[1]
Bird A. Perceptions of epigenetics. Nature 2007; 447(7143): 396-8.
[2]
Araki Y, Mimura T. The histone modification code in the pathogenesis of autoimmune diseases. Mediators Inflamm 2017; 2017: 2608605.
[3]
Sharma S, Taliyan R. Transcriptional dysregulation in Huntington’s disease: The role of histone deacetylases. Pharmacol Res 2015; 100: 157-69.
[4]
Sharma S, Taliyan R. Targeting histone deacetylases: A novel approach in Parkinson’s disease. Park Dis 2015; 2015: 303294.
[5]
Sharma S, Taliyan R. Epigenetic modifications by inhibiting histone deacetylases reverse memory impairment in insulin resistance induced cognitive deficit in mice. Neuropharmacology 2016; 105: 285-97.
[6]
Sharma S, Taliyan R. Histone deacetylase inhibitors: Future therapeutics for insulin resistance and type 2 diabetes. Pharmacol Res 2016; 113: 320-6.
[7]
Seto E, Yoshida M. Erasers of histone acetylation: The histone deacetylase enzymes. Cold Spring Harb Perspect Biol 2014; 6(4): a018713.
[8]
Haberland M, Montgomery RL, Olson EN. The many roles of histone deacetylases in development and physiology: Implications for disease and therapy. Nat Rev Genet 2009; 10(1): 32.
[9]
Rouaux C, Jokic N, Mbebi C, Boutillier S, Loeffler J-P, Boutillier A-L. Critical loss of CBP/p300 histone acetylase activity by caspase-6 during neurodegeneration. EMBO J 2003; 22(24): 6537-49.
[10]
Sadri-Vakili G, Bouzou B, Benn CL, et al. Histones associated with downregulated genes are hypo-acetylated in Huntington’s disease models. Hum Mol Genet 2007; 16(11): 1293-306.
[11]
Henry TR. The history of valproate in clinical neuroscience. Psychopharmacol Bull 2003; 37: 5-16.
[12]
Didonna A, Opal P. The promise and perils of HDAC inhibitors in neurodegeneration. Ann Clin Transl Neurol 2015; 2(1): 79-101.
[13]
Schmitt M, Matthies H. Biochemical studies on histones of the central nervous system. III. Incorporation of [14C]-acetate into the histones of different rat brain regions during a learning experiment]. Acta Biol Med Ger 1979; 38(4): 683-9.
[14]
Oliveira AMM, Wood MA, McDonough CB, Abel T. Transgenic mice expressing an inhibitory truncated form of p300 exhibit long-term memory deficits. Learn Mem 2007; 14(9): 564-72.
[15]
Crepaldi L, Riccio A. Chromatin learns to behave. Epigenetics 2009; 4(1): 23-6.
[16]
Yu IT, Park JY, Kim SH, Lee J, Kim YS, Son H. Valproic acid promotes neuronal differentiation by induction of proneural factors in association with H4 acetylation. Neuropharmacology 2009; 56(2): 473-80.
[17]
Guan JS, Haggarty SJ, Giacometti E, et al. HDAC2 negatively regulates memory formation and synaptic plasticity. Nature 2009; 459(7243): 55.
[18]
Morris MJ, Mahgoub M, Na ES, Pranav H, Monteggia LM. Loss of histone deacetylase 2 improves working memory and accelerates extinction learning. J Neurosci 2013; 33(15): 6401-11.
[19]
Gräff J, Rei D, Guan JS, et al. An epigenetic blockade of cognitive functions in the neurodegenerating brain. Nature 2012; 483(7388): 222.
[20]
Hanson JE, Deng L, Hackos DH, et al. Histone deacetylase 2 cell autonomously suppresses excitatory and enhances inhibitory synaptic function in CA1 pyramidal neurons. J Neurosci 2013; 33(14): 5924-9.
[21]
McQuown SC, Barrett RM, Matheos DP, et al. HDAC3 is a critical negative regulator of long-term memory formation. J Neurosci 2011; 31(2): 764-74.
[22]
Bardai FH, Price V, Zaayman M, Wang L, D’Mello SR. Histone deacetylase (HDAC1) is a molecular switch between neuronal survival and death. J Biol Chem 2012; 287(42): 35444-53.
