Differential Histone Deacetylase mRNA Expression Patterns in Amyotrophic Lateral Sclerosis

Janssen, C.; Schmalbach, Sonja; Boeselt, Sebastian; Sarlette, Alexander; Dengler, Reinhard; Petri, Susanne

doi:10.1097/nen.0b013e3181ddd404

Cited by 92 publications

(76 citation statements)

References 45 publications

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“…18 In amyotrophic lateral sclerosis patients, HDAC2 levels in the motor cortex and spinal cord are elevated. 44 Other studies have shown that HDAC2 negatively regulates synaptic plasticity, spine density, learning, and memory formation. 18 Loss of memory due to the activation and/or overexpression of HDAC2 has been restored by treatment with HDAC inhibitors like sodium valproate, sodium butyrate, and Vorinostat in an animal model of Alzheimer's disease.…”

Section: Discussionmentioning

confidence: 99%

Inhibition of HDAC2 Protects the Retina From Ischemic Injury

Fan

Alsarraf

Dahrouj

et al. 2013

Invest. Ophthalmol. Vis. Sci.

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Section: Discussionmentioning

confidence: 99%

Inhibition of HDAC2 Protects the Retina From Ischemic Injury

Fan

Alsarraf

Dahrouj

et al. 2013

Invest. Ophthalmol. Vis. Sci.

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“…A gene expression profile analysis performed on laser microdissected degenerating motor neurons from sporadic ALS patients revealed the down-regulation of the cbp gene [120]. A comparison of HDAC expression revealed a reduction of HDAC 11 mRNA and increased HDAC 2 levels in postmortem ALS brain and spinal cord specimens [121]. Mouse models bearing a SOD1 mutation have been used to test therapeutic strategies with HDACi.…”

Section: Alsmentioning

confidence: 99%

Acetyltransferases (HATs) as Targets for Neurological Therapeutics

et al. 2013

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The acetylation of histone and non-histone proteins controls a great deal of cellular functions, thereby affecting the entire organism, including the brain. Acetylation modifications are mediated through histone acetyltransferases (HAT) and deacetylases (HDAC), and the balance of these enzymes regulates neuronal homeostasis, maintaining the pre-existing acetyl marks responsible for the global chromatin structure, as well as regulating specific dynamic acetyl marks that respond to changes and facilitate neurons to encode and strengthen longterm events in the brain circuitry (e.g., memory formation). Unfortunately, the dysfunction of these finely-tuned regulations might lead to pathological conditions, and the deregulation of the HAT/HDAC balance has been implicated in neurological disorders. During the last decade, research has focused on HDAC inhibitors that induce a histone hyperacetylated state to compensate acetylation deficits. The use of these inhibitors as a therapeutic option was efficient in several animal models of neurological disorders. The elaboration of new cell-permeant HAT activators opens a new era of research on acetylation regulation. Although pathological animal models have not been tested yet, HAT activator molecules have already proven to be beneficial in ameliorating brain functions associated with learning and memory, and adult neurogenesis in wild-type animals. Thus, HAT activator molecules contribute to an exciting area of research.

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“…A recent human post mortem study provided further evidence for a deregulation of histone acetylation in ALS. Comparing the protein expression levels of all class I, II, and IV HDACs in the ALS brain and spinal cord, HDAC2 and HDAC11 were up-and downregulated, respectively (149). The functional consequences in terms of histone acetylation changes and resulting gene expression changes remain, however, unclear.…”

Section: Amyotrophic Lateral Sclerosismentioning

confidence: 99%

Epigenetic Regulation of Gene Expression in Physiological and Pathological Brain Processes

Gräff

Kim

Dobbin

et al. 2011

Physiological Reviews

323

246

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Over the past decade, it has become increasingly obvious that epigenetic mechanisms are an integral part of a multitude of brain functions that range from the development of the nervous system over basic neuronal functions to higher order cognitive processes. At the same time, a substantial body of evidence has surfaced indicating that several neurodevelopmental, neurodegenerative, and neuropsychiatric disorders are in part caused by aberrant epigenetic modifications. Because of their inherent plasticity, such pathological epigenetic modifications are readily amenable to pharmacological interventions and have thus raised justified hopes that the epigenetic machinery provides a powerful new platform for therapeutic approaches against these diseases. In this review, we give a detailed overview of the implication of epigenetic mechanisms in both physiological and pathological brain processes and summarize the state-of-the-art of “epigenetic medicine” where applicable. Despite, or because of, these new and exciting findings, it is becoming apparent that the epigenetic machinery in the brain is highly complex and intertwined, which underscores the need for more refined studies to disentangle brain-region and cell-type specific epigenetic codes in a given environmental condition. Clearly, the brain contains an epigenetic “hotspot” with a unique potential to not only better understand its most complex functions, but also to treat its most vicious diseases.

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Differential Histone Deacetylase mRNA Expression Patterns in Amyotrophic Lateral Sclerosis

Cited by 92 publications

References 45 publications

Inhibition of HDAC2 Protects the Retina From Ischemic Injury

Inhibition of HDAC2 Protects the Retina From Ischemic Injury

Acetyltransferases (HATs) as Targets for Neurological Therapeutics

Epigenetic Regulation of Gene Expression in Physiological and Pathological Brain Processes

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