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Parkinson's Disease and Type 2 Diabetes: HbA1c Is Associated with Motor and Cognitive Severity

Evidence supporting a relation between Parkinson’s disease (PD) and type 2 diabetes (T2D) has been accumulating, but the relationship is incompletely understood. The aim of this study was to investigate the association between glycated hemoglobin (HbA1c) levels in blood and clinical motor and cognitive severity (Movement Disorder Society Unified Parkinson’s Disease Rating Scale, Part III [MDS-UPDRS III] and MoCA [Montreal Cognitive Assessment] scores) in patients with both PD and T2D participating in the East London PD project. Thirty-six patients had both PD and T2D and a recent HbA1c level recorded. Five patients had HbA1c levels in the normal range (≤41 mmol/mol), 10 patients had mildly raised HbA1c (42–47 mmol/mol), and 21 patients had high HbA1c (≥48 mmol/mol). Multiple linear regression was used to assess the relationship between HbA1c levels and clinical motor and cognitive severity, after adjusting for potential confounding factors. An association was observed between HbA1c level and MDS-UPDRS III score (slope = 0.91, 95% CI [confidence interval] 0.39–1.44; P = 0.001; Fig. 1). After adjusting for age, medication, and time since symptom onset, a 1 mmol/mol increase in HbA1c was associated with 0.85 point increase in the MDS-UPDRS III score (95% CI 0.29–1.41; P = 0.004). An inverse association was also observed between HbA1c levels and MoCA score (slope = 0.18, 95% CI 0.34 to 0.03; P = 0.018; Fig. 1). In adjusted analyses, a 1 mmol/mol increase in HbA1c was associated with a 0.19 point decrease in the MoCA score (95% CI 0.35 to 0.02; P = 0.027). Few studies so far have investigated the relationship between HbA1c and PD severity in PD patients with T2D. Markaki and colleagues showed that in nondiabetic PD patients, low and high HbA1c levels (HbA1c ≤30 mmol/mol or ≥42 mmol/mol) were associated with unfavorable motor outcome (Hoehn & Yahr stage ≥3). Zittel and colleagues have also recently shown an association between increased HbA1c level (HbA1c ≥42 mmol/mol) and motor progression (MDS-UPDRS III increase of >4 points) in PD patients regardless of diabetic status. In a separate study, Yang and colleagues showed that in PD patients, dysglycemia was associated with cognitive impairment. Our study confirms these previous findings in a group of PD patients with confirmed T2D over a range of HbA1c. As HbA1c gives the average blood glucose levels during the preceding 3 months, it is a marker for overall control of diabetes and may explain the associations observed in this study. However, it is plausible that the observed associations may be reverse causal (ie, more severe PD associated with poorer control of diabetes) or due to confounding effects, such that general poor health (eg, sedentary lifestyle, poor diet, lack of self-management) may explain the associations observed in this study. It is recognized that in non-PD patients with T2D, higher HbA1c levels are associated with lower cognitive performance. It is possible