[23]
Krishna K, Behnisch T, Sajikumar S. Inhibition of histone deacetylase 3 restores amyloid-β oligomer-induced plasticity deficit in hippocampal CA1 pyramidal neurons. J Alzheimers Dis 2016; 51(3): 783-91.
[24]
Wang WH, Cheng LC, Pan FY, et al. Intracellular trafficking of histone deacetylase 4 regulates long-term memory formation. Anat Rec Adv Integr Anat Evol Biol 2011; 294(6): 1025-34.
[25]
Kim MS, Akhtar MW, Adachi M, et al. An essential role for histone deacetylase 4 in synaptic plasticity and memory formation. J Neurosci 2012; 32(32): 10879-86.
[26]
Williams SR, Aldred MA, Der Kaloustian VM, et al. Haploinsufficiency of HDAC4 causes brachydactyly mental retardation syndrome, with brachydactyly type E, developmental delays, and behavioral problems. Am J Hum Genet 2010; 87(2): 219-28.
[27]
Agis-Balboa RC, Pavelka Z, Kerimoglu C, Fischer A. Loss of HDAC5 impairs memory function: Implications for Alzheimer’s disease. J Alzheimers Dis 2013; 33(1): 35-44.
[28]
Rivieccio MA, Brochier C, Willis DE, et al. HDAC6 is a target for protection and regeneration following injury in the nervous system. Proc Natl Acad Sci 2009; 106(46): 19599-604.
[29]
Govindarajan N, Rao P, Burkhardt S, et al. Reducing HDAC6 ameliorates cognitive deficits in a mouse model for Alzheimer’s disease. EMBO Mol Med 2013; 5(1): 52-63.
[30]
Peleg S, Sananbenesi F, Zovoilis A, et al. Altered histone acetylation is associated with age-dependent memory impairment in mice. Science 2010; 328(5979): 753-6.
[31]
Zhong T, Guo Q, Zou W, et al. Neonatal isoflurane exposure induces neurocognitive impairment and abnormal hippocampal histone acetylation in mice. PLoS One 2015; 10(4): e0125815.
[32]
Radde R, Bolmont T, Kaeser SA, et al. Aβ42-driven cerebral amyloidosis in transgenic mice reveals early and robust pathology. EMBO Rep 2006; 7(9): 940-6.
[33]
Govindarajan N, Agis-Balboa RC, Walter J, Sananbenesi F, Fischer A. Sodium butyrate improves memory function in an Alzheimer’s disease mouse model when administered at an advanced stage of disease progression. J Alzheimers Dis 2011; 26(1): 187-97.
[34]
Sharma S, Taliyan R, Ramagiri S. Histone deacetylase inhibitor, trichostatin A, improves learning and memory in high-fat diet-induced cognitive deficits in mice. J Mol Neurosci 2015; 56(1): 1-11.
[35]
Subramanian S, Bates SE, Wright JJ, Espinoza-Delgado I, Piekarz RL. Clinical toxicities of histone deacetylase inhibitors. Pharmaceuticals 2010; 3(9): 2751-67.
[36]
Cuadrado-Tejedor M, Garcia-Barroso C, Sanzhez-Arias J, et al. Concomitant histone deacetylase and phosphodiesterase 5 inhibition synergistically prevents the disruption in synaptic plasticity and it reverses cognitive impairment in a mouse model of Alzheimer’s disease. Clin Epigenetics 2015; 7(1): 108.
[37]
Sharma S, Kumar K, Deshmukh R, Sharma PL. Phosphodiesterases: Regulators of cyclic nucleotide signals and novel molecular target for movement disorders. Eur J Pharmacol 2013; 714(1-3): 486-97.
[38]
Sharma S, Deshmukh R. Vinpocetine attenuates MPTP-induced motor deficit and biochemical abnormalities in Wistar rats. Neuroscience 2015; 286: 393-403.
[39]
Johnston TH, Huot P, Damude S, et al. RGFP109, a histone deacetylase inhibitor attenuates l-DOPA-induced dyskinesia in the MPTP-lesioned marmoset: A proof-of-concept study. Parkinsonism Relat Disord 2013; 19(2): 260-4.
