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Diabetes and neuroaxonal damage in Parkinson’s disease
Published July 19, 2022
Output Details
Preprint April 21, 2022
Published July 19, 2022
Description
Uyar and colleagues recently reported on the association between diabetes, non-diabetic elevated glycated hemoglobin levels (HbA1c) and neuroaxonal damage in PD patients from the MARK-PD study. Considering the authors' novel findings of an association between diabetes and neuroaxonal damage, we explored the relationship between serum NfL and diabetes in our previously defined subgroup of the Tracking Parkinson’s study. Our findings affirm Uyar et al’s report of an association between PD-DM and more severe neuroaxonal damage. Furthermore, the data indicate that the more severe phenotype in PD-DM noted to date by several studies is likely to be mediated by additional factors other than vascular risk factor burden that tends to co-exist in these cases. T2DM and PD share several pathological processes encompassing neuroinflammation, lysosomal dysfunction, mitochondrial dysfunction and the development of central insulin resistance that leads to neurodegeneration. This process is in part mediated by hyperglycemia as demonstrated by the MARK-PD study and its downstream impact on alpha synuclein aggregation. It is also possible that some of the observed associations are explained by diabetic neuropathy, as other peripheral neuropathies are known to increase blood NfL concentrations.
Identifier (DOI)
10.1002/mds.29067