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Epigenetic codes in cognition and behaviour.

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TLDR
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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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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Socioeconomic status and the developing brain

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

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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Transcription Factors in Long-Term Memory and Synaptic Plasticity

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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Histone acetylation: molecular mnemonics on the chromatin

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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Finding the engram.

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.
References
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Journal ArticleDOI

Deficiency of methyl-CpG binding protein-2 in CNS neurons results in a Rett-like phenotype in mice

TL;DR: The results indicate that the role of MECp2 is not restricted to the immature brain, but becomes critical in mature neurons, and that Mecp2 deficiency in these neurons is sufficient to cause neuronal dysfunction with symptomatic manifestation similar to Rett syndrome.
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A Transcriptively Active Complex of APP with Fe65 and Histone Acetyltransferase Tip60

TL;DR: It is demonstrated that the cytoplasmic tail of APP forms a multimeric complex with the nuclear adaptor protein Fe65 and the histone acetyltransferase Tip60 that stimulates transcription via heterologous Gal4- or LexA-DNA binding domains, suggesting that release of the cytopsized tail ofAPP by γ-cleavage may function in gene expression.
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Rubinstein-Taybi syndrome caused by mutations in the transcriptional co-activator CBP

TL;DR: It is proposed that the loss of one functional copy of the CBP gene underlies the developmental abnormalities in RTS and possibly the propensity for malignancy.
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Cellular Memory and the Histone Code

TL;DR: Insight is provided into how modification of one residue can influence that of another, even when they are located on different histones, and how modifications at specific genomic locations might be perpetuated on newly assembled chromatin.
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Chromatin Modifications by Methylation and Ubiquitination: Implications in the Regulation of Gene Expression

TL;DR: The recent biochemical, molecular, cellular, and physiological functions of histone methylation and ubiquitination involved in the regulation of gene expression as determined by a combination of enzymological, structural, and genetic methodologies are highlighted.
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