[40]
Gardian G, Yang L, Cleren C, Calingasan NY, Klivenyi P, Beal MF. Neuroprotective effects of phenylbutyrate against MPTP neurotoxicity. Neuromolecular Med 2004; 5(3): 235-41.
[41]
Chauhan NB, Siegel GJ, Lee JM. Depletion of glial cell line-derived neurotrophic factor in substantia nigra neurons of Parkinson’s disease brain. J Chem Neuroanat 2001; 21(4): 277-88.
[42]
Monti B, Gatta V, Piretti F, Raffaelli SS, Virgili M, Contestabile A. Valproic acid is neuroprotective in the rotenone rat model of Parkinson’s disease: Involvement of α-synuclein. Neurotox Res 2010; 17(2): 130-41.
[43]
Wang X, Qin Z-H, Leng Y, et al. Prostaglandin A1 inhibits rotenone-induced apoptosis in SH-SY5Y cells. J Neurochem 2002; 83(5): 1094-102.
[44]
Pan T, Li X, Xie W, Jankovic J, Le W. Valproic acid-mediated Hsp70 induction and anti-apoptotic neuroprotection in SH-SY5Y cells. FEBS Lett 2005; 579(30): 6716-20.
[45]
Laurent RS, O’Brien LM, Ahmad ST. Sodium butyrate improves locomotor impairment and early mortality in a rotenone-induced Drosophila model of Parkinson’s disease. Neuroscience 2013; 246: 382-90.
[46]
Inden M, Kitamura Y, Takeuchi H, et al. Neurodegeneration of mouse nigrostriatal dopaminergic system induced by repeated oral administration of rotenone is prevented by 4-phenylbutyrate, a chemical chaperone. J Neurochem 2007; 101(6): 1491-504.
[47]
Sharma S, Taliyan R, Singh S. Beneficial effects of sodium butyrate in 6-OHDA induced neurotoxicity and behavioral abnormalities: Modulation of histone deacetylase activity. Behav Brain Res 2015; 291: 306-14.
[48]
Contestabile A, Monti B, Mercatelli D. Valproic acid neuroprotection in 6-OHDA lesioned rat, a model for parkinson’s disease. HOAJ Biol 2012; 1(1): 4.
[49]
Nutt J, Williams A, Plotkin C, Eng N, Ziegler M, Calne DB. Treatment of Parkinson’s disease with sodium valproate: Clinical, pharmacological, and biochemical observations. Can J Neurol Sci 1979; 6(3): 337-43.
[50]
Price PA, Parkes JD, Marsden CD. Sodium valproate in the treatment of levodopa-induced dyskinesia. J Neurol Neurosurg Psychiatry 1978; 41(8): 702-6.
[51]
Li SH, Li XJ. Huntingtin protein interactions and the pathogenesis of Huntington’s disease. Trends Genet 2004; 20(3): 146-54.
[52]
DiFiglia M, Sapp E, Chase KO, et al. Aggregation of huntingtin in neuronal intranuclear inclusions and dystrophic neurites in brain. Science 1997; 277(5334): 1990-3.
[53]
Steffan JS, Bodai L, Pallos J, et al. Histone deacetylase inhibitors arrest polyglutamine-dependent neurodegeneration in Drosophila. Nature 2001; 413(6857): 739.
[54]
Bates EA, Victor M, Jones AK, Shi Y, Hart AC. Differential contributions of Caenorhabditis elegans histone deacetylases to huntingtin polyglutamine toxicity. J Neurosci 2006; 26(10): 2830-8.
[55]
Quinti L, Chopra V, Rotili D, et al. Evaluation of histone deacetylases as drug targets in huntington’s disease models: Study of HDACs in brain tissues from R6/2 and CAG140 knock-in HD mouse models and human patients and in a neuronal HD cell model. PLoS Curr 2010; 2.
[56]
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 Huntington’s disease. PLoS One 2011; 6(11): e27746.
[57]
Jia H, Pallos J, Jacques V, et al. Histone deacetylase (HDAC) inhibitors targeting HDAC3 and HDAC1 ameliorate polyglutamine-elicited phenotypes in model systems of Huntington’s disease. Neurobiol Dis 2012; 46(2): 351-61.
