Abstract：
:The rapidly emerging science of epigenetics and epigenomic medicine promises to reveal novel insights into the susceptibility to and the onset and progression of epileptic disorders. Epigenetic regulatory mechanisms are now implicated in orchestrating aspects of neural development (e.g., cell fate specification and maturation), homeostasis and stress responses (e.g., immediate early gene transcription), and neural network function (e.g., excitation-inhibition coupling and activity-dependent plasticity). These same neurobiological processes are responsible for determining the heterogeneous features of complex epileptic disease states. Thus, we highlight recent evidence that is beginning to elucidate the specific roles played by epigenetic mechanisms, including DNA methylation, histone code modifications and chromatin remodeling, noncoding RNAs and RNA editing, in human epilepsy syndromes and in the process of epileptogenesis. The highly integrated layers of the epigenome are responsible for the cell type specific and exquisitely environmentally responsive deployment of genes and functional gene networks that underlie the molecular pathophysiology of epilepsy and its associated comorbidities, including but not limited to neurotransmitter receptors (e.g., GluR2, GLRA2, and GLRA3), growth factors (e.g., BDNF), extracellular matrix proteins (e.g., RELN), and diverse transcriptional regulators (e.g., CREB, c-fos, and c-jun). These important observations suggest that future epigenetic studies are necessary to better understand, classify, prevent, and treat epileptic disorders.
journal_name
Neurobiol Disjournal_title
Neurobiology of diseaseauthors
Qureshi IA,Mehler MFdoi
10.1016/j.nbd.2010.02.005subject
Has Abstractpub_date
2010-07-01 00:00:00pages
53-60issue
1eissn
0969-9961issn
1095-953Xpii
S0969-9961(10)00052-5journal_volume
39pub_type
杂志文章,评审abstract：:Giliosis is a hallmark of prion disease. A neurotoxic prion peptide (PrP106-126) induces astrocyte proliferation in the presence of microglia. This peptide also directly enhances microglial proliferation in culture. We have investigated this further to understand the method by which factors released by microglia and P...
journal_title：Neurobiology of disease
pub_type： 杂志文章
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abstract：:The central nervous system is protected by barriers which control the entry of compounds into the brain, thereby regulating brain homeostasis. The blood-brain barrier, formed by the endothelial cells of the brain capillaries, restricts access to brain cells of blood-borne compounds and facilitates nutrients essential ...
journal_title：Neurobiology of disease
pub_type： 杂志文章,评审
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abstract：:Amyloid-beta (Abeta) accumulation in senile plaques is a hallmark of Alzheimer's disease (AD). Immunotherapy is a leading approach for amyloid clearance, despite the early termination of the Elan clinical trial with active immunization due to a few cases of meningoencephalitis. The mechanisms of immunotherapy-mediated...
journal_title：Neurobiology of disease
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journal_title：Neurobiology of disease
pub_type： 杂志文章
doi：10.1016/j.nbd.2008.05.015
更新日期：2008-09-01 00:00:00
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journal_title：Neurobiology of disease
pub_type： 杂志文章
doi：10.1016/j.nbd.2005.03.014
更新日期：2005-11-01 00:00:00
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journal_title：Neurobiology of disease
pub_type： 杂志文章
doi：10.1016/j.nbd.2005.01.021
更新日期：2005-08-01 00:00:00
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journal_title：Neurobiology of disease
pub_type： 杂志文章
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更新日期：2002-08-01 00:00:00
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journal_title：Neurobiology of disease
pub_type： 杂志文章
doi：10.1016/j.nbd.2012.01.002
更新日期：2012-04-01 00:00:00
abstract：:Prion diseases are disorders of protein conformation that produce neurodegeneration in humans and animals. Studies of transgenic (Tg) mice indicate that a factor designated protein X is involved in the conversion of the normal cellular prion protein (PrPC) into the scrapie isoform (PrPSc); protein X appears to interac...
