1) Anesthesia and Cognitive Impairment
There is concern that exposure to general anesthesia and surgery in both young children and the elderly can cause long-lasting cognitive impairment. The main goal of the laboratory is to identify the molecular and cellular basis that underlies these perioperative cognitive dysfunctions. To this end, we use a multidisciplinary approach in a mouse model system to understand how perturbations at a neuromolecular level alter cognitive behavior. Our hope is that we will be able to understand how anesthesia and surgery alter the developing and aged brain, ultimately leading to safer anesthetic care in these vulnerable patient populations.
2) Identifying new cell signaling pathways activated in the brain following exposure to different anesthetics
Many anesthetics, often having different mechanisms of action, have been shown to cause developmental neurotoxicity in mouse and non-human primate models. This suggests that these diverse agents may be activating a common cell-signaling pathway that triggers neurotoxicity. Using hi-throughput and semi-hi-throughput genomic and proteomic techniques, we are looking to identify potentially novel cell-signaling pathways involved in anesthetic neurotoxicity. Moreover, these techniques allow us to compare the pathways activated between different classes of anesthetics, potentially allowing us to identify new agents or techniques to minimize their harmful properties.
3) Mechanisms of postoperative delirium in older surgical patients
Delirium is prevalent in geriatric surgical patients and is associated with significant morbidity, mortality, and cost. Many older surgical patients suffer from delirium postoperatively and, although numerous factors are likely involved, sedatives, general anesthetics, and depth of anesthesia have been strongly implicated. Nonetheless, the molecular mechanisms underlying the etiology of postoperative delirium remain unclear. Our research on delirium focuses on how general anesthetic-induced changes in neural activity could disrupt normal homeostatic responses in the brains of older surgical patients.