Christos Panagiotis Lisgaras

Biography

Christos Lisgaras is Research Assistant Professor at New York University Grossman School of Medicine, Department of Psychiatry. He also is Research Scientist at the Nathan S. Kline Institute for Psychiatric Research, Center for Dementia Research where his laboratory is located.

My work is primarily focused on developing novel approaches and biomarkers to help treat psychiatric comorbidities and memory deficits for a range of brain disorders including epilepsy, Alzheimer’s disease (AD), and seizure disorders. More specifically, I use electroencephalography (EEG) as a vehicle to better understand the circuits and mechanisms involved in brain disease with a focus on abnormal oscillations such as high frequency oscillations (HFOs>250Hz).

A major arm of my research program investigates the overlap between AD and epilepsy with a focus on common EEG disturbances. In three mouse lines with AD features, I found that HFOs were a new abnormal electrical activity that emerged very early in life and well before neuropathology developed. Notably, HFOs were previously considered a promising epilepsy biomarker but their occurrence in AD was unknown. I also tackled an outstanding question in AD that relates to where abnormal electrical activity originates in the brain. To that end, I employed large-scale electrophysiological recordings in three animal models of AD and found a dominant role of the dentate gyrus in generating abnormal electrical activity.

The second arm of my research program is focused on developing novel neurostimulation protocols to precisely disrupt abnormal electrical activity in both AD and epilepsy. These advanced tools have the potential to uncover circuit mechanisms underlying comorbidities with unprecedented selectivity which may contribute to less side-effects of prolonged treatments.

Last, I am interested in developing new and improved animal models of neurologic disease. To that end, I modified a widely used animal model of epilepsy (intrahippocampal kainic acid model) to show robust chronic convulsive seizures with human seizure onset patterns to better simulate human temporal lobe epilepsy in laboratory mice.