Overview
Mermaid diagram (expand to render)
Study Title: Vagal Nerve Stimulation for Gait and Posture in Parkinson's Disease
Intervention: Vagus Nerve Stimulation (VNS) - implantable device
Phase: Phase 2
Status: Recruiting
Sponsor: University of Oxford / Oxford University Hospitals NHS Foundation Trust
ClinicalTrials.gov Identifier: [NCT07226284](https://clinicaltrials.gov/study/NCT07226284)
Mechanism of Action
Vagal Nerve Stimulation modulates multiple neural circuits implicated in Parkinson's disease pathophysiology:
Neuroanatomical Targets
VNS activates the vagus nerve, which projects to key brainstem nuclei:
Nucleus Tractus Solitarius (NTS): Primary vagal afferent terminus in the dorsal medulla
Locus Coeruleus (LC): Noradrenergic nucleus activated by NTS projections; critical for arousal and motor control
Dorsal Raphe Nucleus: Serotonergic projections that modulate mood and sleep
Parabrachial Nucleus: Integrates viscerosensory informationPutative Disease-Modifying Mechanisms
Recent preclinical research has revealed several mechanisms by which VNS may benefit PD:
Neuroinflammation Reduction:
- VNS activates the cholinergic anti-inflammatory pathway through vagal efferents
- Reduces microglial activation in the substantia nigra and striatum
- Decreases pro-inflammatory cytokines (IL-1β, TNF-α, IL-6) in CNS
Noradrenergic Restoration:
- PD involves early loss of locus coeruleus neurons
- VNS increases norepinephrine release in cortical and subcortical regions
- May protect remaining noradrenergic neurons and enhance compensatory signaling
Alpha-Synuclein Modulation:
- 2024 research demonstrates VNS reduces alpha-synuclein aggregation in mouse models [@h博士后2024]
- Mechanisms include enhanced autophagy and reduced neuroinflammation
Neurotransmitter Modulation:
- Enhances dopaminergic tone indirectly through brainstem-spinal pathways
- Improves serotonergic function which is often compromised in PD depression
Rationale
Clinical Problem
Gait dysfunction and postural instability are among the most disabling symptoms in Parkinson's disease:
Falls and Fractures: Approximately 60% of PD patients experience falls annually; falls cause significant morbidity and mortality
Freezing of Gait: Episodic gait failure affects up to 50% of patients, leading to immobility
Postural Instability: Impaired balance responses contribute to fall risk
Axial Symptoms: Conventional dopaminergic therapies poorly control axial symptomsWhy VNS?
Non-dopaminergic approaches are needed because:
- Dopaminergic medications lose efficacy over time
- Axial symptoms (gait, posture, balance) respond poorly to levodopa
- VNS offers a novel mechanism targeting brainstem circuits
Previous research supports VNS for PD:
- Case series show improved motor scores and gait in PD patients [@sigrist2023]
- Studies in animal models demonstrate neuroprotective effects
- Already FDA-approved for epilepsy and depression with established safety profile [@folkerts2023]
Study Design
Study Type
- Interventional, single-arm open-label trial
- Duration: 12 months active treatment + 6-month follow-up
Inclusion Criteria
- Age 40-80 years
- Diagnosis of Parkinson's disease (UK Brain Bank criteria)
- Hoehn & Yahr stage 2-3
- Stable antiparkinsonian medication for ≥30 days
- Presence of gait dysfunction (TUG > 13.5 seconds) or postural instability
- MMSE ≥ 24
Exclusion Criteria
- Previous VNS implantation
- Significant cardiac disease (pacemaker, arrhythmia)
- Active psychiatric disorder requiring hospitalization
- Uncontrolled medical conditions
- Pregnancy or breastfeeding
Outcome Measures
Primary Endpoints:
- Change in Timed Up and Go (TUG) test at 12 months
- Change in Berg Balance Scale (BBS) at 12 months
Secondary Endpoints:
- MDS-UPDRS Part III (Motor) scores
- Freezing of Gait Questionnaire (FOG-Q)
- Falls frequency (prospective diary)
- PDQ-39 quality of life measure
- MoCA cognitive assessment
- Resting state fMRI connectivity changes
- CSF biomarkers (if available)
Exploratory Endpoints:
- Sleep quality (PDSS-2)
- Autonomic function (SCOPA-AUT)
- Brainstem auditory evoked potentials
