The epigenetic bottleneck of neurodegenerative and psychiatric diseases
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Farahnaz Sananbenesi
Abstract
The orchestrated expression of genes is essential for the development and survival of every organism. In addition to the role of transcription factors, the availability of genes for transcription is controlled by a series of proteins that regulate epigenetic chromatin remodeling. The two most studied epigenetic phenomena are DNA methylation and histone-tail modifications. Although a large body of literature implicates the deregulation of histone acetylation and DNA methylation with the pathogenesis of cancer, recently epigenetic mechanisms have also gained much attention in the neuroscientific community. In fact, a new field of research is rapidly emerging and there is now accumulating evidence that the molecular machinery that regulates histone acetylation and DNA methylation is intimately involved in synaptic plasticity and is essential for learning and memory. Importantly, dysfunction of epigenetic gene expression in the brain might be involved in neurodegenerative and psychiatric diseases. In particular, it was found that inhibition of histone deacetylases attenuates synaptic and neuronal loss in animal models for various neurodegenerative diseases and improves cognitive function. In this article, we will summarize recent data in the novel field of neuroepigenetics and discuss the question why epigenetic strategies are suitable therapeutic approaches for the treatment of brain diseases.
©2009 by Walter de Gruyter Berlin New York
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- Mechanistic insights in light-induced cAMP production by photoactivated adenylyl cyclase alpha (PACα)
- Balance of power – dynamic regulation of chromatin in plant development
- Ultrafast memory loss and relaxation processes in hydrogen-bonded systems
- Memory and neural networks on the basis of color centers in solids
- Dissection of gene regulatory networks in embryonic stem cells by means of high-throughput sequencing
- The epigenetic bottleneck of neurodegenerative and psychiatric diseases
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- Mechanism of activation of Saccharomyces cerevisiae calcineurin by Mn2+
- Structural analysis of the choline-binding protein ChoX in a semi-closed and ligand-free conformation
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Articles in the same Issue
- Editorial
- Highlight: Molecular and Cellular Mechanisms of Memory
- Highlight: 60th Mosbach Colloquium of the GBM ‘Molecular and Cellular Mechanisms of Memory’
- Protein carboxyl methylation and the biochemistry of memory
- Chemotaxis: how bacteria use memory
- Mechanistic insights in light-induced cAMP production by photoactivated adenylyl cyclase alpha (PACα)
- Balance of power – dynamic regulation of chromatin in plant development
- Ultrafast memory loss and relaxation processes in hydrogen-bonded systems
- Memory and neural networks on the basis of color centers in solids
- Dissection of gene regulatory networks in embryonic stem cells by means of high-throughput sequencing
- The epigenetic bottleneck of neurodegenerative and psychiatric diseases
- Protein Structure and Function
- Mechanism of activation of Saccharomyces cerevisiae calcineurin by Mn2+
- Structural analysis of the choline-binding protein ChoX in a semi-closed and ligand-free conformation
- Plasmodium falciparum glyoxalase II: Theorell-Chance product inhibition patterns, rate-limiting substrate binding via Arg257/Lys260, and unmasking of acid-base catalysis
- Genes and Nucleic Acids
- CA/C1 peptidases of the malaria parasites Plasmodium falciparum and P. berghei and their mammalian hosts – a bioinformatical analysis
- Proteolysis
- Placental expression of proteases and their inhibitors in patients with HELLP syndrome
- Irreversible inhibition of human cathepsins B, L, S and K by hypervalent tellurium compounds
