Parkinson’s disease (PD) is a neurodegenerative disorder affecting about 1 person of every 1000 in their fifth decade and rising to 19 out of every 1000 in their eighth decade or older.1 The main clinical symptoms are abnormal involuntary movements, bradykinesia, rigidity, and tremor. Patients also display non-motor symptoms, with high levels of mild cognitive impairment (MCI) even at incident diagnosis and increased likelihood of progression to dementia over time.2 The cholinergic system is severely affected in PD, even at its early stages, with widespread denervation.3, 4 These cholinergic abnormalities are associated with a wide array of clinical features including motor symptoms, levodopa-induced dyskinesias, cognitive deterioration, sleep abnormalities, autonomic dysfunction, and altered olfaction. Molecular imaging of the cholinergic system in PD has focused on the cognitive changes, motivated mainly by the cholinergic hypothesis of dementia. PET studies assessing acetylcholinesterase activity have consistently shown cortical reductions of between 10% and 23% in PD relative to controls.5 Using a nonselective muscarinic receptor tracer, 11C-N-methyl-4-piperidyl benzilate, increased frontal binding has also been reported. Brain connectivity plays an important role in the symptomatology of neurodegenerative disorders.10 In PD, several cholinergic networks have been proposed and thought to affect attention, visuoperceptual, and memory domains.

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