Safety Monitoring
VNS devices carry known risks that are monitored:
Device-related: Infection, lead malfunction, device failure
Stimulation-related: Voice changes, cough, dysphagia, paresthesia
Procedure-related: Surgical complications (bleeding, nerve injury)Surgical Procedure and Device
Implantation Technique
The VNS device implantation involves:
Device Placement: A pulse generator is implanted subcutaneously in the left chest wall
Lead Placement: Electrode leads are wrapped around the left vagus nerve in the carotid sheath
Programming: Device is programmed post-surgery to deliver appropriate stimulation parametersDevice Specifications
| Parameter | Specification |
|-----------|---------------|
| Pulse Generator | Small implantable device (~30g) |
| Electrode | Helical leads on vagus nerve |
| Battery Life | 5-10 years depending on settings |
| Stimulation | Programmable current (0.25-3.5 mA) |
| Frequency | 20-30 Hz typical |
| Pulse Width | 250-500 μs |
| On/Off Cycles | 30s on, 5 min off (typical) |
Stimulation Parameters for PD
The Oxford trial uses parameters optimized for motor and gait outcomes:
- Current: 1.0-2.0 mA (titrated to tolerance)
- Frequency: 30 Hz
- Pulse Width: 300 μs
- Duty Cycle: 30 seconds on, 5 minutes off
Comparison with Other VNS Approaches
Invasive vs. Transcutaneous VNS
| Feature | Invasive VNS (iVNS) | Transcutaneous VNS (tVNS) |
|---------|---------------------|---------------------------|
| Stimulation Site | Cervical vagus nerve (implanted) | Auricular branch (external) |
| Efficacy | Higher (direct nerve activation) | Lower (indirect activation) |
| Invasiveness | Surgical procedure | Non-invasive |
| Cost | $15,000-30,000 | $200-500 |
| Side Effects | Voice changes, cough | Skin irritation |
| Use in PD | Current trial (NCT07226284) | Investigational |
VNS in Other Neurodegenerative Conditions
VNS has been studied in other conditions with overlapping mechanisms:
Alzheimer's Disease:
- VNS may enhance cholinergic signaling via locus coeruleus activation
- Clinical trials ongoing for cognitive enhancement
- Potential for disease modification through neuroinflammation reduction
Multiple System Atrophy:
- Autonomic dysfunction is a key target
- Limited clinical data available
Clinical Outcomes and Expectations
Expected Benefits
Based on prior PD studies and mechanism of action, participants may experience:
Motor Function: 10-20% improvement in MDS-UPDRS Part III scores
Gait: Reduced Timed Up and Go times, improved walking speed
Balance: Improved Berg Balance Scale scores
Falls: Reduced fall frequency through improved postural stability
Non-Motor: Potential improvements in mood and sleepTimeline of Effects
- Acute: Stimulation-related effects may be noticed immediately
- Subacute: Modulation of brainstem circuits over weeks
- Chronic: Disease-modifying effects may require months to years
Limitations and Considerations
- Placebo Response: Single-arm design limits interpretation
- Device Maintenance: Requires battery replacement eventually
- Infection Risk: Surgical site infections possible
- Stimulation Titration: Optimal parameters individualized
Neuroimaging Correlates
Resting State fMRI
The trial includes exploratory neuroimaging to understand mechanism:
Functional Connectivity Changes: Measure changes in brainstem-cortical connectivity
Locus Coeruleus Activation: Indirect measures of noradrenergic enhancement
Motor Network Modulation: Changes in basal ganglia-thalamocortical circuitsPotential Biomarkers
- CSF Neuroinflammatory Markers: IL-1β, TNF-α, IL-6
- Neurodegeneration Markers: Neurofilament light chain (NfL)
- Alpha-Synuclein Species: Total and phosphorylated forms
As of 2026, the trial is actively recruiting at multiple UK sites. Enrollment target: 30 patients.
Neurobiological Mechanisms
Vagus Nerve Anatomy and Function
The vagus nerve (Cranial Nerve X) is the longest cranial nerve and serves as the primary component of the parasympathetic nervous system. Its anatomical course and connections provide insight into the therapeutic potential for neurodegenerative diseases.
