Little is known of the structural and functional properties of abnormal brain networks associated with neurological disorders. We used a social network approach to characterize the properties of the Parkinson’s disease (PD) metabolic topography in 4 independent patient samples and in an experimental non-human primate model. The PD network exhibited distinct features. Dense, mutually facilitating functional connections linked the putamen, globus pallidus, and thalamus to form a metabolically active core. The periphery was formed by weaker connections linking less active cortical regions. Notably, the network contained a separate module defined by interconnected, metabolically active nodes in the cerebellum, pons, frontal cortex, and limbic regions. Exaggeration of the small-world property was a consistent feature of disease networks in parkinsonian humans and in the non-human primate model; this abnormality was only partly corrected by dopaminergic treatment. The findings point to disease-related alterations in network structure and function as the basis for faulty information processing in this disorder.