Glycated haemoglobin (HbA1c) levels and motor symptoms in Parkinson's disease.

Authors

Nikhil Choudhary, Naveen Seervi, Amita Bhargava, Shubhakaran Khichar

Published in

The Indian journal of medical research. Volume 163. Issue 6. Pages 786-792.

Abstract

Background and objectives Emerging evidence indicates a complex relationship between glycated haemoglobin (HbA1c) levels and motor symptom severity in Parkinson's disease. Both elevated (>6.1%) and low (<5.3%) HbA1c have been linked to increased disability. This study examined the association between HbA1c levels and motor symptoms in patients with Parkinson's disease from Jodhpur, India. Methods A cross-sectional observational study was conducted at the department of Neurology, Mathura Das Mathur Hospital, Jodhpur between March 2023 and February 2024. One hundred patients with Parkinson's disease patients fulfilling the UK Parkinson's Disease Society Brain Bank (UKPDSBB) criteria were enrolled. Participants underwent HbA1c testing, motor evaluation with the Unified Parkinson's Disease Rating Scale (UPDRS III) in ON and OFF states, and cognitive screening with the Montreal Cognitive Assessment (MoCA). Patients were categorised into three groups based on HbA1c: ≤4.9% (Low), 5.0-5.9% (Normal-to-Prediabetic), and ≥6.0% (High). Disease duration and medication history were also recorded. Results No significant group differences were found for age, sex, body mass index (BMI), or disease duration, between the three groups, based on HbA1c levels. UPDRS and MoCA scores differed significantly across HbA1c categories (P<0.001). Higher HbA1c strongly correlated with worse motor outcomes (UPDRS ON: Spearman's ρ=0.90; OFF: ρ=0.84) and poorer cognition (MoCA: ρ= -0.79). Interpretation and conclusions Elevated HbA1c levels were significantly associated with greater motor impairment and cognitive dysfunction in Parkinson's disease. These findings highlight the potential role of metabolic dysregulation in progression of Parkinson's disease and underscore the need for longitudinal studies to clarify causal links and therapeutic implications.

PMID:
42295713
Bibliographic data and abstract were imported from PubMed on 15 Jun 2026.

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