Peripheral Course:
The vagus nerve originates in the medulla oblongata and descends through the neck within the carotid sheath, posterior to the internal jugular vein and common carotid artery. It gives rise to branches in the neck (pharyngeal, superior laryngeal, recurrent laryngeal) before entering the thorax, where it contributes to the cardiac plexus and pulmonary plexus. Within the abdomen, it gives off branches to the esophagus, stomach, and celiac ganglion, providing parasympathetic innervation to major abdominal viscera.
Central Connections:
The vagus nerve carries afferent (sensory) fibers whose cell bodies reside in the jugular ganglion and nodose ganglion. These afferents project centrally to the nucleus tractus solitarius (NTS), the primary visceral sensory nucleus in the brainstem. From the NTS, second-order projections reach:
Locus Coeruleus (LC): The LC is the principal noradrenergic nucleus in the brain, with widespread projections to cortex, hippocampus, and spinal cord. Vagal afferent activation increases LC neuronal firing, enhancing norepinephrine release throughout the CNS.
Dorsal Raphe Nucleus (DRN): The DRN is the primary serotonergic nucleus, with projections to limbic structures and cortex. Vagal stimulation increases serotonin turnover, potentially benefiting mood and sleep.
Parabrachial Nucleus (PBN): This nucleus integrates viscerosensory information and projects to limbic structures, including the amygdala and bed nucleus of the stria terminalis.
Hypothalamic Nuclei: Vagal afferents influence hypothalamic activity, affecting autonomic regulation, stress responses, and hormonal secretion.The Cholinergic Anti-Inflammatory Pathway
One of the most significant discoveries in vagus nerve physiology is its role in modulating systemic inflammation through the cholinergic anti-inflammatory pathway.
Mechanism:
Peripheral immune activation triggers afferent vagal signaling to the brain, which in turn activates efferent vagal fibers that release acetylcholine at immune organs. Acetylcholine binds to α7 nicotinic acetylcholine receptors (α7nAChR) on macrophages and other immune cells, inhibiting the release of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, IL-18).
Relevance to Neurodegeneration:
Neuroinflammation is a key pathological feature of both Alzheimer's and Parkinson's disease:
- Microglial activation in substantia nigra and striatum in PD
- Chronic neuroinflammation contributes to tau pathology and amyloid accumulation in AD
- Pro-inflammatory cytokines (IL-1β, TNF-α) are elevated in both disorders
By reducing peripheral and central inflammation, VNS may:
- Decrease microglial activation in key brain regions
- Reduce cytokine-mediated neuronal damage
- Potentially slow disease progression
Alpha-Synuclein and VNS
The 2024 Science Advances paper demonstrating VNS reduces alpha-synuclein pathology provides particular relevance for Parkinson's disease:
Mechanistic Pathways:
- Autophagy enhancement: VNS activates autophagy pathways that clear misfolded α-syn
- Neuroinflammation reduction: Decreased microglial activation reduces α-syn propagation
- Protein clearance: Enhanced lysosomal function improves α-syn degradation
Preclinical Evidence:
- Mouse models of α-syn aggregation show reduced inclusions after VNS
- Improved motor performance in VNS-treated animals
- Reduced Lewy body-like pathology in brainstem regions
Clinical Evidence Base
Historical VNS for Neurological Disorders
VNS has a well-established history in neurological disease:
Epilepsy:
- FDA approved since 1997
- Over 100,000 patients implanted worldwide
- 50% reduction in seizure frequency in responders
Depression:
- FDA approved for treatment-resistant depression since 2005
- Significant improvement in depressive symptoms
- Particularly effective for atypical depression
Pain:
- VNS modulates pain pathways through brainstem mechanisms
- Investigated for fibromyalgia, cluster headache
- Generally well-tolerated
VNS in Movement Disorders
Parkinson's Disease:
- Early case series (2000s) showed motor improvement
- Mechanism likely involves LC-mediated noradrenergic enhancement
- Small sham-controlled trials suggested benefit
- Current Phase 2 trial will provide definitive evidence
Tremor:
- VNS has been tested for essential tremor
- Mixed results, with some patients showing improvement
- May be relevant for PD tremor component
Non-Motor Symptom Effects
VNS may address several non-motor symptoms in PD:
Cognitive Function:
- LC noradrenergic projections to hippocampus support memory
- VNS has improved cognitive function in AD models
- Potential for PD-MCI improvement
Depression:
- Serotonergic and noradrenergic effects benefit mood
- PD depression is common and difficult to treat
- VNS provides non-pharmacological option
Sleep:
- Vagal influences on sleep-wake regulation
- May improve REM sleep behavior disorder
- Potential benefit for PD sleep fragmentation
Study Design Deep Dive
Rationale for Axial Symptoms Focus
The trial specifically targets gait and postural dysfunction for several reasons:
Dopaminergic Resistance:
Axial symptoms (gait, posture, balance) respond poorly to dopaminergic therapy:
- Freezing of gait often persists despite optimized levodopa
- Postural instability is the leading cause of falls
- Falls result in 50% of PD patients experiencing falls annually
- Falls cause significant morbidity (fractures, head injury) and mortality
Non-Dopaminergic Pathways:Gait and posture involve multiple non-dopaminergic systems:
- Noradrenergic (LC) pathways for arousal and motor set
- Serotonergic pathways for timing and coordination
- Cholinergic pathways for attention to task
- Vestibular integration for balance
VNS can modulate all these systems, making it an attractive approach for axial symptoms.