[58]
Hoshino M, Tagawa K, Okuda T, et al. Histone deacetylase activity is retained in primary neurons expressing mutant huntingtin protein. J Neurochem 2003; 87(1): 257-67.
[59]
Bardai FH, D’Mello SR. Selective toxicity by HDAC3 in neurons: Regulation by Akt and GSK3β. J Neurosci 2011; 31(5): 1746-51.
[60]
Bardai FH, Verma P, Smith C, Rawat V, Wang L, D’Mello SR. Disassociation of histone deacetylase-3 from normal huntingtin underlies mutant huntingtin neurotoxicity. J Neurosci 2013; 33(29): 11833-8.
[61]
Mielcarek M, Inuabasi L, Bondulich MK, et al. Dysfunction of the CNS-heart axis in mouse models of Huntington’s disease. PLoS Genet 2014; 10(8): e1004550.
[62]
Yeh HH, Young D, Gelovani JG, et al. Histone deacetylase class II and acetylated core histone immunohistochemistry in human brains with Huntington’s disease. Brain Res 2013; 1504: 16-24.
[63]
Bobrowska A, Paganetti P, Matthias P, Bates GP. Hdac6 knock-out increases tubulin acetylation but does not modify disease progression in the R6/2 mouse model of Huntington’s disease. PLoS One 2011; 6(6): e20696.
[64]
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 Huntington’s disease. PLoS One 2009; 4(6): e5747.
[65]
Thomas EA, Coppola G, Desplats PA, et al. The HDAC inhibitor 4b ameliorates the disease phenotype and transcriptional abnormalities in Huntington’s disease transgenic mice. Proc Natl Acad Sci 2008; 105(40): 15564-9.
[66]
Jia H, Morris CD, Williams RM, Loring JF, Thomas EA. HDAC inhibition imparts beneficial transgenerational effects in Huntington’s disease mice via altered DNA and histone methylation. Proc Natl Acad Sci 2015; 112(1): E56-64.
[67]
Selenica ML, Benner L, Housley SB, et al. Histone deacetylase 6 inhibition improves memory and reduces total tau levels in a mouse model of tau deposition. Alzheimers Res Ther 2014; 6(1): 12.
[68]
Benito E, Urbanke H, Ramachandran B, et al. HDAC inhibitor--dependent transcriptome and memory reinstatement in cognitive decline models. J Clin Invest 2015; 125(9): 3572-84.
[69]
Sewal AS, Patzke H, Perez EJ, et al. Experience modulates the effects of histone deacetylase inhibitors on gene and protein expression in the hippocampus: Impaired plasticity in aging. J Neurosci 2015; 35(33): 11729-42.
[70]
Yoo DY, Kim DW, Kim MJ, et al. Sodium butyrate, a histone deacetylase Inhibitor, ameliorates SIRT2-induced memory impairment, reduction of cell proliferation, and neuroblast differentiation in the dentate gyrus. Neurol Res 2015; 37(1): 69-76.
[71]
Sharma S, Taliyan R. Synergistic effects of GSK-3β and HDAC inhibitors in intracerebroventricular streptozotocin-induced cognitive deficits in rats. Naunyn Schmiedebergs Arch Pharmacol 2015; 388(3): 337-49.
[72]
Blank M, Werenicz A, Velho LA, et al. Enhancement of memory consolidation by the histone deacetylase inhibitor sodium butyrate in aged rats. Neurosci Lett 2015; 594: 76-81.
[73]
Hsing CH, Hung SK, Chen YC, et al. Histone deacetylase inhibitor trichostatin a ameliorated endotoxin-induced neuroinflammation and cognitive dysfunction. Mediators Inflamm 2015; 287(42): 35444-53.
[74]
Kereshi S, Schlagenhauff RE, Richardson KS. Myoclonic and major seizures in early adult Huntington’s chorea: Case-report and electro-clinical findings. Clin Electroencephalogr 1980; 11(2): 44-7.
[75]
Best JD, Carey N. Epigenetic therapies for non-oncology indications. Drug Discov Today 2010; 15(23-24): 1008-14.
120
20
1
2