V. Pando-Naude, L. Andersen
Rhythmic cognition relies on the interplay between endogenous and exogenous temporal structures, allowing organisms to anticipate and adapt to events in time. Neural oscillations, particularly in the beta-band (14-30 Hz), have been implicated in this predictive capacity, coordinating sensorimotor networks that support timing and rhythm perception. Parkinson's disease (PD), a movement disorder characterized by disrupted basal ganglia function, offers a unique framework to probe the neural mechanisms underlying rhythmic cognition. We estimated beta-band source activity and connectivity across the cerebellum, basal ganglia, thalamus, and motor cortex during a rhythmic somatosensory timing task to compare brain activity between participants with PD (n=24) and age-matched controls (n=25). Using magnetoencephalography, participants received tactile stimuli in regular (non-jittered) and irregular (jittered) sequences, with the final stimulus omitted to probe prediction before and evaluation after the omission. We found prediction-related differences between participants with PD and controls in the cerebellum and basal ganglia before the omissions, while replicating earlier findings in controls, consistent with cerebellar evaluation responses after the omissions. In PD, basal ganglia activity showed greater activity for jittered over non-jittered somatosensory rhythms, opposite to controls. Altered cerebellar beta-band responses correlated with PD symptom severity. Connectivity analyzes showed group-by-regularity interactions in a sensory-integration network. These findings suggest that temporal prediction and evaluation in rhythmic cognition rely on coordinated beta-band dynamics across the cerebello-striatal-thalamo-cortical network. In PD, disrupted basal ganglia function may be associated with increased cerebellar engagement and altered network dynamics under irregular temporal conditions, potentially reflecting differences in the processing of rhythmic structure.