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http://dbpedia.org/ontology/abstract Eric Klann is an American neuroscientist wEric Klann is an American neuroscientist who studies how molecular signaling, synaptic plasticity, and behavior are altered in developmental disability, autism, aging, psychiatric disorders, and Alzheimer's disease. His research is focused on the molecular mechanisms underlying activity-dependent, long-lasting changes in neuronal function and the role these mechanisms play in complex behaviors, including cognition. As a postdoctoral fellow in David Sweatt's laboratory at Baylor College of Medicine, Klann was the first to demonstrate that persistent protein kinase activity was associated with long-lasting synaptic plasticity. After becoming an independent investigator, his laboratory was the first to show that at low concentrations, reactive oxygen species (ROS), which are typically considered to be neurotoxic, are in fact signaling molecules that are required for synaptic plasticity and long-term memory. By contrast, Klann's laboratory has also shown that removal of ROS can prevent age- and Alzheimer's disease-related impairments in synaptic plasticity and memory. Klann's laboratory made additional breakthroughs in the mid-2000s. It has been known since the 1960s that new protein synthesis (translation) was necessary for the formation of long-term memory. However, the mechanisms that regulate this process were not understood until Klann's laboratory published a number of seminal studies describing the translational control mechanisms that are required for proper long-lasting synaptic plasticity and long-term memory. In addition, Klann's laboratory subsequently demonstrated that dysregulated translational control mechanisms are involved in several brain disorders, including fragile X syndromeand autism. His laboratory uses a number of experimental approaches to dissect the molecular mechanisms necessary for maintaining long-lasting changes in synaptic strength and memory. Detailed biochemical and sophisticated imaging experiments are employed to delineate the molecular signaling cascades that are activated and required for long-lasting synaptic plasticity in the hippocampus, amygdala, cortex, and striatum, and whether these signaling events are required for memory formation, social behaviors, and behavioral flexibility. Klann's laboratory also conducts electrophysiological, biochemical, imaging, and behavioral studies with various knockout and transgenic mice to determine how precise genetic manipulations that either activate or abolish signaling cascades alter synaptic function and behavior. Klann serves as a reviewing editor for The Journal of Neuroscience and as an associate editor for Neurobiology of Learning and Memory, and serves on the editorial boards of several other journals. He is a former member and chair of both the Neural Oxidative Metabolism & Death and the Molecular & Cellular Substrates of Complex Disorders Study Sections of the National Institutes of Health. Klann serves on the Scientific Advisory Boards of the Foundation for Angelman Syndrome Therapeutics and Pitt Hopkins Syndrome International Network. He also served on the Fragile X Outcomes Measures Group and the Fragile X Syndrome Research Plan Working Group of the National Institutes of Health. Klann also was the treasurer (2010-2012) and is a past president of the Molecular and Cellular Cognition Society. Klann received his Ph.D. from the Medical College of Virginia, did postdoctoral training at Baylor College of Medicine, and held faculty positions at the University of Pittsburgh (1994-2001) and Baylor College of Medicine (2001-2006) before joining the faculty of New York University in 2006.he faculty of New York University in 2006.
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rdfs:comment Eric Klann is an American neuroscientist wEric Klann is an American neuroscientist who studies how molecular signaling, synaptic plasticity, and behavior are altered in developmental disability, autism, aging, psychiatric disorders, and Alzheimer's disease. His research is focused on the molecular mechanisms underlying activity-dependent, long-lasting changes in neuronal function and the role these mechanisms play in complex behaviors, including cognition.in complex behaviors, including cognition.
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