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Brain signal decoding promises significant advances in the development of clinical brain computer interfaces (BCI). In Parkinson's disease (PD), first bidirectional BCI implants for adaptive deep brain stimulation (DBS) are now available. Brain signal decoding can extend the clinical utility of adaptive DBS but the impact of neural source, computational methods and PD pathophysiology on decoding performance are unknown. This represents an unmet need for the development of future neurotechnology. To address this, we developed an invasive brain-signal decoding approach based on intraoperative sensorimotor electrocorticography (ECoG) and subthalamic LFP to predict grip-force, a representative movement decoding application, in 11 PD patients undergoing DBS. We demonstrate that ECoG is superior to subthalamic LFP for accurate grip-force decoding. Gradient boosted decision trees (XGBOOST) outperformed other model architectures. ECoG based decoding performance negatively correlated with motor impairment, which could be attributed to subthalamic beta bursts in the motor preparation and movement period. This highlights the impact of PD pathophysiology on the neural capacity to encode movement vigor. Finally, we developed a connectomic analysis that could predict grip-force decoding performance of individual ECoG channels across patients by using their connectomic fingerprints. Our study provides a neurophysiological and computational framework for invasive brain signal decoding to aid the development of an individualized precision-medicine approach to intelligent adaptive DBS.
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http://dx.doi.org/10.7554/eLife.75126 | DOI Listing |
ACS Chem Neurosci
September 2025
Chemical and Biomolecular Engineering Dept, University of California, Los Angeles, Los Angeles, California 90095, United States.
Simulations in three dimensions and time provide guidance on implantable, electroenzymatic glutamate sensor design; relative placement in planar sensor arrays; feasibility of sensing synaptic release events; and interpretation of sensor data. Electroenzymatic sensors based on the immobilization of oxidases on microelectrodes have proven valuable for the monitoring of neurotransmitter signaling in deep brain structures; however, the complex extracellular milieu featuring slow diffusive mass transport makes rational sensor design and data interpretation challenging. Simulations show that miniaturization of the disk-shaped device size below a radius of ∼25 μm improves sensitivity, spatial resolution, and the accuracy of glutamate concentration measurements based on calibration factors determined .
View Article and Find Full Text PDFArch Pharm Res
September 2025
College of Pharmacy, Hanyang University, Ansan, 15588, Republic of Korea.
c-Jun N-terminal kinases (JNKs), a subfamily of mitogen-activated protein kinases (MAPKs), are key mediators of cellular responses to environmental stress, inflammation, and apoptotic signals. The three isoforms-JNK1, JNK2, and JNK3 exhibit both overlapping and isoform-specific functions. While JNK1 and JNK2 are broadly expressed across tissues and regulate immune signaling, cell proliferation, and apoptosis, JNK3 expression is largely restricted to the brain, heart, and testis, where it plays a crucial role in neuronal function and survival.
View Article and Find Full Text PDFMetab Brain Dis
September 2025
Department of Pharmacology and Toxicology, Faculty of Pharmacy, Cairo University, Cairo, Egypt.
Acute or chronic liver damage can result in Hepatic Encephalopathy (HE), a potentially fatal neuropsychiatric condition that leads to cerebral and neurological alterations. Dapagliflozin (DAPA), an orally active Sodium/Glucose cotransporter 2 inhibitor with long duration of action. The study aim was to evaluate the potential protective impact of DAPA against HE caused by Thioacetamide (TAA) in rats.
View Article and Find Full Text PDFNeurochem Res
September 2025
International Translational Neuroscience Research Institute, Zhejiang Chinese Medical University, Hangzhou, 310053, Zhejiang, China.
The concept of the central nervous system (CNS) reserve emerged from the mismatch often observed between the extent of brain pathology and its clinical manifestations. The cognitive reserve reflects an "active" capacity, driven by the plasticity of CNS cellular components and shaped by experience, learning, and memory processes that increase resilience. We propose that neuroglial cells are central to defining this resilience and cognitive reserve.
View Article and Find Full Text PDFBrain
September 2025
Central European Institute of Technology Masaryk University (CEITEC MU), 625 00 Brno, Czech Republic.
Mutations in the human ADAR gene encoding adenosine deaminase acting on RNA 1 (ADAR1) cause Aicardi-Goutières syndrome 6 (AGS6); a severe auto-inflammatory encephalopathy with aberrant interferon (IFN) induction. AdarΔ2-13 null mutant mouse embryos lacking ADAR1 protein die with high levels of IFN-stimulated gene (ISG) transcripts. In Adar Mavs double mutants also lacking the Mitochondrial antiviral signaling (MAVS) adaptor, the aberrant IFN induction is prevented.
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