Outcome Measure Selection
Primary Endpoints:
Timed Up and Go (TUG):
- Time to rise from chair, walk 3m, turn, walk back, sit
- Validated, reliable, sensitive to change
- Cutoff >13.5 seconds indicates fall risk
- PD-specific norms available
Berg Balance Scale (BBS):
- 14-item functional balance assessment
- Scoring: 0-56 (higher = better)
- <40 indicates fall risk
- Excellent inter-rater reliability
Secondary Endpoints Rationale:
- MDS-UPDRS Part III: Gold-standard motor assessment
- FOG-Q: Specific for freezing of gait, a major cause of falls
- PDQ-39: Quality of life, captures functional impact
- MoCA: Cognitive screening, important for overall function
- Resting state fMRI: Mechanism validation, connectivity changes
Patient Selection Considerations
Why Hoehn & Yahr Stage 2-3?
- Stage 2: "Unilateral involvement with no postural instability"
- Stage 3: "Mild to moderate bilateral disease, some postural instability"
- Early enough for intervention benefit
- Late enough to have significant gait/posture impairment
- Excludes very advanced patients unlikely to benefit
Exclusion Rationale:
- Previous VNS: Prior device would confound results
- Cardiac disease: VNS affects heart rate; pre-existing arrhythmia is safety concern
- Psychiatric disease: Depression/anxiety may confound outcomes
- Pregnancy: Safety consideration for reproductive-age subjects
Safety Profile
Adverse Event Frequency
VNS has a well-characterized safety profile based on 25+ years of use:
| Adverse Event | Frequency | Severity | Management |
|---------------|-----------|----------|------------|
| Hoarseness/dysphonia | 30-50% | Mild-moderate | Usually resolves |
| Cough | 10-20% | Mild | Often transient |
| Dyspnea | 5-10% | Mild-moderate | Usually transient |
| Paresthesia | 5-10% | Mild | Often during stimulation |
| Headache | 5-10% | Mild | Usually transient |
| Dysphagia | 3-7% | Mild-moderate | Usually resolves |
| Device infection | 1-3% | Moderate-severe | Requires antibiotic/intervention |
Serious Adverse Events
Rare but Important:
- Vocal cord paralysis (usually transient)
- Cardiac arrhythmia (rare with proper screening)
- Device malfunction requiring revision
- Surgical complications (bleeding, infection)
Safety Monitoring:
- Cardiac telemetry during device placement
- Regular device parameter checks
- Symptom diary for AEs
- Regular ENT assessment for hoarseness
Future Directions
Larger-Scale Trials
If this Phase 2 trial shows positive results:
Phase 3 Trial Design:
- Randomized, sham-controlled
- Larger sample size (100-200 participants)
- Longer duration (12-24 months)
- Multi-center, international
Endpoints:
- Adding clinical endpoints (fall frequency)
- Considering biomarker co-primary endpoints
- Quality of life as key secondary
Combination Approaches
VNS may be combined with other PD therapies:
With Deep Brain Stimulation:
- Different mechanisms (electrical vs pharmacological)
- VNS may address non-motor symptoms DBS doesn't help
- Combined approach under investigation
With Pharmacological Therapy:
- VNS may allow reduced medication doses
- Synergistic effects with dopaminergic therapy
- Non-motor symptom benefits beyond medication
Transcutaneous VNS (tVNS)
An alternative to implantable VNS:
Advantages:
- Non-invasive (no surgery)
- Lower risk profile
- Easier to implement
- Reversible
Limitations:
- Less robust activation of vagal pathways
- Variable stimulation delivery
- May not achieve same efficacy
Current Status:
- Being investigated for PD
- May serve as screening tool before implantation
- Useful for patients unsuitable for surgery
Device Technology
VNS Device Components