journal_title：Neurobiology of disease
pub_type： 杂志文章
doi：10.1006/nbdi.1997.0130
更新日期：1997-01-01 00:00:00
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journal_title：Neurobiology of disease
pub_type： 杂志文章,评审
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更新日期：2020-01-01 00:00:00
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journal_title：Neurobiology of disease
pub_type： 杂志文章,评审
doi：10.1006/nbdi.2000.0305
更新日期：2000-06-01 00:00:00
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journal_title：Neurobiology of disease
pub_type： 杂志文章
doi：10.1016/j.nbd.2011.06.003
更新日期：2011-10-01 00:00:00
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journal_title：Neurobiology of disease
pub_type： 杂志文章
doi：10.1016/j.nbd.2018.05.008
更新日期：2018-09-01 00:00:00
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journal_title：Neurobiology of disease
pub_type： 杂志文章
doi：10.1016/j.nbd.2005.01.029
更新日期：2005-08-01 00:00:00
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journal_title：Neurobiology of disease
pub_type： 杂志文章,评审
doi：10.1016/j.nbd.2016.07.022
更新日期：2016-11-01 00:00:00
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journal_title：Neurobiology of disease
pub_type： 杂志文章
doi：10.1016/j.nbd.2006.11.003
更新日期：2007-03-01 00:00:00
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journal_title：Neurobiology of disease
pub_type： 杂志文章
doi：10.1016/j.nbd.2010.11.008
更新日期：2011-03-01 00:00:00
abstract：:Several neurodegenerative diseases like Huntington's, a polyglutamine (PolyQ) disease, are initiated by protein aggregation in neurons. Furthermore, these diseases are also associated with a multitude of responses in non-neuronal cells in the brain, in particular glial cells, like astrocytes. These non-neuronal respon...
journal_title：Neurobiology of disease
pub_type： 杂志文章
doi：10.1016/j.nbd.2018.10.017
更新日期：2019-04-01 00:00:00
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journal_title：Neurobiology of disease
pub_type： 杂志文章,评审
doi：10.1016/j.nbd.2014.08.029
更新日期：2015-11-01 00:00:00
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journal_title：Neurobiology of disease
pub_type： 杂志文章
doi：10.1016/j.nbd.2011.03.006
更新日期：2011-06-01 00:00:00
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journal_title：Neurobiology of disease
pub_type： 杂志文章
doi：10.1016/j.nbd.2004.09.018
更新日期：2005-02-01 00:00:00
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journal_title：Neurobiology of disease
pub_type： 杂志文章
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更新日期：2016-09-01 00:00:00
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journal_title：Neurobiology of disease
pub_type： 杂志文章
doi：10.1016/j.nbd.2016.07.005
更新日期：2016-11-01 00:00:00
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journal_title：Neurobiology of disease
pub_type： 杂志文章
doi：10.1016/j.nbd.2017.09.009
更新日期：2018-01-01 00:00:00
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journal_title：Neurobiology of disease
pub_type： 杂志文章
doi：10.1016/j.nbd.2019.104627
更新日期：2020-02-01 00:00:00
abstract：:Seizures occur in the basal ganglia (BG) of epileptic patients and in animal models of epilepsy, but there is relatively little known about how these events are gated and/or propagated through this structure. Here, we present and characterize a model of in vitro seizure-like events (SLEs) in the striatum by applying c...
journal_title：Neurobiology of disease
pub_type： 杂志文章
doi：10.1016/j.nbd.2012.11.019
更新日期：2013-04-01 00:00:00
abstract：:The epsilon4 allele of the apolipoprotein E gene (APOE) is associated with sporadic and familial late-onset Alzheimer's disease (AD). Oxidative stress is believed to play an important role in neuronal dysfunction and cell death in AD. We now provide evidence that in the hippocampus of AD, the level of thiobarbituric a...
journal_title：Neurobiology of disease
pub_type： 杂志文章
doi：10.1006/nbdi.1999.0273
更新日期：2000-02-01 00:00:00
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journal_title：Neurobiology of disease
pub_type： 杂志文章
doi：10.1016/j.nbd.2020.105152
更新日期：2021-01-01 00:00:00
abstract：:We identified a novel spontaneous mutant mouse showing motor symptoms that are similar to those of the dystonia musculorum (dt) mouse. The observations suggested that the mutant mice inherited the mild dt phenotype as an autosomal recessive trait. Linkage analysis showed that the causative gene was located near D1Mit3...
journal_title：Neurobiology of disease
pub_type： 杂志文章
doi：10.1016/j.nbd.2016.09.016
更新日期：2016-12-01 00:00:00
abstract：:Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by motor neuron death. A 20% of familial ALS cases are associated with mutations in the gene coding for superoxide dismutase 1 (SOD1). The accumulation of abnormal aggregates of different proteins is a common feature in motor neurons of p...
journal_title：Neurobiology of disease
pub_type： 杂志文章
doi：10.1016/j.nbd.2019.104497
更新日期：2019-10-01 00:00:00
