Diabetes, Glycated Hemoglobin (HbA1c), and Neuroaxonal Damage in Parkinson's Disease (MARK-PD Study)
- PMID: 35384057
- DOI: 10.1002/mds.29009
Diabetes, Glycated Hemoglobin (HbA1c), and Neuroaxonal Damage in Parkinson's Disease (MARK-PD Study)
Abstract
Background: Diabetes is associated with incidence and prevalence of Parkinson's disease (PD). Furthermore, glycated hemoglobin (HbA1c) levels have been linked with motor function and progression.
Objectives: We evaluated the relationship between prevalent diabetes and HbA1c levels with serum neurofilament light chain (NfL) levels as marker of neuroaxonal damage.
Methods: NfL concentrations were analyzed with Simoa in serum of 195 PD patients with available HbA1c values. Motor (MDS-UPDRS III, Hoehn & Yahr [H&Y]) and cognitive (Montreal Cognitive Assessment [MoCA]) function was assessed and vascular comorbidities were documented from medical records.
Results: PD patients with prevalent diabetes had higher serum NfL levels and lower MoCA scores independent of age, body mass index (BMI), and vascular risk factors. Furthermore, diabetes was associated with higher H&Y stages in unadjusted and age/BMI-adjusted models. Higher HbA1c levels were associated with increased NfL in unadjusted and age/BMI-adjusted models.
Conclusions: In PD patients, diabetes and high HbA1c are associated with increased neuroaxonal damage and cognitive impairment. © 2022 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson Movement Disorder Society.
Keywords: Simoa; glycemia; neurofilament.
© 2022 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson Movement Disorder Society.
Comment in
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Reply to: "Diabetes and Neuroaxonal Damage in Parkinson's Disease".Mov Disord. 2022 Jul;37(7):1569-1570. doi: 10.1002/mds.29064. Mov Disord. 2022. PMID: 35856728 No abstract available.
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Diabetes and Neuroaxonal Damage in Parkinson's Disease.Mov Disord. 2022 Jul;37(7):1568-1569. doi: 10.1002/mds.29067. Mov Disord. 2022. PMID: 35856732 Free PMC article. No abstract available.
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