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Unraveling the molecular mechanisms of alcohol dependence

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Unraveling the molecular mechanisms of alcohol dependence. / Kalsi, Gursharan; Prescott, Carol A.; Kendler, Kenneth S.; Riley, Brien P.

In: Trends in Genetics, Vol. 25, No. 1, N/A, 01.2009, p. 49-55.

Research output: Contribution to journalLiterature review

Harvard

Kalsi, G, Prescott, CA, Kendler, KS & Riley, BP 2009, 'Unraveling the molecular mechanisms of alcohol dependence', Trends in Genetics, vol. 25, no. 1, N/A, pp. 49-55. https://doi.org/10.1016/j.tig.2008.10.005

APA

Kalsi, G., Prescott, C. A., Kendler, K. S., & Riley, B. P. (2009). Unraveling the molecular mechanisms of alcohol dependence. Trends in Genetics, 25(1), 49-55. [N/A]. https://doi.org/10.1016/j.tig.2008.10.005

Vancouver

Kalsi G, Prescott CA, Kendler KS, Riley BP. Unraveling the molecular mechanisms of alcohol dependence. Trends in Genetics. 2009 Jan;25(1):49-55. N/A. https://doi.org/10.1016/j.tig.2008.10.005

Author

Kalsi, Gursharan ; Prescott, Carol A. ; Kendler, Kenneth S. ; Riley, Brien P. / Unraveling the molecular mechanisms of alcohol dependence. In: Trends in Genetics. 2009 ; Vol. 25, No. 1. pp. 49-55.

Bibtex Download

@article{5865f8c085544da98366b800873ba15a,
title = "Unraveling the molecular mechanisms of alcohol dependence",
abstract = "Alcohol dependence (AD) is a common, chronic, relapsing disorder. Compelling epidemiological evidence indicates that >50{\%} of the risk for becoming alcoholic stems from genetic susceptibility and genetic studies have identified several risk genes. Alcohol intake alters gene expression patterns, thereby producing long-lasting cellular and molecular adaptations that might explain the development and maintenance of AD. The heterogeneous nature of AD indicates a complex etiology involving mechanisms related to motivational behavior, reward and learning, adaptations in signaling pathways owing to interactions between alcohol and target molecules, and chromatin remodeling. Emerging methodologies present opportunities to determine how alcohol might disrupt the synergistic actions of molecular systems and to assess gene-environment interactions for elucidating the behavioral and physiological dysfunctions underlying AD.",
keywords = "GABA(A) RECEPTORS, ETHANOL EXPOSURE, MALE TWINS, INDUCED NEUROPLASTICITY, DELTA-FOSB, GENE-EXPRESSION, BRAIN, CANDIDATE GENES, SYSTEMS BIOLOGY, ELEMENT-BINDING PROTEIN",
author = "Gursharan Kalsi and Prescott, {Carol A.} and Kendler, {Kenneth S.} and Riley, {Brien P.}",
year = "2009",
month = "1",
doi = "10.1016/j.tig.2008.10.005",
language = "English",
volume = "25",
pages = "49--55",
journal = "Trends in Genetics",
issn = "0168-9525",
publisher = "Elsevier Limited",
number = "1",

}

RIS (suitable for import to EndNote) Download

TY - JOUR

T1 - Unraveling the molecular mechanisms of alcohol dependence

AU - Kalsi, Gursharan

AU - Prescott, Carol A.

AU - Kendler, Kenneth S.

AU - Riley, Brien P.

PY - 2009/1

Y1 - 2009/1

N2 - Alcohol dependence (AD) is a common, chronic, relapsing disorder. Compelling epidemiological evidence indicates that >50% of the risk for becoming alcoholic stems from genetic susceptibility and genetic studies have identified several risk genes. Alcohol intake alters gene expression patterns, thereby producing long-lasting cellular and molecular adaptations that might explain the development and maintenance of AD. The heterogeneous nature of AD indicates a complex etiology involving mechanisms related to motivational behavior, reward and learning, adaptations in signaling pathways owing to interactions between alcohol and target molecules, and chromatin remodeling. Emerging methodologies present opportunities to determine how alcohol might disrupt the synergistic actions of molecular systems and to assess gene-environment interactions for elucidating the behavioral and physiological dysfunctions underlying AD.

AB - Alcohol dependence (AD) is a common, chronic, relapsing disorder. Compelling epidemiological evidence indicates that >50% of the risk for becoming alcoholic stems from genetic susceptibility and genetic studies have identified several risk genes. Alcohol intake alters gene expression patterns, thereby producing long-lasting cellular and molecular adaptations that might explain the development and maintenance of AD. The heterogeneous nature of AD indicates a complex etiology involving mechanisms related to motivational behavior, reward and learning, adaptations in signaling pathways owing to interactions between alcohol and target molecules, and chromatin remodeling. Emerging methodologies present opportunities to determine how alcohol might disrupt the synergistic actions of molecular systems and to assess gene-environment interactions for elucidating the behavioral and physiological dysfunctions underlying AD.

KW - GABA(A) RECEPTORS

KW - ETHANOL EXPOSURE

KW - MALE TWINS

KW - INDUCED NEUROPLASTICITY

KW - DELTA-FOSB

KW - GENE-EXPRESSION

KW - BRAIN

KW - CANDIDATE GENES

KW - SYSTEMS BIOLOGY

KW - ELEMENT-BINDING PROTEIN

U2 - 10.1016/j.tig.2008.10.005

DO - 10.1016/j.tig.2008.10.005

M3 - Literature review

VL - 25

SP - 49

EP - 55

JO - Trends in Genetics

JF - Trends in Genetics

SN - 0168-9525

IS - 1

M1 - N/A

ER -

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