<scp>HbA1c</scp> and Motor Outcome in Parkinson's Disease in the <scp>Mark‐PD</scp> Study

Zittel, Simone; Uyar, Merve; Lezius, Susanne; Gerloff, Christian; Choe, Chi‐un

doi:10.1002/mds.28689

Cited by 11 publications

(10 citation statements)

References 5 publications

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“…4,5 In addition to prevalent diabetes, recent studies suggested that hyperglycemia, that is glycated hemoglobin (HbA1c) ≥42 mmol/mol, is an independent predictor of faster motor progression determined by Hoehn & Yahr (H&Y) stage ≥3 or Movement Disorder Society-Unified Parkinson's Disease Rating Scale Part III (MDS-UPDRS III) >4 points. 6,7 In line with these findings, a cross-sectional study revealed that high HbA1c levels in PD patients are associated with more severe motor impairment (MDS-UPDRS III). 8 Interestingly, interventional trials using antidiabetic drugs indicate that there might be a causal relationship between glycemic control and motor severity in PD patients.…”

Section: Supporting Datamentioning

confidence: 68%

“…Besides PD risk, prevalent diabetes was also associated with greater motor symptoms and faster motor progression in patients with PD 4,5 . In addition to prevalent diabetes, recent studies suggested that hyperglycemia, that is glycated hemoglobin (HbA1c) ≥42 mmol/mol, is an independent predictor of faster motor progression determined by Hoehn & Yahr (H&Y) stage ≥3 or Movement Disorder Society‐Unified Parkinson's Disease Rating Scale Part III (MDS‐UPDRS III) >4 points 6,7 . In line with these findings, a cross‐sectional study revealed that high HbA1c levels in PD patients are associated with more severe motor impairment (MDS‐UPDRS III) 8 .…”

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confidence: 65%

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Diabetes, Glycated Hemoglobin (HbA1c), and Neuroaxonal Damage in Parkinson's Disease (MARK‐PD Study)

et al. 2022

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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.

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Section: Supporting Datamentioning

confidence: 68%

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confidence: 65%

Diabetes, Glycated Hemoglobin (HbA1c), and Neuroaxonal Damage in Parkinson's Disease (MARK‐PD Study)

et al. 2022

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“…Diabetes was associated with motor and cognitive progression in PD patients. In addition to diabetes, increased glycated hemoglobin (HbA1c) was associated with an unfavorable motor outcome in different PD cohorts (Zittel et al 2021 ). Unsurprisingly, prevalent diabetes and high HbA1c levels were both linked with increased neuroaxonal damage quantified by neurofilament light chain (NfL) levels (Uyar et al 2022 ).…”

Section: Introductionmentioning

confidence: 99%

The heterogeneity of Parkinson’s disease

et al. 2023

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The heterogeneity of Parkinson’s disease (PD), i.e. the various clinical phenotypes, pathological findings, genetic predispositions and probably also the various implicated pathophysiological pathways pose a major challenge for future research projects and therapeutic trail design. We outline several pathophysiological concepts, pathways and mechanisms, including the presumed roles of α-synuclein misfolding and aggregation, Lewy bodies, oxidative stress, iron and melanin, deficient autophagy processes, insulin and incretin signaling, T-cell autoimmunity, the gut–brain axis and the evidence that microbial (viral) agents may induce molecular hallmarks of neurodegeneration. The hypothesis is discussed, whether PD might indeed be triggered by exogenous (infectious) agents in susceptible individuals upon entry via the olfactory bulb (brain first) or the gut (body-first), which would support the idea that disease mechanisms may change over time. The unresolved heterogeneity of PD may have contributed to the failure of past clinical trials, which attempted to slow the course of PD. We thus conclude that PD patients need personalized therapeutic approaches tailored to specific phenomenological and etiologic subtypes of disease.

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“…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. 4 In a separate study, Yang and colleagues showed that in PD patients, dysglycemia was associated with cognitive impairment. 5 Our study confirms these previous findings in a group of PD patients with confirmed T2D over a range of HbA1c.…”

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confidence: 99%