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Many neurodevelopmental and psychiatric diseases (i.e., autism spectrum disorder, social anxiety) are characterized by severe social impairments.

To understand the neural mechanisms responsible for these diseases, we investigate the brain function required to drive social interactions. We use a combination of neural tracing, optogenetic/chemogenetic, and in vivo electrophysiological techniques to understand how epigenetic regulation affects social-related functional connectivity within neural circuits.

On-going projects:

The neural and behavioural effects of mouse models of bacterial and viral
prenatal infection. Funded by Research Nova Scotia (Establishment).

Infections during pregnancy, like bacterial urinary tract infections or viral influenza infections, are thought to be risk factors for two neurodevelopmental disorders in offspring: autism spectrum disorder (ASD) and schizophrenia. We aim to understand how exposure to an immune response during gestation acts as a risk factor for these disorders by using mouse models of bacterial and viral prenatal infection. Our recent research has discovered that mice exposed to bacterial maternal immune activation during prenatal development have increased levels of an activated form of an important signaling molecule (mechanistic target of rapamycin (Mtor)) at birth. Prior research has also observed dysregulation of Mtor in both schizophrenia and ASD patients suggesting that this may be an important link between prenatal infection and these disorders. This research program will define a developmental window during which Mtor function is dysregulated as a result of maternal immune activation. It will further investigate a process that mTOR regulates in the brain, called autophagy, that is critical for normal brain development. Lastly, we will measure pup and adult behaviour to understand how quickly the behavioural effects of maternal immune activation are presented, and how long these behavioural effects persist. Findings from this study will describe Mtor dysregulation in mouse models of neurodevelopmental disease precipitated by prenatal infection, and will describe a time window during which Mtor and/or autophagy can be therapeutically targeted by pharmacological or environmental interventions.

Social Dominance: mechanisms of the prefrontal cortex. Funded by NSERC Discovery grant (RGPIN-2017-06490).

Living in large social groups requires us to fulfill particular roles, with some individuals dominant within their social environment, and others subordinate. Our research program is focused on understanding how the brains of dominant individuals differ from the brains of individuals that are subordinate within their social hierarchy. To do this, we use mice, a social mammal that forms complex dominance hierarchies. We are currently investigating the role that a histone deacetylase plays in dominance behaviour. We are specifically focusing on its function within the prefrontal cortex, a brain area that plays a central role in generating social behaviours.

Investigating transgenerational information transfer resulting from adolescent stress in mice. Funded by Nova Scotia Health Research Foundation Development/Innovative (#1534).

We are investigating the direct and transgenerational behavioural effects of adolescent stress on female and male adult social behaviours.

Understanding the neural bases for social deficits in Alzheimer's Disease. Funded by the Alzheimer's Association research grant award (2016-MNIRGD-391961).

Alzheimer鈥檚 disease patients present symptoms of social withdrawal and aggression that negatively impact the patients, their families, and caregivers. Despite this, the majority of current research focuses on how disease-related brain changes cause learning and memory deficits in Alzheimer鈥檚 disease patients. Few studies are aimed at understanding the underlying causes for the social deficits often observed in this patient population. Our research aims to describe changes in the brain that cause deficits in social behaviour related to Alzheimer鈥檚 disease, and to reverse social dysfunction in an Alzheimer鈥檚 disease mouse model by manipulating brain activity. We are currently characterizing social behaviours in a mouse that models many of the features of Alzheimer鈥檚 disease (5x FAD)