• Longitudinal clinical and neurophysiological metrics in Parkinson’s disease over four and a half years have been characterized.1
  • These dynamics inform biomarker development and DBS/neuroprosthetics trial design.1
  • The work is tier-1 (Nature) with a disease-progression and clinical-neurophysiology focus.1 1

Weekly enrichment (2026-07-20)

  • The primary study is a 4.5-year cohort study published in Scientific Reports (2025; DOI 10.1038/s41598-025-13558-3), described by the authors as one of the longest clinical-electrophysiological follow-ups in Parkinson’s disease (PD) to date.2
  • The cohort comprised 22 patients spanning early and advanced PD, assessed with both Movement Disorder Society-Unified Parkinson’s Disease Rating Scale (MDS-UPDRS) scores and transcranial magnetic stimulation (TMS) measures of cortical excitability.2 3
  • The cortical silent period (CSP), a marker of GABAergic inhibition, progressively lengthened over time and was associated with motor decline, supporting its potential as a dynamic, non-invasive, and scalable biomarker of disease progression.2 3
  • Resting motor threshold (rMT) and motor asymmetry also deteriorated longitudinally, and the changes were most pronounced following the COVID-19 pandemic, suggesting environmental stressors may accelerate PD pathophysiology.2
  • Reported effect sizes across both the more-affected and less-affected hemispheres were significant for rMT (p = 0.001, partial η² = 0.31–0.32), MEP duration (p < 0.015, partial η² = 0.18–0.27), and CSP (p < 0.001, partial η² = 0.34–0.51).2
  • CSP duration increases were especially prominent in early-stage PD, and the longitudinal changes were independent of sex, indicating persistent cortical reorganization over several years.2 3
  • Broader neurophysiology work supports subthalamic beta oscillations (13–35 Hz) as symptom-specific biomarkers of bradykinesia and rigidity; a 33-patient local-field-potential study found beta power, center frequency, and spatial distribution remained stable enough for beta-guided DBS programming, with active therapeutic contacts showing higher normalized beta power than inactive contacts (p < 0.0001).4
  • These physiomarkers underpin adaptive/closed-loop deep brain stimulation (aDBS), where clinical severity correlates with cumulative beta-burst time and burst rate, informing sensing-guided neuroprosthetic and DBS trial design referenced in this topic’s clinical links.4 5

Footnotes

  1. https://news.google.com/rss/articles/CBMiX0FVX3lxTE5vZXFZN2tBTjhIeU9DcTJNWFAxemg2ZTROTFJrV0NrWElKNmpGTmtVQU5abkQ5VG0tY0YzbkdObFRtdTNtSU5sMmluSWFvVkRlUTB3cEl2UEZPQ05fXzl3?oc=5 2 3 4

  2. https://www.nature.com/articles/s41598-025-13558-3 2 3 4 5 6

  3. https://doi.org/10.21203/rs.3.rs-6246415/v1 2 3

  4. https://doi.org/10.1002/mds.30169 2

  5. https://doi.org/10.1002/mds.70198