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Mov Disord. 2016 Jun;31(6):782-90. doi: 10.1002/mds.26566. Epub 2016 Mar 4.

Glycation in Parkinson's disease and Alzheimer's disease.

Author information

1
CEDOC - Chronic Diseases Research Center, NOVA Medical School, Lisboa, Portugal.
2
Neurological Disorders Center, Qatar Biomedical Research Institute, and College of Science and Engineering, Hamad Bin Khalifa University (HBKU), Education City, Qatar Foundation, P.O. Box 5825 Doha, Qatar.
3
Department of Neurodegeneration and Restorative Research, Center for Nanoscale Microscopy and Molecular Physiology of the Brain (CNMPB), University Medical Center Goettingen, Goettingen, Germany.
4
Max Planck Institute for Experimental Medicine, Goettingen, Germany.

Abstract

Glycation is a spontaneous age-dependent posttranslational modification that can impact the structure and function of several proteins. Interestingly, glycation can be detected at the periphery of Lewy bodies in the brain in Parkinson's disease. Moreover, α-synuclein can be glycated, at least under experimental conditions. In Alzheimer's disease, glycation of amyloid β peptide exacerbates its toxicity and contributes to neurodegeneration. Recent studies establish diabetes mellitus as a risk factor for several neurodegenerative disorders, including Parkinson's and Alzheimer's diseases. However, the mechanisms underlying this connection remain unclear. We hypothesize that hyperglycemia might play an important role in the development of these disorders, possibly by also inducing protein glycation and thereby dysfunction, aggregation, and deposition. Here, we explore protein glycation as a common player in Parkinson's and Alzheimer's diseases and propose it may constitute a novel target for the development of strategies for neuroprotective therapeutic interventions.

KEYWORDS:

Alzheimer's disease; Parkinson's disease; glycation; neurodegenerative diseases

PMID:
26946341
DOI:
10.1002/mds.26566
[Indexed for MEDLINE]

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