1)Polymeropoulos MH, Lavedan C, Leroy E, et al. Mutation in the alpha-synuclein gene identified in families with Parkinsonʼs disease. Science. 1997; 276: 2045-7
|
|
|
2)Singleton AB, Farrer M, Johnson J, et al. alpha-Synuclein locus triplication causes Parkinsonʼs disease. Science. 2003; 302: 841
|
|
|
3)Matsumoto L, Takuma H, Tamaoka A, et al. CpG demethylation enhances alpha-synuclein expression and affects the pathogenesis of Parkinsonʼs disease. PloS One. 2010; 5: e15522
|
|
|
4)Jowaed A, Schmitt I, Kaut O, et al. Methylation regulates alpha-synuclein expression and is decreased in Parkinsonʼs disease patientsʼ brains. J Neurosci. 2010; 30: 6355-9
|
|
|
5)Chiba-Falek O, Lopez GJ, Nussbaum RL. Levels of alpha-synuclein mRNA in sporadic Parkinson disease patients. Mov Disord. 2006; 21: 1703-8
|
|
|
6)Grundemann J, Schlaudraff F, Haeckel O, et al. Elevated alpha-synuclein mRNA levels in individual UV-laser-microdissected dopaminergic substantia nigra neurons in idiopathic Parkinsonʼs disease. Nucleic Acids Res. 2008; 36: e38
|
|
|
7)Desplats P, Spencer B, Coffee E, et al. Alpha-synuclein sequesters Dnmt1 from the nucleus: a novel mechanism for epigenetic alterations in Lewy body diseases. J Biol Chem. 2011; 286: 9031-7
|
|
|
8)Tan YY, Wu L, Zhao ZB, et al. Methylation of alpha-synuclein and leucine-rich repeat kinase 2 in leukocyte DNA of Parkinsonʼs disease patients. Parkinsonism Relat Disord. 2014; 20: 308-13
|
|
|
9)Ai SX, Xu Q, Hu YC, et al. Hypomethylation of SNCA in blood of patients with sporadic Parkinsonʼs disease. J Neurol Sci. 2014; 337: 123-8
|
|
|
10)Richter J, Appenzeller S, Ammerpohl O, et al. No evidence for differential methylation of alpha-synuclein in leukocyte DNA of Parkinsonʼs disease patients. Mov Disord. 2012; 27: 590-1
|
|
|
11)Song Y, Ding H, Yang J, et al. Pyrosequencing analysis of SNCA methylation levels in leukocytes from Parkinsonʼs disease patients. Neurosci Lett. 2014; 569: 85-8
|
|
|
12)Masliah E, Dumaop W, Galasko D, et al. Distinctive patterns of DNA methylation associated with Parkinson disease: identification of concordant epigenetic changes in brain and peripheral blood leukocytes. Epigenetics. 2013; 8: 1030-8
|
|
|
13)Kang JH, Irwin DJ, Chen-Plotkin AS, et al. Association of cerebrospinal fluid beta-amyloid 1-42, T-tau, P-tau181, and alpha-synuclein levels with clinical features of drug-naive patients with early Parkinson disease. JAMA Neurol. 2013; 70: 1277-87
|
|
|
14)Coupland KG, Mellick GD, Silburn PA, et al. DNA methylation of the MAPT gene in Parkinsonʼs disease cohorts and modulation by vitamin E in vitro. Mov Disord. 2014; 29: 1606-14
|
|
|
15)De Mena L, Cardo LF, Coto E, et al. No differential DNA methylation of PARK2 in brain of Parkinsonʼs disease patients and healthy controls. Mov Disord. 2013; 28: 2032-3
|
|
|
16)Cai M, Tian J, Zhao GH, et al. Study of methylation levels of parkin gene promoter in Parkinsonʼs disease patients. Int J Neurosci. 2011; 121: 497-502
|
|
|
17)Monti B, Gatta V, Piretti F, et al. Valproic acid is neuroprotective in the rotenone rat model of Parkinsonʼs disease: involvement of alpha-synuclein. Neurotox Res. 2010; 17: 130-41
|
|
|
18)Kidd SK, Schneider JS. Protection of dopaminergic cells from MPP+-mediated toxicity by histone deacetylase inhibition. Brain Res. 2010; 1354: 172-8
|
|
|
19)Song C, Kanthasamy A, Jin H, et al. Paraquat induces epigenetic changes by promoting histone acetylation in cell culture models of dopaminergic degeneration. Neurotoxicology. 2011; 32: 586-95
|
|
|
20)Fuso A, Scarpa S. One-carbon metabolism and Alzheimerʼs disease: is it all a methylation matter? Neurobiol Aging. 2011; 32: 1192-5
|
|
|
21)Bottiglieri T, Godfrey P, Flynn T, et al. Cerebrospinal fluid S-adenosylmethionine in depression and dementia: effects of treatment with parenteral and oral S-adenosylmethionine. J Neurol Neurosurg Psychiatry. 1990; 53: 1096-8
|
|
|
22)Morrison LD, Smith DD, Kish SJ. Brain S-adenosylmethionine levels are severely decreased in Alzheimerʼs disease. J Neurochem. 1996; 67: 1328-31
|
|
|
23)Clarke R, Smith AD, Jobst KA, et al. Folate, vitamin B12, and serum total homocysteine levels in confirmed Alzheimer disease. Arch Neurol. 1998; 55: 1449-55
|
|
|
24)Kennedy BP, Bottiglieri T, Arning E, et al. Elevated S-adenosylhomocysteine in Alzheimer brain: influence on methyltransferases and cognitive function. J Neural Transm. 2004; 111: 547-67
|
|
|
