Raul Chavez-Valdez, co-director of the neurosciences intensive care nursery program at Johns Hopkins, discusses his latest research on the consequences of injury to the neonatal brain, with a particular focus on birth asphyxia. The goal of this research is to identify mechanisms of injury that are responsive to treatment to improve some of the devastating outcomes seen in survivors.
Hello, my name is Raul Chavez Valdez. I am an associate professor of pediatrics in the Department of Neonatology, Johns Hopkins. I am the co-director of the Neuroscience Intensive Care Nursery Program and the fellowship program. Today, I would like to introduce you to some of the important research that we are working on in my laboratory of Developmental Neuroscience at Johns Hopkins. In my lab, we studied the short term and long term cellular and biochemical consequences of injury to the neonatal brain with a particular focus in neonatal hypoxic ischemic injury commonly known as bury. Our ultimate goal is to identify mechanisms of injury and enable to treatment to improve some of the devastating outcomes seen in survivors. In 2017, we were the first to report the burs as fix your results in the late deficit in inhibitory inputs to memory circuits in the developing brain. The visit persists to adult knowing that those inhibitory circuits develop for decades after birth and that these developmental processes are necessary for appropriate moderation of many behavioral and cognitive abilities later in our lives. Our findings have helped us and all the researchers to understand some of the neurodevelopmental imper documented in survivors at the age allowing us now to test various delay therapies to prevent these future deficits experiments which are currently ongoing because genetic variability encoding our DNA changes the way how our brain cells responds to birth asphyxia. My lab is also focused in the study of the human apo epsilon four A L, the strongest genetic risk factor for late onset Alzheimer's disease and its influence in the outcomes of birth asphyxia. One of the most intriguing and persistent findings in our mice car in the human apo for A L is a long time after birth exi they develop progressive brain inflammation and neurodegeneration leading to cognitive deterioration at the human equivalent as young as 30 to 40 years of age. These results suggest the birth asphyxia may accelerate the neurodegeneration more commonly seen in A 04 carriers. We believe that we have identified the brain cell initiating these pathological processes and we have initiated the testing of therapeutic agents hoping to redirect cellular dysfunction. Our hope is that by using high quality experimental approaches, we will continue making strides in the discovery of novel treatments to improve the life of our little patients and their families, preventing worsening deficits as they age. Thank you.
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