Epigenetics and the nervous system

Mehler, Mark F.

doi:10.1002/ana.21595

Cited by 87 publications

(49 citation statements)

References 188 publications

(420 reference statements)

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“…These mechanisms suppress expression of genes by the methylation of DNA or acetylation of the proteins (histones) that cover the DNA molecule (Mehler 2008). Epigenetic modifications are important in neural development, (Fagiolini et al 2009;Mathers and McKay 2009;O'Shea 2001) neural function, and plasticity (Borrelli et al 2008;Covic et al 2010;Day and Sweatt 2011;Levenson and Sweatt 2005;Lubin 2011;Lubin et al 2011;Puckett and Lubin 2011) as well as in neuropathology (Denk and McMahon 2012;Feinberg 2007;Hwang et al 2013;Lee and Ryu 2010;Qureshi and Mehler 2010;Smith 2011;Tsankova et al 2007).…”

Section: Asd and Developmental Mechanismsmentioning

confidence: 98%

Autism, Development and Neural Plasticity

Robinson-Agramonte

Fraguela

Bergado-Rosado

2015

Translational Approaches to Autism Spectrum Disorder

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In this chapter, we show evidences derived from carefully designed animal experiments and clinical data, supporting a role of neuroplasticty on the development and physiopathology of autism. Although the exact mode in which genetic and environmental factors interact in various psychiatric conditions, including autism remains largely unclear, a comprehensive understanding of these complex interactions, including the contribution of immune molecules, in the establishment of neuronal connectivity that may drive into phenotypes of autism spectrum disorder (ASD) is of the greatest importance to understand its causes and develop successful strategies to treat and revert its consequences. Available evidence strongly supports the involvement of maladaptive neuroplasticity, mutations, epigenetic modification, and individual miRNA-related pathways in the pathogenesis and pathophysiology of the complex clinical phenotypes that is included in ASD.

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Section: Asd and Developmental Mechanismsmentioning

confidence: 98%

Autism, Development and Neural Plasticity

Robinson-Agramonte

Fraguela

Bergado-Rosado

2015

Translational Approaches to Autism Spectrum Disorder

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“…In the central nervous system (CNS), epigenetic mechanisms such as DNA methylation and histone modification has been shown to be important for brain development, cellular migration, neural stem cell maintenance, proliferation, neurogenesis, gliogenesis, and synaptic and neural network connectivity (Mehler 2008). Although these epigenetic processes have been considered to be important in the pathogenesis of epilepsy, most studies have focused on histone modification (Huang et al 2002;Phiel et al 2001;Sng et al 2006;Tsankova et al 2004), and the function of DNA methylation in epileptogenesis is unclear.…”

Section: Introductionmentioning

confidence: 99%

Increased Expression of DNA methyltransferase 1 and 3a in Human Temporal Lobe Epilepsy

et al. 2011

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DNA methylation is a key epigenetic modification of DNA that is catalyzed by DNA methyltransferase (DNMT). Increasing evidence suggests that DNA methylation in neurons regulates synaptic plasticity as well as neuronal network activity. Here, we evaluated DNA methyltransferase 1 (Dnmt1) and Dnmt3a expression in brain tissues of epileptic patients to explore their possible role in epileptogenesis. Tissue samples from temporal neocortices of 25 patients with intractable temporal lobe epilepsy (TLE) and ten histologically normal temporal lobes from control patients were used to detect Dnmt1 and Dnmt3a expression through immunohistochemistry, immunofluorescence, and Western blotting analysis. We found that both Dnmt1 and Dnmt3a expression were principally expressed in the nucleus and the cytoplasm of NeuN-positive neurons, but not in GFAP-positive astrocytes. Levels of the two DNMT proteins were significantly increased in patients with TLE. Our study suggests that DNMT1 and DNMT3a may play a role in the pathogenesis of TLE.

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“…Histone deacetylase inhibitors (HDACi) have therefore opened a new field of promising treatment alternatives primarily for elderly patients who do not qualify for intensive cancer chemotherapy regimens (5). Recently, the use of HDACi was also considered in children and non-oncologic chronic diseases (6,7).…”

Section: Introductionmentioning

confidence: 99%

HDAC inhibition radiosensitizes human normal tissue cells and reduces DNA double-strand break repair capacity

Purrucker

Fricke²,

Ong³

et al. 2009

Oncol Rep

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Abstract. HDAC inhibitors (HDACi) are gaining increasing attention in the treatment of cancer, particularly in view of their therapeutic effectiveness and assumed mild toxicity profile. While numerous studies have investigated the role of HDACi in tumor cells, little is known about their effects on normal tissue cells. We studied the effect of suberoylanilide hydroxamic acid (SAHA), MS275, sodium-butyrate and valproic acid in healthy human fibroblasts and found HDACi-treatment to go along with increased radiosensitivity and reduced DSB repair capacity. In view of the potential genotoxic effects of HDACi-treatment, particularly when being administered long-term for chronic disease or when given to children, to women of childbearing age or their partners or in combination with radiotherapy, an extensive education of patients and prescribing physicians as well as a stringent definition of clinical indications is urgently required.

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Epigenetics and the nervous system

Cited by 87 publications

References 188 publications

Autism, Development and Neural Plasticity

Autism, Development and Neural Plasticity

Increased Expression of DNA methyltransferase 1 and 3a in Human Temporal Lobe Epilepsy

HDAC inhibition radiosensitizes human normal tissue cells and reduces DNA double-strand break repair capacity

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