Network connectivity determines cortical thinning in early Parkinson’s disease progression

TLDR

The atrophy pattern in the ventral frontal lobes resembles that seen in certain Alzheimer’s disease cases. The study tests whether Parkinson’s disease neurodegeneration spreads stereotypically along neural networks, potentially via toxic alpha‑synuclein propagation. The authors performed longitudinal T1‑MRI scans on 105 PD patients and 57 controls over one year as part of the Parkinson’s Progression Markers Initiative. PD patients showed greater cortical thinning over one year, especially in left occipital, bilateral frontal, and right somatomotor‑sensory regions, and this thinning correlated with functional or structural connectivity to a baseline disease reservoir, suggesting that cortical spread follows neuronal networks and may predict cognitive decline.

Abstract

Here we test the hypothesis that the neurodegenerative process in Parkinson's disease (PD) moves stereotypically along neural networks, possibly reflecting the spread of toxic alpha-synuclein molecules. PD patients (n = 105) and matched controls (n = 57) underwent T1-MRI at entry and 1 year later as part of the Parkinson's Progression Markers Initiative. Over this period, PD patients demonstrate significantly greater cortical thinning than controls in parts of the left occipital and bilateral frontal lobes and right somatomotor-sensory cortex. Cortical thinning is correlated to connectivity (measured functionally or structurally) to a "disease reservoir" evaluated by MRI at baseline. The atrophy pattern in the ventral frontal lobes resembles one described in certain cases of Alzheimer's disease. Our findings suggest that disease propagation to the cortex in PD follows neuronal connectivity and that disease spread to the cortex may herald the onset of cognitive impairment.