The brain is central in coordinating the organism’s response to environmental factors such as stress, and at the same time, a very sensitive target when such response is not controlled. In fact, in humans stress is associated with the onset and exacerbation of a number of neurological disorders, including anxiety, depression, drug addiction, and post-traumatic stress disorder (PTSD). Stress is also a contributing factor in unhealthy aging and neurodegenerative disorders, including Alzheimer’s.

Current projects in the lab include:

• Exercise-derived myokines (such as Irisin) as possible anti-stress and anti-neurodegeneration agents. Irisin is a skeletal muscle-derived protein that contributes to regulating metabolism and thermogenesis.  Irisin is also released after physical activity, which is known to have positive effects on cognitive function and overall health. We will use electrophysiology and behavioral analysis to investigate the effects of Irisin on hippocamapal function as a stress resilience molecule. Further, we will also use Alzheimer’s disease mouse models to test Irisin as anti-neurodegeneration agent.
• Neuropeptide Y (NPY) and resilience to stress. Amongst the many pathways involved in stress processing in the brain, NPY has emerged as a promising “resilience molecule” due to its robust anxiolytic, anti-epileptic and pro-neurogenesis properties. Moreover, NPY levels in specific brain regions, such as the hippocampus, are decreased by stressful conditions, yet the role of endogenously released NPY and the impact of stress-induced changes in NPY on hippocampal function are not clear.
• Effect of early life stress (ELS) on hippocampal function. Adverse conditions during early development can cause dramatic changes in the brain, however the precise mechanisms involved are far from clear. We will use well known paradigms for early stress to fully characterize changes in hippocampal synaptic function and behavior in adult mice. We are specially interested in social behavior and avoidance.
• High Salt diet (HSD), altered gut microbiome, and autism spectrum disorder (ASD) in the offspring. Parental HSD has been associated with alterations in gut microbiome and autoimmunity. Other studies have found an increased incidence of ASD in children whose parents suffered from autoimmune disorders. Therefore, using our own mouse model of HSD, we will test the hypothesis that autoimmunity and gut microbiome alterations in the parental generation can result in behavioral changes associated with ASD-like behavior in the offspring.