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Alpha-synuclein glycation and the action of anti-diabetic agents in Parkinson's disease

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Outeiro,  Tiago F.
Experimental Neurodegeneration, Max Planck Institute of Experimental Medicine, Max Planck Society;

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König, A., Miranda, H. V., & Outeiro, T. F. (2018). Alpha-synuclein glycation and the action of anti-diabetic agents in Parkinson's disease. Journal of Parkinson's Disease: JPD, 8(1), 33-43. doi:10.3233/JPD-171285.


Cite as: https://hdl.handle.net/21.11116/0000-0002-18B8-4
Abstract
Parkinson’s disease (PD) is a neurodegenerative disorder with complex etiology and variable pathology. While a subset of cases is associated with single-gene mutations, the majority originates from a combination of factors we do not fully understand. Thus, understanding the underlying causes of PD is indispensable for the development of novel therapeutics. Glycation, the non-enzymatic reaction between reactive dicarbonyls and amino groups, gives rise to a variety of different reaction products known as advanced glycation end products (AGEs). AGEs accumulate over a proteins life-time, and increased levels of glycation reaction products play a role in diabetic complications. It is now also becoming evident that PD patients also display perturbed sugar metabolism and protein glycation, including that of alpha-synuclein, a key player in PD. Here, we hypothesize that anti-diabetic drugs targeting the levels of glycation precursors, or promoting the clearance of glycated proteins may also prove beneficial for PD patients.