Moritz Haaf
Transcript for the 3-Minute SIRS Early Career Video
Hello, my name is Moritz Haaf, and I’m researching the role of the neurotransmitter glutamate in schizophrenia. While a dysfunction of glutamatergic neurotransmission has been implicated in schizophrenia for three decades, no pharmacological treatments targeting the glutamate system are clinically available today. Finding markers to identify the group of people who might benefit from this type of therapy could help us address difficult-to-treat symptoms such as negative symptoms and cognitive challenges.
In this context it is important to consider the essential role of glutamate for the delicate balance between neuronal excitation and inhibition. A central piece to the disbalance found in people with schizophrenia is a hypofunction of the NMDA receptor. Despite our understanding of these dysfunctions, current biomarkers fall short in capturing the complex impact on neural activity. Traditional EEG methods may overlook key dynamics hidden in the aperiodic, or non-oscillatory, aspects of the signal. To tackle this challenge, we modelled NMDA receptor hypofunction in healthy volunteers using the receptor antagonist ketamine.
Each participant underwent separate sessions one with ketamine and one with a placebo during which we recorded resting-state EEGs. This allowed us to investigate the changes in neural dynamics associated with NMDA receptor hypofunction compared with placebo. On the one hand we were able to demonstrate changes in the background or aperiodic EEG activity that could explain previously reported changes in gamma activity. On the other hand, we used an approach to geometrically capture the alterations in neural dynamics, to leverage the benefit of EEG’s high temporal solution.
Why does this matter? By linking alterations in the aperiodic slope and EEG complexity directly to NMDA receptor hypofunction, we open the possibility of using these measures as potential biomarkers for schizophrenia. This could be transformative, not only in improving diagnosis but also in tailoring targeted interventions using glutamatergic agents. By leveraging EEG's accessibility, especially in resource-limited settings, corresponding biomarkers could help us to improve outcomes for individuals affected by schizophrenia worldwide.
I invite you to ask questions about our methodology, our results, and the implications of these findings at our poster. Thank you for your attention!
