Histone-acetylation: a link between Alzheimer's disease and post-traumatic stress disorder?

Bahari‐Javan, Sanaz; Sananbenesi, Farahnaz; Fischer, André

doi:10.3389/fnins.2014.00160

Cited by 38 publications

(28 citation statements)

References 87 publications

(113 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Class I HDACs HDAC 2 and 3 [185,188,[195][196][197] and Class II HDACs HDAC 5 [198] and 6 [188,195,197] could be potential targets for improving cognition in neuropsychiatric disorders. HDAC 1 appears to have inconsistent effects on cognition [184,188,195,[198][199][200] . Representative HDAC inhibitors that have effects on cognition in preclinical and/or clinical studies for a variety of neuropsychiatric disorders are summarized in Table 2.…”

Section: Hdac and Dnmt Inhibitors For The Treatment Of Cognitive Defementioning

confidence: 99%

GABAergic inhibitory neurons as therapeutic targets for cognitive impairment in schizophrenia

Wong

2018

Acta Pharmacol Sin

102

View full text Add to dashboard Cite

Schizophrenia is considered primarily as a cognitive disorder. However, functional outcomes in schizophrenia are limited by the lack of effective pharmacological and psychosocial interventions for cognitive impairment. GABA (gamma-aminobutyric acid) interneurons are the main inhibitory neurons in the central nervous system (CNS), and they play a critical role in a variety of pathophysiological processes including modulation of cortical and hippocampal neural circuitry and activity, cognitive function-related neural oscillations (eg, gamma oscillations) and information integration and processing. Dysfunctional GABA interneuron activity can disrupt the excitatory/inhibitory (E/I) balance in the cortex, which could represent a core pathophysiological mechanism underlying cognitive dysfunction in schizophrenia. Recent research suggests that selective modulation of the GABAergic system is a promising intervention for the treatment of schizophrenia-associated cognitive defects. In this review, we summarized evidence from postmortem and animal studies for abnormal GABAergic neurotransmission in schizophrenia, and how altered GABA interneurons could disrupt neuronal oscillations. Next, we systemically reviewed a variety of up-to-date subtype-selective agonists, antagonists, positive and negative allosteric modulators (including dual allosteric modulators) for α5/α3/α2 GABA and GABA receptors, and summarized their pro-cognitive effects in animal behavioral tests and clinical trials. Finally, we also discuss various representative histone deacetylases (HDAC) inhibitors that target GABA system through epigenetic modulations, GABA prodrug and presynaptic GABA transporter inhibitors. This review provides important information on current potential GABA-associated therapies and future insights for development of more effective treatments.

show abstract

Section: Hdac and Dnmt Inhibitors For The Treatment Of Cognitive Defementioning

confidence: 99%

GABAergic inhibitory neurons as therapeutic targets for cognitive impairment in schizophrenia

Wong

2018

Acta Pharmacol Sin

102

View full text Add to dashboard Cite

show abstract

“…Increasing evidence has demonstrated the critical role of histone acetylation/deacetylation in gene transcription (1,2). Histone acetylation mediated by histone acetyltransferases promotes an open chromatin formation, which provides binding sites for basal transcription factors and RNA polymerase II to facilitate gene transcription.…”

Section: Introductionmentioning

confidence: 99%

Sirtuin 1: A Target for Kidney Diseases

Kong

Zhou

et al. 2015

Mol Med

View full text Add to dashboard Cite

Sirtuin 1 (SIRT1) is an evolutionarily conserved NAD + -dependent histone deacetylase that is necessary for caloric restriction-related lifespan extension. SIRT1, as an intracellular energy sensor, detects the concentration of intracellular NAD + and uses this information to adapt cellular energy output to cellular energy requirements. Previous studies on SIRT1 have confirmed its beneficial effects on cellular immunity to oxidative stress, reduction of fibrosis, suppression of inflammation, inhibition of apoptosis, regulation of metabolism, induction of autophagy and regulation of blood pressure. All of the above biological processes are involved in the pathogenesis of kidney diseases. Therefore, the activation of SIRT1 may become a therapeutic target to improve the clinical outcome of kidney diseases. In this review, we give an overview of SIRT1 and its molecular targets as well as SIRT1-modulated biological processes, with a particular focus on the role of SIRT1 in kidney diseases.

show abstract

“…A large number of genetic and environmental factors impacting within the extended (prenatal to young adult) period of brain development result in cognitive and behavioural deficits only at much later periods. Unsurprisingly, therefore, considerable time and effort has been invested exploring long-term adaptations of neuronal and glial transcriptomes and epigenomes in a wide range of disease models 1 2 3 4 . However, functional neurogenomics faces a key limitation, owing to the fact that, to date, even the most powerful genome-scale assays for chromatin modifications (chromatin immunoprecipitation (ChIP) sequencing), transcription (RNA sequencing) or chromosomal conformations (Hi-C) essentially provide only a single snapshot of genome organization and function at the time of tissue harvest.…”

mentioning

confidence: 99%

Longitudinal assessment of neuronal 3D genomes in mouse prefrontal cortex

et al. 2016

View full text Add to dashboard Cite

Neuronal epigenomes, including chromosomal loopings moving distal cis-regulatory elements into proximity of target genes, could serve as molecular proxy linking present-day-behaviour to past exposures. However, longitudinal assessment of chromatin state is challenging, because conventional chromosome conformation capture assays essentially provide single snapshots at a given time point, thus reflecting genome organization at the time of brain harvest and therefore are non-informative about the past. Here we introduce ‘NeuroDam' to assess epigenome status retrospectively. Short-term expression of the bacterial DNA adenine methyltransferase Dam, tethered to the Gad1 gene promoter in mouse prefrontal cortex neurons, results in stable GmethylATC tags at Gad1-bound chromosomal contacts. We show by NeuroDam that mice with defective cognition 4 months after pharmacological NMDA receptor blockade already were affected by disrupted chromosomal conformations shortly after drug exposure. Retrospective profiling of neuronal epigenomes is likely to illuminate epigenetic determinants of normal and diseased brain development in longitudinal context.

show abstract

Histone-acetylation: a link between Alzheimer's disease and post-traumatic stress disorder?

Cited by 38 publications

References 87 publications

GABAergic inhibitory neurons as therapeutic targets for cognitive impairment in schizophrenia

GABAergic inhibitory neurons as therapeutic targets for cognitive impairment in schizophrenia

Sirtuin 1: A Target for Kidney Diseases

Longitudinal assessment of neuronal 3D genomes in mouse prefrontal cortex

Contact Info

Product

Resources

About