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J Parkinsons Dis. 2018;8(1):33-43. doi: 10.3233/JPD-171285.

Alpha-Synuclein Glycation and the Action of Anti-Diabetic Agents in Parkinson's Disease.

Author information

1
Department of Experimental Neurodegeneration, Center for Biostructural Imaging of Neurodegeneration, Center for Nanoscale Microscopy and Molecular Physiology of the Brain, University Medical Center Göttingen, Göttingen, Germany.
2
CEDOC, Chronic Diseases Research Center, NOVA Medical School, Faculdade de Ciências Médicas, Universidade Nova de Lisboa, Campo dos Mártires da Pátria, Lisboa, Portugal.
3
Max Planck Institute for Experimental Medicine, Göttingen, Germany.
4
Institute of Neuroscience, The Medical School, Newcastle University, Framlington Place, Newcastle Upon Tyne, UK.

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.

KEYWORDS:

Glycation; Maillard-reaction; Parkinson’s disease; alpha-synuclein

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