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Transcriptional Regulators as Targets for Alcohol Pharmacotherapies

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The Neuropharmacology of Alcohol

Part of the book series: Handbook of Experimental Pharmacology ((HEP,volume 248))

Abstract

Alcohol use disorder (AUD) is a chronic relapsing brain disease that currently afflicts over 15 million adults in the United States. Despite its prevalence, there are only three FDA-approved medications for AUD treatment, all of which show limited efficacy. Because of their ability to alter expression of a large number of genes, often with great cell-type and brain-region specificity, transcription factors and epigenetic modifiers serve as promising new targets for the development of AUD treatments aimed at the neural circuitry that underlies chronic alcohol abuse. In this chapter, we will discuss transcriptional regulators that can be targeted pharmacologically and have shown some efficacy in attenuating alcohol consumption when targeted. Specifically, the transcription factors cyclic AMP-responsive element binding protein (CREB), peroxisome proliferator-activated receptors (PPARs), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), and glucocorticoid receptor (GR), as well as the epigenetic enzymes, the DNA methyltransferases (DNMTs) and histone deacetylases (HDACs), will be discussed.

The original version of this chapter was revised. A correction to this chapter is available at https://doi.org/10.1007/164_2018_194.

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Change history

  • 29 January 2019

    Figure 1 was published incorrectly in this chapter. The original chapter was corrected.

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Acknowledgements

A.W.L. is supported by the National Institute on Alcohol Abuse and Alcoholism (INIA U01 AA020912 and the Center for Alcohol Research in Epigenetics P50 AA022538).

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Correspondence to Amy W. Lasek .

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Savarese, A.M., Lasek, A.W. (2018). Transcriptional Regulators as Targets for Alcohol Pharmacotherapies. In: Grant, K., Lovinger, D. (eds) The Neuropharmacology of Alcohol . Handbook of Experimental Pharmacology, vol 248. Springer, Cham. https://doi.org/10.1007/164_2018_101

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