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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Journal Article•DOI•

Covalent Modification of DNA Regulates Memory Formation

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Courtney A. Miller¹, J. David Sweatt¹•Institutions (1)

University of Alabama at Birmingham¹

15 Mar 2007-Neuron

TL;DR: The results demonstrate that DNA methylation is dynamically regulated in the adult nervous system and that this cellular mechanism is a crucial step in memory formation.

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1,100 citations

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

...A more direct link was recently established y the demonstration that contextual fear conditioning is associted with increased methylation and decreased transcription of he memory suppressor gene PP1, and at the same time, with ecreased methylation and increased transcription of reelin, a emory promoting gene [48]....
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...In addition, epigenetic mechanisms nvolving DNA methylation were demonstrated to be dynamic rocesses in the adult brain [48], suggesting that long-term memry traces may be stabilized by a complex and flexible interplay f multiple molecular marks....
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...irs spatial memory Hippocampus Mice [43] 1, a memory eased while memory promoting ntext learning Hippocampus Rats [48]...
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...In ontrast, BDNF expression is significantly upregulated and H4 yperacetylated at BDNF promoter P2 by pilocarpine treatment. lectroconvulsive seizures (ECS) also modulate H4 acetylation n the promoter region of c-Fos, BDNF and CREB genes, and corelate with altered mRNA expression in that H4 hyperacetylation s associated with increased gene expression and vice versa [45]. owever, there is no clear correlation for H3 acetylation on K9 or 14, or for the combined phosphorylation/acetylation of Ser10 nd K14, suggesting a general role for H4 acetylation but a more Brain area Organism References ces LTP Hippocampus Mice [43] ctivity blocks LTP Hippocampus Mice [42] irs spatial memory Hippocampus Mice [43] 1, a memory eased while memory promoting ntext learning Hippocampus Rats [48] 4K8 acetylation on AT CBP Sensory-motor neurons Aplysia [29] ion is accompanied tion Hippocampus Rats [36] X repressor group of y is accompanied by Hippocampus Mice [38] in H2B e-phase LTP Hippocampus Mice [39] Bdnf, H4 R2 observed in acute cetylation only in Hippocampus Rats [44,45] APK is regulating in novel taste Insular cortex Mice [49] loinsufficiency Hippocampus and forebrain Mice [39,50] spatial memory Hippocampus Mice [51] creased by spatial Hippocampus Rats [36] Bdnf promoters is d fear Prefrontal cortex Mice [55] is regulated by the nd increased upon ning Hippocampus Rats [53] g protein; C/EBP, CCAAT/enhancer binding protein; DNMT1, DNA methyl HAT, histone acetyl transferase; LTF, long-term facilitation; LTP, long-term protein 1; NMDA, N-methyl d-aspartate; PP1, protein phosphatase 1....
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...It took, howver, another 8 years until DNA methylation was found to be a ynamic process in the brain that is critical for memory foration [48]....
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Journal Article•DOI•

Methylation of Lysine 4 on Histone H3: Intricacy of Writing and Reading a Single Epigenetic Mark

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Alexander J. Ruthenburg¹, C. David Allis¹, Joanna Wysocka²•Institutions (2)

Rockefeller University¹, Stanford University²

12 Jan 2007-Molecular Cell

TL;DR: It is hypothesize how the unique properties of the polyvalent chromatin fiber and associated effectors may amplify small differences in methyl-lysine recognition, simultaneously allowing for a dynamic chromatin architecture.

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1,093 citations

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

...[23] Ruthenburg AJ, Allis CD, Wysocka J....
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...These rosstalks can enhance chromatin condensation when trancriptional silence is required, or chromatin opening when ranscriptional activity is needed [22,23]....
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Journal Article•DOI•

The neuronal MAP kinase cascade : A biochemical signal integration system subserving synaptic plasticity and memory

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J. D. Sweatt¹•Institutions (1)

Baylor College of Medicine¹

10 Oct 2008-Journal of Neurochemistry

TL;DR: The mitogen-activated protein kinase (MAP kinase, MAPK) cascade was originally discovered as a critical regulator of cell division and differentiation as mentioned in this paper, and it became clear that the MAPK cascade is in fact a prototype for a family of signaling cascades that share the motif of three serially linked kinases regulating each other by sequential phosphorylation.

