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Wolf-Julian Neumann - Invasive Brain Computer Interfaces for Parkinson's disease - BrainMeeting 2023
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Talk abstract:
Dopamine and the basal ganglia have been conserved over 500 million years of evolution. They are fundamental to animal and human behaviour. Parkinson’s disease (PD) is associated with loss of dopaminergic innervation to the basal ganglia. Over six million people suffer from the debilitating symptoms of PD that span disturbance of emotion, cognition and movement. There is a pressing need to understand the pathogenesis of these symptoms, but an integrated account of dopamine and basal ganglia function is lacking. This constitutes a significant roadblock to scientific and therapeutic advances. Deep brain stimulation (DBS) is an emerging neurotechnological treatment for which electrodes are implanted directly into the depth of the patients’ brains and connected to an implantable pulse generator for chronic neurostimulation. In the past decades, DBS has shown clinical efficacy and provided unique access to invasive neurophysiology from the human basal ganglia. Nevertheless, the precise therapeutic mechanisms of DBS remain unknown. The leading hypothesis is that DBS can disrupt pathological brain circuit communication through local suppression and modulation of neural activity. In the present lecture, I will introduce how our centre uses DBS to develop a better understanding of the brain circuit computations of the basal ganglia and their alterations underlying PD symptoms. Next, I will highlight how a better understanding can directly inform machine learning models for the development of invasive brain computer interfaces that adapt to the individual challenges that PD patients are facing. To achieve this, we leverage the unprecedented spatiotemporal precision of closed-loop neurostimulation to reinstate physiological brain network activity in cortex - basal ganglia networks that are affected by dopaminergic neurodegeneration in PD. If successful, this could open new horizons for the interdisciplinary treatment of brain disorders affecting the dopaminergic system.
Funding statement:
WJN received funding from the European Union (ERC, ReinforceBG, project 101077060 ), Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) – Project-ID – TRR 295 and the Bundesministerium für Bildung und Forschung (BMBF, project FKZ01GQ1802).
Twitter accounts to tag in promotional posts:
@neumann_wj
@ICNeuromodulate
Background of the speaker:
Wolf-Julian Neumann is a clinician scientist (MD) at the Movement Disorders and Neuromodulation Unit at Charité Berlin with an expertise in movement disorders, neurophysiology and deep brain stimulation. The challenge his group, the @icneuromodulation174 group is currently working on is to try and integrate insights from PD pathophyisology, basal ganglia function, dopamine and neural reinforcement into a holistic cortex – basal ganglia – circuit model. I am actively engaging in programs and activities that aim to improve the scientific landscapes in terms of openness, reproducibility, diversity, equity and inclusiveness. I am severely hearing impaired.
Dopamine and the basal ganglia have been conserved over 500 million years of evolution. They are fundamental to animal and human behaviour. Parkinson’s disease (PD) is associated with loss of dopaminergic innervation to the basal ganglia. Over six million people suffer from the debilitating symptoms of PD that span disturbance of emotion, cognition and movement. There is a pressing need to understand the pathogenesis of these symptoms, but an integrated account of dopamine and basal ganglia function is lacking. This constitutes a significant roadblock to scientific and therapeutic advances. Deep brain stimulation (DBS) is an emerging neurotechnological treatment for which electrodes are implanted directly into the depth of the patients’ brains and connected to an implantable pulse generator for chronic neurostimulation. In the past decades, DBS has shown clinical efficacy and provided unique access to invasive neurophysiology from the human basal ganglia. Nevertheless, the precise therapeutic mechanisms of DBS remain unknown. The leading hypothesis is that DBS can disrupt pathological brain circuit communication through local suppression and modulation of neural activity. In the present lecture, I will introduce how our centre uses DBS to develop a better understanding of the brain circuit computations of the basal ganglia and their alterations underlying PD symptoms. Next, I will highlight how a better understanding can directly inform machine learning models for the development of invasive brain computer interfaces that adapt to the individual challenges that PD patients are facing. To achieve this, we leverage the unprecedented spatiotemporal precision of closed-loop neurostimulation to reinstate physiological brain network activity in cortex - basal ganglia networks that are affected by dopaminergic neurodegeneration in PD. If successful, this could open new horizons for the interdisciplinary treatment of brain disorders affecting the dopaminergic system.
Funding statement:
WJN received funding from the European Union (ERC, ReinforceBG, project 101077060 ), Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) – Project-ID – TRR 295 and the Bundesministerium für Bildung und Forschung (BMBF, project FKZ01GQ1802).
Twitter accounts to tag in promotional posts:
@neumann_wj
@ICNeuromodulate
Background of the speaker:
Wolf-Julian Neumann is a clinician scientist (MD) at the Movement Disorders and Neuromodulation Unit at Charité Berlin with an expertise in movement disorders, neurophysiology and deep brain stimulation. The challenge his group, the @icneuromodulation174 group is currently working on is to try and integrate insights from PD pathophyisology, basal ganglia function, dopamine and neural reinforcement into a holistic cortex – basal ganglia – circuit model. I am actively engaging in programs and activities that aim to improve the scientific landscapes in terms of openness, reproducibility, diversity, equity and inclusiveness. I am severely hearing impaired.