Parkinson's disease (PD) is a common neurodegenerative disorder associated with motor and cognitive impairments. The mechanisms underlying the pathophysiology and treatments have traditionally focused on basal ganglia-thalamo-cortical pathways due to striatal dopamine loss, but more recent evidence has highlighted the role of the cerebellum. Here we review evidence from neuroimaging and non-invasive brain stimulation that demonstrate altered cerebellar activity in PD may be both a pathophysiological and compensatory mechanism depending on dopaminergic medication and symptoms.
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