CORDIS - EU research results
CORDIS

Interrogating basal ganglia reinforcement with deep brain stimulation in Parkinson’s disease.

Project description

Adaptive neurostimulation for brain disorders

Parkinson’s disease is a movement disorder associated with a gradual loss of dopamine-producing neurons. Funded by the European Research Council, the ReinforceBG project proposes the novel hypothesis that loss of dopamine does not impair movement per se but impedes crucial mechanisms that help sustain neuronal communication. Researchers aim to address this hypothesis by combining invasive brain signal recordings with behaviour-specific adaptive neurostimulation. They aim to pilot a neuroprosthetic brain-computer interface based on machine learning, which supports patients with Parkinson's disease with the individual challenges they are facing. In the future, this could open new horizons for the treatment of brain disorders affecting the dopaminergic system.

Objective

Dopamine and the basal ganglia have been conserved over more than 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 6 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. To overcome this roadblock, ReinforceBG poses the novel unconventional hypothesis that loss of dopamine in PD does not impair movement per se but leads to chronic negative reinforcement of neural population dynamics. Conversely, in the healthy state, transient dopamine signals may stabilize cortex–basal ganglia activity to facilitate reentry and refinement of cortical output. To address this hypothesis, ReinforceBG will combine invasive electrocorticography and local field potential recordings with closed-loop deep brain stimulation in PD patients. Aim 1 will investigate how basal ganglia pathways coordinate neuromuscular adaptation. Aim 2 will shed light on basal ganglia reinforcement in multiple behavioural domains, including movement, gait, speech, and spatial navigation in virtual reality. Aim 3 will develop a neuroprosthetic brain-computer interface that aims to modulate basal ganglia reinforcement. ReinforceBG deviates from outdated models on pro- vs. antikinetic “Go” and “NoGo” pathways and promises a holistic-reinforcement centred view of basal ganglia function. It will leverage the unprecedented spatiotemporal precision of neuromodulation for the development of an innovative brain circuit intervention that modulates neural reinforcement in real time. This opens new horizons for the interdisciplinary treatment of brain disorders affecting the dopaminergic system.

Host institution

CHARITE - UNIVERSITAETSMEDIZIN BERLIN
Net EU contribution
€ 1 499 580,00
Address
Chariteplatz 1
10117 Berlin
Germany

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Region
Berlin Berlin Berlin
Activity type
Higher or Secondary Education Establishments
Links
Total cost
€ 1 499 580,00

Beneficiaries (1)