Dopaminergic and Cholinergic Brain Activity and Performance on MMSE and MoCA in Parkinson's Disease (P03.127)

Abstract

Objective: To investigate the relationship between performance on the Montreal Cognitive Assessment (MoCA) and Mini-Mental State Exam (MMSE) and PET measures (dopaminergic/cholinergic) of brain activity. Background Executive dysfunction seen in early Parkinson9s disease (PD) is believed to result from striatal dopaminergic denervation, while the degree of cognitive impairment in PD dementia is thought to correlate with cortical cholinergic activity. Because it contains tasks that evaluate executive function, performance on the MoCA may correlate more strongly with striatal dopaminergic activity, while performance on the MMSE may better correlate with cortical cholinergic activity. Design/Methods: 19 non-demented men with PD (mean age 66.4 ± 7.5; mean disease duration 5.7 ± 3.5 years) underwent (+)-[ 11 C] dihydrotetrabenazine (DTBZ) vesicular monoamine transporter 2 and [ 11 C]methyl-4-piperidinyl propionate (PMP) acetylcholinesterase (AChE) PET imaging as well as the Unified PD Rating Scale (UPDRS), MoCA and MMSE. Results: Stepwise regression analysis was performed, with MoCA or MMSE as the dependent variable and the PET measures (cortical PMP, basal ganglia, putamen and caudate DTBZ) as regressors. Results for the MOCA show that cortical PMP was the only variable that met entry criteria in the model (F=6.12, P=0.024). The DTBZ measures did not meet entry criteria. Similar results were seen for the MMSE, with the cortical PMP variable as the only significant variable in the model (F=5.76, P=0.028). Conclusions: Both MoCA and MMSE performance were associated with cortical AChE activity in PD patients. Surprisingly, we did not find a significant relationship between the MoCA and striatal dopaminergic denervation, but we may not have had the power to detect such a relationship. Nevertheless, these findings suggest that both the MoCA and the MMSE may be reliable measures of the cognitive decline attributable to cortical cholinergic denervation seen in early PD. Supported by: NIH P01 NS15655, NIH R01 NS070856 (PI), and a grant from the Department of Veterans Affairs. Disclosure: Dr. Lenhart has nothing to disclose. Dr. Bohnen has nothing to disclose. Dr. Koeppe has nothing to disclose. Dr. Chou has received personal compensation for activities with Medtronic, Inc. and Merz Pharma.