Epigenetic codes in cognition and behaviour.

doi:10.1016/J.BBR.2008.01.021

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Epigenetic codes in cognition and behaviour.

Journal Article•DOI•

Epigenetic codes in cognition and behaviour.

Johannes Gräff¹, Isabelle M. Mansuy¹•Institutions (1)

École Polytechnique Fédérale de Lausanne¹

01 Sep 2008-Behavioural Brain Research (Elsevier)-Vol. 192, Iss: 1, pp 70-87

TL;DR: Recent findings on the role and mechanisms of epigenetic codes in the brain are described, and their implication in synaptic plasticity, cognitive functions and psychiatric disorders are discussed.

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About: This article is published in Behavioural Brain Research.The article was published on 2008-09-01. It has received 260 citations till now. The article focuses on the topics: Epigenetic code & Epigenetics.

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Journal Article•DOI•

Socioeconomic status and the developing brain

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Daniel A. Hackman¹, Martha J. Farah¹•Institutions (1)

University of Pennsylvania¹

01 Feb 2009-Trends in Cognitive Sciences

TL;DR: These studies indicate that SES is an important predictor of neurocognitive performance, particularly of language and executive function, and that S ES differences are found in neural processing even when performance levels are equal.

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1,258 citations

Journal Article•DOI•

Lasting epigenetic influence of early-life adversity on the BDNF gene.

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Tania L. Roth¹, Farah D. Lubin¹, Adam J. Funk¹, J. David Sweatt¹•Institutions (1)

University of Alabama at Birmingham¹

01 May 2009-Biological Psychiatry

TL;DR: An epigenetic molecular mechanism potentially underlying lifelong and transgenerational perpetuation of changes in gene expression and behavior incited by early abuse and neglect is highlighted.

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1,176 citations

Journal Article•DOI•

Transcription Factors in Long-Term Memory and Synaptic Plasticity

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Cristina M. Alberini¹•Institutions (1)

Icahn School of Medicine at Mount Sinai¹

01 Jan 2009-Physiological Reviews

TL;DR: The results of this work suggest that patterns of transcription regulation represent the molecular signatures of long-term synaptic changes and memory formation.

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Abstract: Transcription is a molecular requisite for long-term synaptic plasticity and long-term memory formation. Thus, in the last several years, one main interest of molecular neuroscience has been the identification of families of transcription factors that are involved in both of these processes. Transcription is a highly regulated process that involves the combined interaction and function of chromatin and many other proteins, some of which are essential for the basal process of transcription, while others control the selective activation or repression of specific genes. These regulated interactions ultimately allow a sophisticated response to multiple environmental conditions, as well as control of spatial and temporal differences in gene expression. Evidence based on correlative changes in expression, genetic mutations, and targeted molecular inhibition of gene expression have shed light on the function of transcription in both synaptic plasticity and memory formation. This review provides a brief overview ...

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902 citations

Cites background from "Epigenetic codes in cognition and b..."

...[From Gräff and Mansuy (82), with permission from Elsevier....
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...[From Gräff and Mansuy (82), with permission from Elsevier.]...
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Journal Article•DOI•

Histone acetylation: molecular mnemonics on the chromatin

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Johannes Gräff¹, Li-Huei Tsai², Li-Huei Tsai¹•Institutions (2)

Massachusetts Institute of Technology¹, Picower Institute for Learning and Memory²

01 Feb 2013-Nature Reviews Neuroscience

TL;DR: As histone acetylation and cognitive functions can be pharmacologically restored by histone deacetylase inhibitors, this epigenetic modification might constitute a molecular memory aid on the chromatin and, by extension, a new template for therapeutic interventions against cognitive frailty.

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Abstract: Long-lasting memories require specific gene expression programmes that are, in part, orchestrated by epigenetic mechanisms. Of the epigenetic modifications identified in cognitive processes, histone acetylation has spurred considerable interest. Whereas increments in histone acetylation have consistently been shown to favour learning and memory, a lack thereof has been causally implicated in cognitive impairments in neurodevelopmental disorders, neurodegeneration and ageing. As histone acetylation and cognitive functions can be pharmacologically restored by histone deacetylase inhibitors, this epigenetic modification might constitute a molecular memory aid on the chromatin and, by extension, a new template for therapeutic interventions against cognitive frailty.

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506 citations

Journal Article•DOI•

Finding the engram.

