Preclinical dementia neurophysiology: We are studying the impact of dementia related pathologies such as tau and Aβ disrupt neuronal circuit function. We are particularly interested in how neural coding of spatial information and memories are affected in mouse models of dementia pathology and the contributions made by specific cell subtypes to circuit dysfunction in dementia models. 

Neuropharmacology: In collaboration with leading pharmaceutical and biotech companies, we are working to establish the neural mechanisms of actions of clinically relevant drugs. 

Circuit connectivity:  We are using optogenetic and neuroanatomical circuit mapping techniques to understand how dementia-linked pathologies disrupt synaptic communication throughout the brain’s memory centres. We are also developing a closed-loop system combining optogenetic stimulation, imaging of neuronal activity, and mathematical modelling of synaptic connections, to manipulate connectivity in neuronal networks. This system will enable testing theories on how connectivity constrains the activity patterns of networks. 

Neuroimmune interactions: We are working to understand mechanisms of communication between neurons and glia cells and how these signalling pathways can be leveraged using pharmacology or brain stimulation for dementia treatment.   

Single-cell electrophysiology: We use the dynamic clamp technique to determine the role of leak channels in setting the electrical excitability of hormone-releasing cells. This is the first step in determining how hormone release is regulated by messages from the brain. 

Neuroendocrine oscillations: We are investigating how hypothalamic circuits and pituitary cell networks regulate oscillations in stress hormone secretion, and how in turn these hormone oscillations feedback to regulate the activity of stress-sensitive neuroendocrine systems. To do this, we are using a combination of ex vivo and in vivo calcium imaging, hormone assay, and mathematical modelling.