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RESEARCH PAPER ANALYSIS

Mobile EEG assessment of inhibitory control during dual-task walking in Parkinson's disease.

Proof-of-concept study showing mobile EEG can detect condition-dependent behavioral and event-related potential changes during an inhibitory-control task while walking in Parkinson's disease, with levodopa primarily modulating early sensory-perceptual components and DBS affecting later cognitive…

PMID41962423
JournalParkinsonism & related disorders
Publication Date2026-04-08
Ingested2026-04-28 08:58 PM
EXECUTIVE SUMMARY

What the AI sees

Proof-of-concept study showing mobile EEG can detect condition-dependent behavioral and event-related potential changes during an inhibitory-control task while walking in Parkinson's disease, with levodopa primarily modulating early sensory-perceptual components and DBS affecting later cognitive…

WHY IT MATTERS

Research significance

Provides a feasible ambulatory neurophysiological biomarker for cognition–gait interactions that can help design and power trials of levodopa/DBS and other interventions, though it offers limited direct therapeutic mechanistic targets.

ABSTRACT

Source abstract

BACKGROUND: How levodopa and deep brain stimulation (DBS) modulate the cognitive processing underlying dual-task walking in Parkinson's disease remains poorly characterized, in part due to methodological challenges in capturing neural signals during walking. OBJECTIVES: To evaluate the feasibility and signal characteristics of combining mobile EEG with an inhibitory control task during walking, and to generate preliminary, group-level evidence on how levodopa and DBS may differentially modulate cognitive processing during dual-task walking in Parkinson's disease. METHODS: Ten people with Parkinson's disease completed an inhibitory control task while walking under four levodopa/DBS conditions. Behavioral measures (response accuracy, treadmill-walking speed) and event-related potentials were collected. Data from the off-levodopa/off-DBS condition were compared with data from 37 control participants, and within-subject differences across levodopa/DBS conditions were explored to assess sensitivity of behavioral and mobile EEG measures. RESULTS: Compared with controls, participants with Parkinson's disease off-levodopa/off-DBS demonstrated reduced response accuracy and treadmill-walking speed. Exploratory within-subject analyses suggested that response accuracy improved primarily in the on-levodopa/on-DBS condition compared to the off-levodopa/off-DBS condition. Event-related potentials showed condition-dependent modulation, with levodopa primarily affecting early sensory-perceptual components over bilateral frontocentral regions, and DBS modulating later cognitive components over right prefrontal and right parietal regions. CONCLUSIONS: This proof-of-concept study demonstrates the feasibility and sensitivity of using mobile EEG to assess inhibitory control while walking in Parkinson's disease. The observed condition-dependent behavioral and electrophysiological patterns are hypothesis-generating and provide preliminary guidance for the design of future, adequately powered studies examining combined levodopa and DBS effects on cognition-gait interactions.

