The 19th Annual UNC Neuroscience Symposium will be held on Thursday, October 11th at the Carolina Club. The annual Andrew S Rachlin UNC Neuroscience Symposium will be held on October 11th, 2018 at the Carolina Club (150 Stadium Dr, … Continued
Angelman Syndrome is a severe neurodevelopmental disorder that is caused by loss of the maternal copy of the Ube3a gene. Using the gene editing technology CRISPR/Cas9, a team of scientists in the Zylka lab was able to correct the underlying molecular deficiency in the Angelman mouse model. The Zylka Lab was awarded a grant from the Angelman Syndrome Foundation to expand this finding towards a gene therapy.
María Luisa, a graduate student in the the McElligott lab at the Bowles Center for Alcohol Studies, received an NRSA from the NIAAA entitled “Examining Alcohol Induced Plasticity in Amygdala Hind Brain Circuits.” She will work to determine whether a history of alcohol consumption in mice can alter the behavioral and physiological properties of amygdalar circuits targeting the hindbrain.
Mark J. Zylka, PhD, Professor/Director, W.R. Kenan Distinguished Professor of Cell Biology and Physiology, and American Association for the Advancement of Science Fellow, was one of the awardees of the Center for Environmental Health and Susceptibility (CEHS) Pilot Projects Program. His project, “Does prenatal pesticide exposure exacerbate phenotypes in a mouse model of autism?”, submitted for the 2018-2019 CEHS Standard Pilot Projects Program, was approved for funding on April 1, 2018.
Hiroyuki Kato, PhD, has been selected as a Pew Scholar in Biological Sciences, which provides funding to young investigators of outstanding promise in science relevant to the advancement of human health.
The Kato Lab will use this award to study the circuit mechanisms underlying the extraction of complex sounds in the auditory cortex. Findings in the simple mouse cortex should provide a first step towards an ultimate understanding of the neuronal circuits underlying vocal communications, and how they fail in diseased brains.
The Dokholyan and Deshmukh labs published a report in PNAS where they examined the neurotoxicity of various SOD1 protein aggregates in a model of Amyotrophic Lateral Sclerosis (ALS). The large SOD1 aggregates, which are a hallmark of ALS, are generally considered to contribute to motor neuron death in ALS. However, the study found that the large SOD1 aggregates are less toxic than the smaller SOD1 trimers. These results suggest that therapies targeted towards the SOD1 trimers, rather than the larger SOD1 fibrils, may be more effective for the treatment of ALS.