Implantable Generator:
- Small device (approximately 4cm x 5cm x 1cm)
- Implanted subcutaneously in chest wall
- Battery life: 5-10 years depending on stimulation parameters
- Rechargeable and non-rechargeable options available
Stimulation Electrodes:
- Bipolar electrode coil wrapped around vagus nerve
- Helical design minimizes nerve trauma
- Internal and external versions available
- Most commonly placed on left vagus (less cardiac effects)
Programming System:
- Handheld wand for device communication
- Clinician programmer for parameter adjustment
- Patient magnet for on-demand stimulation (optional)
Stimulation Parameters
Key Parameters:
- Output current: 0.25-3.5 mA (programmable)
- Pulse width: 250-500 μs
- Frequency: 1-30 Hz (typically 20-30 Hz for therapeutic effect)
- On-time: 30 seconds (typical)
- Off-time: 5 minutes (typical)
Dosing:
- Intermittent stimulation (duty cycle approach)
- Typical: 30 seconds ON, 5 minutes OFF
- Continuous stimulation possible but associated with more side effects
Advances in VNS Technology
Closed-Loop Systems:
- Responsive stimulation based on physiological markers
- Auto-adjusting output based on heart rate, respiration
- Potentially more efficient and personalized
Directional Leads:
- Newer electrode designs allow directional stimulation
- Can selectively activate vagal fibers
- May reduce side effects, improve efficacy
MRI Compatibility:
- Most modern devices are MRI-conditional
- Specific scan parameters required
- Important for PD patients who may need brain imaging
Neuroimaging Correlates
VNS-Induced Brain Changes
Functional neuroimaging studies have characterized VNS effects on brain activity:
Increased Activity:
- Locus coeruleus (noradrenergic)
- Dorsal raphe (serotonergic)
- Hippocampus (memory circuits)
- Prefrontal cortex (executive function)
- Thalamus (relay)
Decreased Activity:
- Amygdala (stress response)
- Hypothalamus (stress axis)
- Brainstem pain centers
Resting State Functional Connectivity
Connectivity Changes with VNS:
The Oxford VNS trial includes resting state fMRI as a secondary endpoint, building on prior research:
- Enhanced connectivity between NTS and LC
- Improved prefrontal-limbic connectivity
- Normalization of default mode network abnormalities
- Potential biomarker for treatment response
Molecular Imaging
PET Studies:
- [11C]WAY-100635: 5-HT1A receptor binding changes with VNS
- [11C]raclopride: Dopaminergic changes](/entities/dopamine)
- [18F]FDG: Metabolic pattern changes
Future Directions:
- α-Syn PET ligands to track pathology
- Microglial activation (TSPO) PET
- Tau PET in combined PD/DLB cases
Comparison with Other Neuromodulation Approaches
VNS vs. Deep Brain Stimulation
| Parameter | VNS | DBS |
|-----------|-----|-----|
| Invasiveness | Moderate (minor surgery) | High (craniotomy) |
| Target | Peripheral nerve | Brain nuclei (STN, GPi) |
| Mechanism | Modulatory | Network modulation |
| Side effects | Hoarseness, cough | Dysarthria, cognitive effects |
| Battery | 5-10 years | 3-5 years |
| MRI compatibility | Generally safe | Conditional |
| Reversibility | Complete | Partial (hardware remains) |
VNS vs. Transcranial Magnetic Stimulation
| Parameter | VNS | TMS |
|-----------|-----|-----|
| Invasiveness | Moderate | Minimal |
| Depth of stimulation | Peripheral → central | Direct brain (limited depth) |
| Frequency of treatments | Continuous (implanted) | Repeated sessions |
| Mechanism | Autonomic | Direct neural |
| Side effects | Hoarseness | Headache, seizure risk |
VNS vs. Transcutaneous VNS (tVNS)
| Parameter | VNS | tVNS |
|-----------|-----|------|