SUPPORTING PAPER SET

32 more papers to review

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1 The cGAS-STING-Glymphatic-gut Axis in Parkinson's disease: A proposed self-amplifying triad of Neuroinflammation and therapeutic opportunity. International immunopharmacology 91.0 2 Immunosenescence and Inflammaging as Drivers of Neurodegeneration: Cellular Mechanisms, Neuroimmune Crosstalk, and Therapeutic Implications. Cells 91.0 3 Flavonoids improve neurotransmitters for Parkinson's treatment: mechanism and therapeutic potential. Frontiers in pharmacology 88.0 4 Alpha-Lipoic Acid and Biotin in Neurodegenerative Diseases: Convergent Mechanistic Insights from Preclinical Models to Clinical Perspectives. Neurology international 78.0 5 The Gut Microbiota in Parkinson's Disease: Mechanistic Insights into Microbial-Host Interactions. Microorganisms 85.0 6 Linking inflammation, metabolic dysfunction, and neurodegeneration: a comprehensive review of TLR2 pathways in type 2 diabetes. Frontiers in clinical diabetes and healthcare 80.0 7 Neuroprotective effects of GLP-2 and a GLP-2/GIP dual receptor agonist in an MPTP-induced mouse model of Parkinson's disease. Peptides 86.0 8 TNF alpha unmasks enteric malate aspartate shuttle dysfunction bridging Parkinson disease and intestinal inflammation. Nature communications 91.5 9 Lipid Metabolism and Neurodegeneration: Mechanistic Insights and Therapeutic Targets. Ageing research reviews 82.0 10 Shared functional microbiome signatures in Parkinson's disease and constipation predominate irritable bowel syndrome despite taxonomic divergence. Brain, behavior, & immunity - health 80.0 11 Benzimidazole as a Versatile Scaffold for Developing Neurotherapeutics Against Neurodegenerative Diseases. ChemMedChem 74.0 12 Biomimicking neuromelanin reverses the gait deficits and dopaminergic neuronal loss in the Parkinson's disease. Colloids and surfaces. B, Biointerfaces 86.0 13 Neuroprotective roles of klotho: Molecular pathways and therapeutic implications for cognitive health in neurological and psychiatric diseases. Experimental physiology 84.0 14 Flavonoid Rutin Reduces Intestinal Inflammation in an Experimental Model of Parkinson's Disease. Neurotoxicity research 70.0 15 Nanostructured Lipid Carriers Enhance Brain Delivery and Antioxidant Efficacy of a Small-Molecule MAO B Inhibitor for Neurodegenerative Disease Therapy. Molecular pharmaceutics 78.0 16 Pathophysiological Role of the Gut Brain Axis in Parkinson's Disease: From Microbial Metabolites and Intestinal Permeability to Central Neuroinflammation. Current neurovascular research 86.0 17 Parkinson's Disease: From Metabolism to Genetics-A Comprehensive Review. Current issues in molecular biology 86.0 18 Navigating the cholesterol maze: Key insights on use of statins in neurodegenerative disorders. Neuroprotection (Chichester, England) 76.0 19 Integrative network pharmacology delineates dual GPCR and non-GPCR mechanisms of blended and individual Taikong Blue lavender and Pingyin rose essential oils in neurodegenerative and psychiatric disorders. Computers in biology and medicine 65.0 20 Models of neuroprotection in Parkinson's disease: Exploring cellular, molecular, and microenvironmental targets. Experimental neurology 78.0 21 Hyaluronic acid: emerging roles and biomaterial innovations in Alzheimer's and Parkinson's disease therapy. Frontiers in pharmacology 75.2 22 Molecular mechanisms underlying Parkinson's disease and role of phytochemicals, α-synuclein, sirtuins, and incretin mimetics in potential therapy. Frontiers in pharmacology 75.0 23 Lipid droplets in neurodegenerative diseases: pathological drivers and therapeutic vulnerabilities. Cell death discovery 82.0 24 Brain-gut-microbiota axis: a review on the bidirectional regulatory mechanisms between gut microbiota and brain and their disease interactions. Frontiers in microbiology 74.0 25 Long non-coding RNAs in neurodegenerative diseases - Molecular mechanisms, liquid biopsy biomarkers, and therapeutic targets: A review. Biomolecules & biomedicine 84.0 26 Neurosyphilis and Parkinsonism: Overlapping Pathophysiology and Emerging Therapeutic Insights. Current neurovascular research 76.0 27 Molecular biochemistry of soluble epoxide hydrolase in lipid mediator pathways and neuroinflammatory responses. The Journal of steroid biochemistry and molecular biology 82.0 28 Multifaceted role of CNPY2 beyond ER stress: Disease implications and therapeutic potential. Cell stress 83.3 29 Neuroprotective Role of Exercise-based Physiotherapy Combined with Pharmacological Agents in Parkinson's Disease. Central nervous system agents in medicinal chemistry 64.0 30 Distinct metabolomic and proteomic signatures in Parkinson's disease patients with REM sleep behavior disorder. Signal transduction and targeted therapy 84.0 31 HMGB1-mediated neuroinflammation: molecular mechanisms and emerging therapeutic approaches. Inflammopharmacology 78.0 32 Beyond acid-base dyshomeostasis: Dynamic instability of neuronal lysosomal pH as a pathogenic mechanism and therapeutic target in neurological diseases. Biochemical pharmacology 88.0
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