increases in synaptic connectivity. These probes will then serve as developmental platforms for future generations of drugs that treat a wide range of brain disorders.

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