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. Author manuscript; available in PMC: 2019 Apr 23.
Published in final edited form as: Prog Neurobiol. 2015 Jun 11;131:21–64. doi: 10.1016/j.pneurobio.2015.05.002

Table 8.

Epigenetic dysregulation in Parkinson’s disease: chromatin remodeling.

Chromatin remodeling target Regulation Epigenetic modification Observed in Sample size Methods Reference

Histones (Globally) Deacetylation via binding of α-
synuclein to PGC1-α promoter element
PD patients (SN) 16 GWES Zheng et al., 2010
H3 Acetylation via the interaction of
α-synuclein with SIRT1
α-Synuclein-transfected
SH-SY5Y cells
PD Drosophila model
-

N.S.
WB

WB
Kontopoulos et al., 2006
Acetylation due to Paraquat and/
or Dieldrin exposure
N27 dopaminergic cells - WB Song et al., 2010, 2011a
H3K4 Tri-methylation due to MPTP-
induced toxicity
Mice (striatum)
Macaque monkeys (striatum)
5
18
WB Nicholas et al., 2008
H4 Acetylation due to Dieldrin exposure N27 dopaminergic cells - WB Song et al., 2011a
Heterozygous A53T
SNCA mutation
Epigenetically silenced affected
allele via histone modifications
fPD patient 1 PCR Voutsinas et al., 2010

indicates increased expression levels,

indicates decreased expression levels, and

indicates a genetic mutation affecting epigenetic regulation.

Abbreviations: fPD, familial PD; H, histone; K, lysine; MPTP, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; PD, Parkinson’s disease; PGC1-α, peroxisome proliferator receptor gamma coactivator-1 alpha; SH-SY5Y cells, human neuroblastoma cell line; SIRT1, sirtuin 1; SN, substantia nigra; SNCA, synuclein alpha; N.S., not specified; GWES, genome-wide epistasis studies; WB, Western blot; PCR, polymerase chain reaction.