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Sheena A. Josselyn, Stefan Köhler¹, Paul W. Frankland•Institutions (1)

University of Western Ontario¹

01 Sep 2015-Nature Reviews Neuroscience

TL;DR: This Review develops four defining criteria that enable us to critically assess the recent progress that has been made towards finding the engram, and proposes that findings from 'capture' studies represent considerable progress in allowing us to observe, erase and express the engrams.

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Abstract: Many attempts have been made to localize the physical trace of a memory, or engram, in the brain However, until recently, engrams have remained largely elusive In this Review, we develop four defining criteria that enable us to critically assess the recent progress that has been made towards finding the engram Recent 'capture' studies use novel approaches to tag populations of neurons that are active during memory encoding, thereby allowing these engram-associated neurons to be manipulated at later times We propose that findings from these capture studies represent considerable progress in allowing us to observe, erase and express the engram

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464 citations

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References

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Book•

Epigenetic mechanisms of gene regulation

[...]

V. E. A. Russo, Robert A. Martienssen, Arthur D. Riggs

01 Jan 1996

TL;DR: Historical overview of epigenetic mechanisms DNA methylation paramutation, imprinting and X inactivation repeated genes and gene silencing nuclear organization and chromatin structure transposable elements and viruses.

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Abstract: Historical overview of epigenetic mechanisms DNA methylation paramutation, imprinting and X inactivation repeated genes and gene silencing nuclear organization and chromatin structure transposable elements and viruses. Appendices.

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901 citations

"Epigenetic codes in cognition and b..." refers background in this paper

...[3] Russo VEA, Martienssen RA, Riggs AD, editors....
[...]
...ot be explained by changes in the DNA sequence itself [3] reviewed in [4,5])....
[...]

Journal Article•DOI•

Chromatin acetylation, memory, and LTP are impaired in CBP+/- mice: a model for the cognitive deficit in Rubinstein-Taybi syndrome and its amelioration.

[...]

Juan Marcos Alarcon¹, Gaël Malleret¹, Khalid Touzani¹, Svetlana Vronskaya¹, Shunsuke Ishii, Eric R. Kandel¹, Eric R. Kandel², Angel Barco¹ - Show less +4 more•Institutions (2)

Columbia University¹, Howard Hughes Medical Institute²

24 Jun 2004-Neuron

TL;DR: Some of the cognitive and physiological deficits observed on RTS are not simply due to the reduction of CBP during development but may also result from the continued requirement throughout life for both the CREB co-activation and the histone acetylation function of CBp.

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891 citations

"Epigenetic codes in cognition and b..." refers background in this paper

...Several mouse models with CBP mutations were generated nd confirmed the involvement of CBP in the molecular mechnisms of the disease [39,50,60,61]....
[...]
...[43] Zhao X, Ueba T, Christie BR, Barkho B, McConnell MJ, Nakashima K, et al. Mice lacking methyl-CpG binding protein 1 have deficits in adult neurogenesis and hippocampal function....
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...Mammalian synaptic plasticity The most prominent forms of synaptic plasticity in mamals are long-term potentiation (LTP) and LTD....
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...In mice, an FMR2 deficiency nduced by gene knock-out impairs spatial memory, however, t enhances LTP [74]....
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...Treatment of such slices with he HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) meliorates late-phase LTP. Importantly, a similar effect is bserved in wild-type rats, in which administration of the HDAC nhibitors trichostatin A (TSA) or sodium butyrate enhances the nduction of LTP in the hippocampus [36], suggesting a causal ink between histone acetylation and LTP....
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Journal Article•DOI•

Reversal of Maternal Programming of Stress Responses in Adult Offspring through Methyl Supplementation: Altering Epigenetic Marking Later in Life

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Ian C. G. Weaver, Frances A. Champagne, Shelley E. Brown¹, Sergiy Dymov¹, Shakti Sharma, Michael J. Meaney, Moshe Szyf¹ - Show less +3 more•Institutions (1)

McGill University¹

23 Nov 2005-The Journal of Neuroscience

TL;DR: It is reported that methionine infusion reverses the effect of maternal behavior on DNA methylation, nerve growth factor-inducible protein-A binding to the exon 17 promoter, GR expression, and hypothalamic-pituitary-adrenal and behavioral responses to stress, suggesting a causal relationship among epigenomic state, GRexpression, and stress responses in the adult offspring.