| Invasiveness | Surgical | Non-invasive |
| Efficacy | Established | Investigational |
| Specificity | Direct vagus | Auricular branch |
| Side effects | Moderate | Minimal |
| Cost | High (device) | Low (device) |
Pharmacoeconomic Considerations
Cost-Effectiveness
Implant Costs:
- Device cost: $15,000-30,000
- Surgical cost: $5,000-10,000
- Total initial cost: $20,000-40,000
Ongoing Costs:
- Battery replacement (if applicable): $5,000-10,000
- Programming visits: $500-1,000/year
- Device check: $200-500/year
Potential Savings:
- Reduced hospitalization (falls, complications)
- Delayed nursing home placement
- Reduced medication needs
- Improved productivity for caregivers
Budget Impact
UK NHS Perspective:
- Per-patient cost: ~£15,000-25,000 over 5 years
- If effective for axial symptoms in PD:
- 120,000 PD patients in UK
- ~20% with significant gait/freeze symptoms
- Potential eligible: 24,000 patients
- Full adoption: £360M-600M over 5 years
Reimbursement
UK:
- NHS England considers VNS for epilepsy and depression
- No current coverage for PD
- Would require positive Phase 3 data and NICE appraisal
US:
- Medicare covers VNS for epilepsy and depression
- No current FDA indication for PD
- Would require FDA approval for PD indication
Research Gaps
Unmet Clinical Needs
Biomarkers: No established biomarker for VNS response prediction
Patient Selection: Optimal patient characteristics unclear
Long-term Effects: Multi-year safety and efficacy unknown
Mechanism: Precise mechanisms in PD not fully elucidated
Combination: Optimal combination with other therapiesOngoing Research
Clinical:
- Oxford VNS-PD trial (NCT07226284)
- Other VNS-PD trials in Europe and US
- tVNS trials for PD
Basic Science:
- α-Syn propagation mechanisms
- Optimal stimulation parameters
- Closed-loop system development
- Combination with neuroprotective agents
Cross-Links to NeuroWiki
[Vagal nerve stimulation for Parkinson's disease motor symptoms - A systematic review (Parkinsonism Relat Disord, 2023)](https://doi.org/10.1016/j.parkreldis.2023.105265)
[Vagal nerve stimulation activates the locus coeruleus to improve gait in parkinsonian models (Nature Scientific Reports, 2022)](https://doi.org/10.1038/s41598-022-15389-4)
[Long-term effects of vagal nerve stimulation on neurodegenerative diseases (Brain, 2021)](https://doi.org/10.1093/brain/awab159)
[Transcutaneous vagal nerve stimulation for neurological disorders (Clin Neurophysiol, 2023)](https://doi.org/10.1016/j.clinph.2023.02.375)
[Vagus nerve stimulation reduces alpha-synuclein pathology in preclinical models (Science Advances, 2024)](https://doi.org/10.1126/sciadv.adh8321)
[ClinicalTrials.gov: NCT07226284](https://clinicaltrials.gov/study/NCT07226284)Related Pages
- [Parkinson's Disease Motor Complications](/diseases/parkinsons-disease)](/proteins/parkin)
- [Parkinson's Disease Non-Motor Symptoms](/diseases/parkinsons-disease-non-motor-symptoms)](/proteins/parkin)
- [Gait Dysfunction in Parkinson's Disease](/diseases/parkinsons-gait-freezing)](/proteins/parkin)
- [Locus Coeruleus in Neurodegeneration](/cell-types/locus-coeruleus-neurons)](/cell-types/locus-coeruleus)
- [Alpha-Synuclein Propagation](/experiments/alpha-synuclein-spreading-neurodegeneration-pd)
See Also
Related Experiments:
- [ER-Golgi Secretory Pathway Dysfunction in PD - Experiment Design](/experiment/exp-wiki-experiments-er-golgi-secretory-pathway-parkinsons)
- [Cytochrome Therapeutics](/experiment/exp-wiki-experiments-lipid-droplet-lysosome-axis-parkinsons)
- [MLCS Quantification in Parkinson's Disease](/experiment/exp-wiki-experiments-mlcs-quantification-parkinsons)