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Parkinson’s Disease (PD) is a progressive neurodegenerative disorder characterized by motor and cognitive deficits. The neurodegenerative process is thought to move stereotypically from the brainstem up to the cerebral cortex, possibly reflecting the spread of toxic alpha-synuclein molecules. Using a large, longitudinal, multi-center database of de novo PD patients, we tested whether focal reductions in cortical thickness could be explained by disease spread from a subcortical disease reservoir along the brain’s connectome. PD patients (n=105) and matched controls (n=57) underwent T1-MRI at entry and one year later. Over this period, PD patients demonstrated significantly greater loss of cortical thickness than healthy controls in parts of the left occipital and bilateral frontal lobes and right somatomotor-sensory cortex. Cortical regions with greater connectivity (measured functionally or structurally) to a disease reservoir evaluated via MRI at baseline demonstrated greater atrophy one year later. The atrophy pattern in the frontal lobes resembled that described in Alzheimer’s disease. Moreover, path models suggest that cerebrospinal fluid amyloid-{beta}42 predicted left frontal cortical thinning, which in turn was associated with reduced cognitive scores. Our findings suggest that disease propagation to the cortex follows neural connectivity, and that cognitive impairments occur earlier than previously thought in PD.