# A Canonical Neural Map and Its Deviations Shape Parkinson’s Disease Phenotypes

**Authors:** Koorosh Mirpour, Amirreza Alijanpourotaghsara, Vibhash Sharma, Yvette Bordelon, Nader Pouratian

PMC · DOI: 10.21203/rs.3.rs-8239383/v1 · Research Square · 2026-01-12

## TL;DR

This study shows that Parkinson's disease has a common brain activity pattern but individual differences in this pattern explain varied symptoms and could guide personalized treatments.

## Contribution

The study introduces a canonical spatio-spectral map of Parkinson’s disease and shows how deviations from it correlate with clinical variability.

## Key findings

- A canonical spatio-spectral map of network dysfunction was identified in Parkinson’s disease.
- Clinical variability is explained by systematic deviations from the canonical map, which predict symptom severity.
- Data-driven clustering of these deviations reveals distinct clinical phenotypes in Parkinson’s disease.

## Abstract

Parkinson’s disease (PD) presents a paradox: patients exhibit generally highly stereotyped network oscillations (excessive beta activity) yet patients manifest profound clinical heterogeneity and the literature is still sometimes inconsistent about the clinical significance of beta oscillations in PD. We resolve this discrepancy using multisite intracranial human recordings from the motor cortex and basal ganglia to define a robust, disease-specific “canonical spatio-spectral map” of network dysfunction. Crucially, we demonstrate that clinical variability is not random but is encoded by systematic, patient-specific deviations from this common template. The spatial regions exhibiting the highest inter-individual physiological variance specifically predict motor symptom severity, and data-driven clustering of these features reveals distinct clinical phenotypes. This framework establishes that individual deviations from a normative pathological map, often treated as noise, actually correlate with clinical symptoms. We provide a unified model of PD pathophysiology, linking the canonical beta signature to individual phenotypic diversity, and offer a quantitative blueprint for the development of personalized, circuit-specific therapeutic strategies.

## Linked entities

- **Diseases:** Parkinson’s disease (MONDO:0005180)

## Full-text entities

- **Genes:** MFSD11 (major facilitator superfamily domain containing 11) [NCBI Gene 79157] {aka ET}, GPI (glucose-6-phosphate isomerase) [NCBI Gene 2821] {aka AMF, CNSHA4, GNPI, NLK, PGI, PHI}
- **Diseases:** motor deficits (MESH:D009461), PIGD (MESH:D054972), resting tremor (MESH:D014202), akinesia (MESH:C537921), PD (MESH:D010300), brain atrophy (MESH:C566985), Rigidity (MESH:D009127), bradykinesia (MESH:D018476), neurodegeneration (MESH:D019636), Motor Impairment (MESH:D000068079), motor disability (MESH:D009069), Symptom (MESH:D012816), ET (MESH:D016751), PSD (MESH:D001851)
- **Chemicals:** iridium (MESH:D007495), platinum (MESH:D010984), levodopa (MESH:D007980)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

7 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12869688/full.md

## References

36 references — full list in the complete paper: https://tomesphere.com/paper/PMC12869688/full.md

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Source: https://tomesphere.com/paper/PMC12869688