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Abstract: Stress responses in the adult rat are programmed early in life by maternal care and associated with epigenomic marking of the hippocampal exon 17 glucocorticoid receptor (GR) promoter. To examine whether such epigenetic programming is reversible in adult life, we centrally infused the adult offspring with the essential amino acid l-methionine, a precursor to S-adenosyl-methionine that serves as the donor of methyl groups for DNA methylation. Here we report that methionine infusion reverses the effect of maternal behavior on DNA methylation, nerve growth factor-inducible protein-A binding to the exon 17 promoter, GR expression, and hypothalamic-pituitary-adrenal and behavioral responses to stress, suggesting a causal relationship among epigenomic state, GR expression, and stress responses in the adult offspring. These results demonstrate that, despite the inherent stability of the epigenomic marks established early in life through behavioral programming, they are potentially reversible in the adult brain.

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876 citations

"Epigenetic codes in cognition and b..." refers background in this paper

...Likewise, maternal programming of stress esponses via glucocorticoid receptors can be reversed by methyl upplementation via the administration of L-methionine, a SAM recursor [111]....
[...]
...[111] Weaver ICG, Champagne FA, Brown SE, Dymov S, Sharma S, Meaney...
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...Predisposition to stress GR Poor maternal care decreases GR expression through increased DNA methylation SAM precursor l-methionine reverses the maternal care effect on DNA methylation [108,111]...
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Journal Article•DOI•

Suberoylanilide hydroxamic acid, a histone deacetylase inhibitor, ameliorates motor deficits in a mouse model of Huntington's disease

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Emma Hockly, Victoria M. Richon, Benjamin Woodman, Donna L. Smith, Xianbo Zhou, E. Rosa, Kirupa Sathasivam, Shabnam Ghazi-Noori, Amarbirpal Mahal, Philip A. S. Lowden, Joan S. Steffan, J.L. Marsh, Leslie M. Thompson, Cathryn M. Lewis, Paul A. Marks, Gillian P. Bates - Show less +12 more

18 Feb 2003-Proceedings of the National Academy of Sciences of the United States of America

TL;DR: Preclinical trials with suberoylanilide hydroxamic acid (SAHA), a potent HDAC inhibitor, show that SAHA crosses the blood–brain barrier and increases histone acetylation in the brain, clearly validating the pursuit of this class of compounds as HD therapeutics.

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Abstract: Huntington's disease (HD) is an inherited, progressive neurological disorder that is caused by a CAG/polyglutamine repeat expansion and for which there is no effective therapy. Recent evidence indicates that transcriptional dysregulation may contribute to the molecular pathogenesis of this disease. Supporting this view, administration of histone deacetylase (HDAC) inhibitors has been shown to rescue lethality and photoreceptor neurodegeneration in a Drosophila model of polyglutamine disease. To further explore the therapeutic potential of HDAC inhibitors, we have conducted preclinical trials with suberoylanilide hydroxamic acid (SAHA), a potent HDAC inhibitor, in the R6/2 HD mouse model. We show that SAHA crosses the blood-brain barrier and increases histone acetylation in the brain. We found that SAHA could be administered orally in drinking water when complexed with cyclodextrins. SAHA dramatically improved the motor impairment in R6/2 mice, clearly validating the pursuit of this class of compounds as HD therapeutics.

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862 citations

"Epigenetic codes in cognition and b..." refers background in this paper

...[86] Hockly E, Richon VM, Woodman B, Smith DL, Zhou X, Rosa E, et al....
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...In mouse models of HD, the administraion of several types of HDAC inhibitors significantly attenuates otor deficits [85,86] and neuronal atrophy [87], which are ccompanied by increased histone acetylation and decreased istone methylation....
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Journal Article•DOI•

Regulation of histone methylation by demethylimination and demethylation.

[...]

Robert J. Klose¹, Yi Zhang¹•Institutions (1)

University of North Carolina at Chapel Hill¹

07 Mar 2007-Nature Reviews Molecular Cell Biology

TL;DR: The enzymatic and structural basis for the mechanisms that these enzymes use to counteract histone methylation are examined and insights into their substrate specificity and biological function are provided.

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Abstract: Histone methylation has important roles in regulating transcription, genome integrity and epigenetic inheritance. Historically, methylated histone arginine and lysine residues have been considered static modifications because of the low levels of methyl-group turnover in chromatin. The recent identification of enzymes that antagonize or remove histone methylation has changed this view and now the dynamic nature of these modifications is being appreciated. Here, we examine the enzymatic and structural basis for the mechanisms that these enzymes use to counteract histone methylation and provide insights into their substrate specificity and biological function.

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838 citations