25)Condliffe D, Wong A, Troakes C, et al. Cross-region reduction in 5-hydroxymethylcytosine in Alzheimerʼs disease brain. Neurobiol Aging. 2014; 35: 1850-4
|
|
|
26)Chouliaras L, Mastroeni D, Delvaux E, et al. Consistent decrease in global DNA methylation and hydroxymethylation in the hippocampus of Alzheimerʼs disease patients. Neurobiol Aging. 2013; 34: 2091-9
|
|
|
27)Mastroeni D, McKee A, Grover A, et al. Epigenetic differences in cortical neurons from a pair of monozygotic twins discordant for Alzheimerʼs disease. PloS One. 2009; 4: e6617
|
|
|
28)Coppieters N, Dieriks BV, Lill C, et al. Global changes in DNA methylation and hydroxymethylation in Alzheimerʼs disease human brain. Neurobiol Aging. 2014; 35: 1334-44
|
|
|
29)Iwata A, Nagata K, Hatsuta H, et al. Altered CpG methylation in sporadic Alzheimerʼs disease is associated with APP and MAPT dysregulation. Hum Mol Genet. 2014; 23: 648-56
|
|
|
30)Sanchez-Mut JV, Aso E, Heyn H, et al. Promoter hypermethylation of the phosphatase DUSP22 mediates PKA-dependent TAU phosphorylation and CREB activation in Alzheimerʼs disease. Hippocampus. 2014; 24: 363-8
|
|
|
31)Chen KL, Wang SS, Yang YY, et al. The epigenetic effects of amyloid-beta (1-40) on global DNA and neprilysin genes in murine cerebral endothelial cells. Biochem Biophys Res Commun. 2009; 378: 57-61
|
|
|
32)Mastroeni D, Grover A, Delvaux E, et al. Epigenetic changes in Alzheimerʼs disease: decrements in DNA methylation. Neurobiol Aging. 2010; 31: 2025-37
|
|
|
33)Sung HY, Choi EN, Ahn Jo S, et al. Amyloid protein-mediated differential DNA methylation status regulates gene expression in Alzheimerʼs disease model cell line. Biochem Biophys Res Commun. 2011; 414: 700-5
|
|
|
34)Delage B, Dashwood RH. Dietary manipulation of histone structure and function. Ann Rev Nutr. 2008; 28: 347-66
|
|
|
35)Szyf M, McGowan P, Meaney MJ. The social environment and the epigenome. Environ Mol Mutagen. 2008; 49: 46-60
|
|
|
36)Wu J, Basha MR, Brock B, et al. Alzheimerʼs disease (AD) -like pathology in aged monkeys after infantile exposure to environmental metal lead (Pb): evidence for a developmental origin and environmental link for AD. J Neurosci. 2008; 28: 3-9
|
|
|
37)Bakulski KM, Dolinoy DC, Sartor MA, et al. Genome-wide DNA methylation differences between late-onset Alzheimerʼs disease and cognitively normal controls in human frontal cortex. J Alzheimerʼs Dis. 2012; 29: 571-88
|
|
|
38)Steffan JS, Bodai L, Pallos J, et al. Histone deacetylase inhibitors arrest polyglutamine-dependent neurodegeneration in Drosophila. Nature. 2001; 413: 739-43
|
|
|
39)Pallos J, Bodai L, Lukacsovich T, et al. Inhibition of specific HDACs and sirtuins suppresses pathogenesis in a Drosophila model of Huntingtonʼs disease. Hum Mol Genet. 2008; 17: 3767-75
|
|
|
40)Mielcarek M, Benn CL, Franklin SA, et al. SAHA decreases HDAC 2 and 4 levels in vivo and improves molecular phenotypes in the R6/2 mouse model of Huntingtonʼs disease. PloS One. 2011; 6: e27746
|
|
|
41)Jia H, Pallos J, Jacques V, et al. Histone deacetylase (HDAC) inhibitors targeting HDAC3 and HDAC1 ameliorate polyglutamine-elicited phenotypes in model systems of Huntingtonʼs disease. Neurobiol Dis. 2012; 46: 351-61
|
|
|
42)Moumne L, Campbell K, Howland D, et al. Genetic knock-down of HDAC3 does not modify disease-related phenotypes in a mouse model of Huntingtonʼs disease. PloS One. 2012; 7: e31080
|
|
|
43)Thomas EA, Coppola G, Desplats PA, et al. The HDAC inhibitor 4b ameliorates the disease phenotype and transcriptional abnormalities in Huntingtonʼs disease transgenic mice. Proc Natl Acad Sci U S A. 2008; 105: 15564-9
|
|
|
44)Bobrowska A, Paganetti P, Matthias P, et al. Hdac6 knock-out increases tubulin acetylation but does not modify disease progression in the R6/2 mouse model of Huntingtonʼs disease. PloS One. 2011; 6: e20696
|
|
|
45)Benn CL, Butler R, Mariner L, et al. Genetic knock-down of HDAC7 does not ameliorate disease pathogenesis in the R6/2 mouse model of Huntingtonʼs disease. PloS One. 2009; 4: e5747
|
|
|
46)Hathorn T, Snyder-Keller A, Messer A. Nicotinamide improves motor deficits and upregulates PGC-1alpha and BDNF gene expression in a mouse model of Huntingtonʼs disease. Neurobiol Dis. 2011; 41: 43-50
|
|
|
47)Mangiarini L, Sathasivam K, Seller M, et al. Exon 1 of the HD gene with an expanded CAG repeat is sufficient to cause a progressive neurological phenotype in transgenic mice. Cell. 1996; 87: 493-506
|
|
|