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Abstract: The mitogen-activated protein kinase (MAP kinase, MAPK) cascade, as the name implies, was originally discovered as a critical regulator of cell division and differentiation. As further details of this signaling cascade were worked out, it became clear that the MAPK cascade is in fact a prototype for a family of signaling cascades that share the motif of three serially linked kinases regulating each other by sequential phosphorylation. Thus, a revised nomenclature arose that uses the term MAPK to refer to the entire superfamily of signaling cascades (comprising the erks, the JNKs and the p38 stress activated protein kinases), and specifies the prototype MAPK as the extracellular signal-regulated kinase (erk). The two erk MAPK isoforms, p44 MAPK and p42 MAPK, are referred to as erk1 and erk2, respectively. The erks are abundantly expressed in neurons in the mature central nervous system, raising the question of why the prototype molecular regulators of cell division and differentiation are present in these non-dividing, terminally differentiated neurons. This review will describe the beginnings of an answer to this question. Interestingly, the general model has begun to emerge that the erk signaling system has been co-opted in mature neurons to function in synaptic plasticity and memory. Moreover, recent insights have led to the intriguing prospect that these molecules serve as biochemical signal integrators and molecular coincidence detectors for coordinating responses to extracellular signals in neurons. In this review I will first outline the essential components of this signal transduction cascade, and briefly describe recent results implicating the erks in mammalian synaptic plasticity and learning. I will then proceed to outline recent results implicating the erks as molecular signal integrators and, potentially, coincidence detectors. Finally, I will speculate on what the critical downstream effectors of the erks are in neurons, and how they might provide a readout of the integrated signal.

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1,086 citations

Journal Article•DOI•

Inherited epigenetic variation--revisiting soft inheritance.

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Eric J. Richards¹•Institutions (1)

Washington University in St. Louis¹

01 May 2006-Nature Reviews Genetics

TL;DR: The line between these two components is blurred by inherited epigenetic variation, which is potentially sensitive to environmental inputs.

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Abstract: A growing body of evidence indicates that epigenetic states can be influenced by the environment. Considering that erasure of epigenetic marks between generations is not universal among multicellular organisms, what are the potential implications of inherited epigenetic variation for current theories of inheritance and evolutionary change? Phenotypic variation is traditionally parsed into components that are directed by genetic and environmental variation. The line between these two components is blurred by inherited epigenetic variation, which is potentially sensitive to environmental inputs. Chromatin and DNA methylation-based mechanisms mediate a semi-independent epigenetic inheritance system at the interface between genetic control and the environment. Should the existence of inherited epigenetic variation alter our thinking about evolutionary change?

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1,071 citations

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

...This has been referred to as “soft inheritance” [117] and references therein) and can reflect an adaptive or pathological process....
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...see [117] and references therein), both of which can be altered y environmental factors (Fig....
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Journal Article•DOI•

Regulation of histone acetylation during memory formation in the hippocampus.

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Jonathan M. Levenson¹, Kenneth J. O’Riordan¹, Karen D. Brown¹, Mimi A. Trinh¹, David L. Molfese¹, J. David Sweatt¹ - Show less +2 more•Institutions (1)

Baylor College of Medicine¹

24 Sep 2004-Journal of Biological Chemistry

TL;DR: Results indicate that histone-associated heterochromatin undergoes changes in structure during the formation of long term memory, which enhances a cellular process thought to underlie longterm memory formation, hippocampal long term potentiation, and memory formation itself.

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1,071 citations

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

...[36] Levenson JM, O’Riordan KJ, Brown KD, Trinh MA, Molfese DL, Sweatt...
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...Intriguingly, 3 acetylation remains unchanged after latent inhibition, a ehavioural test based on the inhibition of conditioning, whereas 4 acetylation (on several residues) is increased [36]....
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...Activation of the MAPK cascade was also reported o increase H3K14 acetylation during memory formation [36], ointing to a role for the MAPK cascade in the epigenetic egulation of histones, in addition to its classical functions in euronal signaling....
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...ion is accompanied tion Hippocampus Rats [36]...
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...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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