SWEBAGS proudly present the following Keynote Speakers for 2024
Henry Yin
Professor of Psychology and Neuroscience, Professor in Neurobiology,
Affiliation: Affiliate of the Duke Regeneration Center, Faculty Network Member of the Duke Institute for Brain Sciences. Duke University
Web: https://www.neuro.duke.edu/profile/henry-yin
Web: https://www.neuro.duke.edu/profile/henry-yin
Emanuela Santini
Assistant Professor
Wolf-Julian Neumann
Assistant Professor for Interventional and Cognitive Neuromodulation
Affiliation: Charité – Universitätsmedizin Berlin
Web: https://neurologie.charite.de/en/
Bio: I am associate professor for invasive neurotechnology at Charité – Universitätsmedizin Berlin. The primary aim of my research is to translate invasive brain data from human patients with neurological and psychiatric disorders into neurotechnological brain circuit interventions. During my postdoctoral career I have characterized invasively recorded brain activity in hundreds of patients suffering from Parkinson’s disease (PD), Major Depressive Disorder, Tourette’s Syndrome, Obsessive Compulsive Disorder and Dystonia. My group now combines causal brain stimulation experiments, with MRI based connectomics and machine learning to understand how to a) optimally decode symptoms and behavior for clinical brain computer interfaces and closed-loop neuromodulation, b) discover pathophysiological changes in brain networks and c) develop the most spatiotemporally precise treatment strategies possible. I am convinced that success and progress in neurotechnology and BCI will depend on continuous research on the fundamental principles of human brain function and precise knowledge on pathophysiological circuit changes and their interaction. I have made the circuit changes in dopaminergic brain disorders my primary clinical research interest. Building on subthalamic deep brain stimulation, my dream would be to develop an invasive neuroprosthetic that can mimic the effect of dopamine release in the human brain and counteract the development of symptoms of Parkinson’s disease.
Title: Shared network mechanisms of dopamine and deep brain stimulation for the treatment of Parkinson’s disease: From modulation of oscillatory cortex – basal ganglia communication to intelligent clinical brain computer interfaces.
Abstract: Deep brain stimulation (DBS) is a brain circuit intervention that can modulate distinct neural pathways for the alleviation of neurological symptoms in patients with brain disorders. In Parkinson’s disease, subthalamic DBS clinically mimics the effect of dopaminergic drug treatment, but the shared network mechanisms on cortex – basal ganglia networks are matter of ongoing research. In our effort to elucidate therapeutic circuit effects and inspire novel treatment avenues, we combine fully-invasive neural multisite recordings in patients undergoing DBS surgery with MRI-based whole-brain connectomics and machine learning based brain signal decoding. Our findings demonstrate that dopamine and DBS exert distinct mesoscale effects through modulation of local neural population synchrony, while at the macroscale, DBS mimics dopamine in its suppression of excessive interregional network synchrony associated with indirect and hyperdirect cortex – basal ganglia pathways and akinesia. Our results provide a better understanding of the circuit mechanisms of dopamine and DBS, laying the foundation for advanced closed-loop neurostimulation therapies that can use brain signal decoding to adapt neurotherapies to the individual challenges that our patients are facing, right when their symptoms occur.
Web: https://neurologie.charite.de/en/
Bio: I am associate professor for invasive neurotechnology at Charité – Universitätsmedizin Berlin. The primary aim of my research is to translate invasive brain data from human patients with neurological and psychiatric disorders into neurotechnological brain circuit interventions. During my postdoctoral career I have characterized invasively recorded brain activity in hundreds of patients suffering from Parkinson’s disease (PD), Major Depressive Disorder, Tourette’s Syndrome, Obsessive Compulsive Disorder and Dystonia. My group now combines causal brain stimulation experiments, with MRI based connectomics and machine learning to understand how to a) optimally decode symptoms and behavior for clinical brain computer interfaces and closed-loop neuromodulation, b) discover pathophysiological changes in brain networks and c) develop the most spatiotemporally precise treatment strategies possible. I am convinced that success and progress in neurotechnology and BCI will depend on continuous research on the fundamental principles of human brain function and precise knowledge on pathophysiological circuit changes and their interaction. I have made the circuit changes in dopaminergic brain disorders my primary clinical research interest. Building on subthalamic deep brain stimulation, my dream would be to develop an invasive neuroprosthetic that can mimic the effect of dopamine release in the human brain and counteract the development of symptoms of Parkinson’s disease.
Title: Shared network mechanisms of dopamine and deep brain stimulation for the treatment of Parkinson’s disease: From modulation of oscillatory cortex – basal ganglia communication to intelligent clinical brain computer interfaces.
Abstract: Deep brain stimulation (DBS) is a brain circuit intervention that can modulate distinct neural pathways for the alleviation of neurological symptoms in patients with brain disorders. In Parkinson’s disease, subthalamic DBS clinically mimics the effect of dopaminergic drug treatment, but the shared network mechanisms on cortex – basal ganglia networks are matter of ongoing research. In our effort to elucidate therapeutic circuit effects and inspire novel treatment avenues, we combine fully-invasive neural multisite recordings in patients undergoing DBS surgery with MRI-based whole-brain connectomics and machine learning based brain signal decoding. Our findings demonstrate that dopamine and DBS exert distinct mesoscale effects through modulation of local neural population synchrony, while at the macroscale, DBS mimics dopamine in its suppression of excessive interregional network synchrony associated with indirect and hyperdirect cortex – basal ganglia pathways and akinesia. Our results provide a better understanding of the circuit mechanisms of dopamine and DBS, laying the foundation for advanced closed-loop neurostimulation therapies that can use brain signal decoding to adapt neurotherapies to the individual challenges that our patients are facing, right when their symptoms occur.
