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Brain. 2017 Apr 1;140(4):878-886. doi: 10.1093/brain/aww227.

The yin and yang of α-synuclein-associated epigenetics in Parkinson's disease.

Author information

1
Department of NeuroDegeneration and Restorative Research, Center for Nanoscale Microscopy and Molecular Physiology of the Brain, University Medical Center Göttingen, Göttingen, Germany.
2
Faculty of Medicine, University of Porto, 4099-002, Porto, Portugal.
3
Max Planck Institute for Experimental Medicine, Göttingen, Germany.

Abstract

Parkinson's disease is the second most prevalent neurodegenerative disorder. The main neuropathological hallmarks of the disease are the degeneration of dopaminergic neurons in the substantia nigra pars compacta and the accumulation of protein inclusions known as Lewy bodies. Recently, great attention has been given to the study of genes associated with both familial and sporadic forms of Parkinson's disease. Among them, the α-synuclein gene is believed to play a central role in the disease and is, therefore, one of the most studied genes. Parkinson's disease is a complex disorder and, as such, derives from the interaction between genetic and environmental factors. Here, we offer an update on the landscape of epigenetic-mediated regulation of gene expression that has been linked with α-synuclein and associated with Parkinson's disease. We also provide an overview of how epigenetic modifications can influence the transcription and/or translation of the α-synuclein gene and, on the other hand, how α-synuclein function/dysfunction can, per se, affect the epigenetic landscape. Finally, we discuss how a deeper understanding of the epigenetic profile of α-synuclein may enable the development of novel therapeutic approaches for Parkinson's disease and other synucleinopathies.

KEYWORDS:

Parkinson’s disease; epigenetic modifications; protein aggregation; α-synuclein

PMID:
27585855
DOI:
10.1093/brain/aww227
[Indexed for MEDLINE]

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