This hypothesis differentiates cognitively impaired Parkinson’s disease patients into two groups. This heterogeneity has led to the emergence of the dual syndrome hypothesis 14. Response to cholinergic medications has been reported to be different among cognitively impaired Parkinson’s patients: while Parkinson’s disease dementia is routinely treated with cholinesterase inhibitors, these are not consistently used in patients with MCI 13. The presence of cortical Lewy bodies in the frontal cortex could also contribute to this impairment 12. Several possible mechanisms have been proposed for cognitive impairment in Parkinson’s disease, including dopamine depletion in the frontostriatal pathway 6, and imbalance in neurotransmitters, such as acetylcholine 7, serotonin 8, 9, 10, and norepinephrine 11.

Some MCI patients experience deficits in working memory and executive function 4 others are more impaired in visuospatial function 5. Clinical presentation of cognitive impairment therefore varies. Cognitive impairment in Parkinson’s disease affects several cognitive domains, such as executive function, attention, visuospatial, memory and language 1. However, reconversion from MCI to normal cognition is not uncommon (~ 20% at one-year follow up 3). MCI can present at time of diagnosis in about 35% of cases, and it has been estimated that about 62% of those patients progress to dementia over 5 years 2. These range from mild cognitive impairment (MCI) to severe dementia 1. Parkinson’s disease is traditionally thought of as a movement disorder, but the majority of patients have varying degrees of cognitive impairment. Our findings support and complement the dual syndrome hypothesis. Increased caudate connectivity may be related to a compensatory mechanism found in cognitively normal patients with Parkinson’s disease. We found that Alzheimer’s disease-like metabolic/perfusion pattern score correlated with MoCA scores in healthy controls, but not in Parkinson’s disease. Interestingly, PDNC’s functional connectivity of the right caudate was significantly higher than both PDLC and healthy controls, while PDLC and healthy controls were not significantly different from each other.

A strong positive correlation was found between the functional connectivity of the right caudate nucleus and MoCA scores in Parkinson’s patient groups, but not in healthy control subjects. We analyzed these data for graph theory metrics and Alzheimer’s disease-like pattern score, respectively. All subjects were scanned with resting-state functional magnetic resonance imaging (MRI) and perfusion MRI. We recruited 18 Parkinson’s disease patients-10 PDNC, 8 PDLC (low cognition Parkinson’s disease MoCA < 26) -and 10 age-matched healthy controls. The aim of this study was to investigate functional connectivity changes of the caudate nucleus in cognitively impaired Parkinson’s patients. However, its underlying mechanism is not well understood, which has hindered new treatment discoveries specific to MCI. Mild cognitive impairment (MCI) is common in Parkinson’s disease patients.

Moca test score bell curve