Clock genes in human alcohol abuse and comorbid conditions

Partonen, Timo

doi:10.1016/j.alcohol.2014.08.013

Cited by 34 publications

(25 citation statements)

References 72 publications

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“…Both male and female mice display escalated alcohol intake after 3 weeks of chronic IA exposure, mainly occurring at the first 4-hour dark cycle (25-30% in total daily intake), without much change in the other two-time periods [Zhou et al, 2017a, b]. Of interest, hypothalamic POMC deficient mice displayed lower alcohol intake than wild-type mice during the first 4-hour dark cycle in both sexes [Zhou et al, 2017b], suggesting a potential contribution of hypothalamic POMC to the genetically determined tendency of hypothalamic POMC deficient mice towards reduced alcohol consumption, with potential clock genes' influence, as found in other studies with alcohol [Spanagel et al, 2005;Agapito et al, 2010;Partonen, 2015].…”

Section: Pro-opiomelanocortin (Pomc)/β-endorphin and Mu-opioid Rementioning

confidence: 47%

“…Other stress responsive systems discussed here ( [Bond et al, 1998;Bart et al, 2004;Kreek and LaForge, 2007;Anton et al, 2008], the single-target pharmacotherapy has relatively modest therapeutic value, also suggesting a need for better efficacy [Müller et al, 2014]. , 2015;Zhou and Leri, 2016]. There are several precedents to study the combinations of NTN with other compounds in rodent models, like acamprosate [Heyser et al, 2003], or prazosin [Froehlich et al, 2013].…”

Section: Discussionmentioning

confidence: 99%

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Involvement of Activated Brain Stress Responsive Systems in Excessive and “Relapse” Alcohol Drinking in Rodent Models: Implications for Therapeutics

Zhou

Kreek

2018

J Pharmacol Exp Ther

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Addiction to specific drugs (such as alcohol, psychostimulants and opioids) shares some common direct or downstream effects on the brain stress-responsive systems, including arginine vasopressin and its V1b receptors, dynorphin and the kappa opioid receptors, proopiomelanocortin/β-endorphin and the mu opioid receptors, and the endocannabinoids. Further study of these systems, through laboratory-based and translational research, could lead to the discovery of novel treatment targets and the early optimization of interventions (for example, combination) for the pharmacological therapy of alcoholism.

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Section: Pro-opiomelanocortin (Pomc)/β-endorphin and Mu-opioid Rementioning

confidence: 47%

Section: Discussionmentioning

confidence: 99%

Involvement of Activated Brain Stress Responsive Systems in Excessive and “Relapse” Alcohol Drinking in Rodent Models: Implications for Therapeutics

Zhou

Kreek

2018

J Pharmacol Exp Ther

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“…Although associations of certain clock gene variants and AUD and SUDs could not always be replicated (Malison et al, 2006; Surovtseva et al, 2012), in sum these genetic studies link clock gene function and addictive behavior in humans (Partonen, 2015). …”

Section: Clock Genes – New Key Players In Aud and Sudsmentioning

confidence: 99%

Clock genes × stress × reward interactions in alcohol and substance use disorders

Perreau-Lenz

Spanagel

2015

Alcohol

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Adverse life events and highly stressful environments have deleterious consequences for mental health. Those environmental factors can potentiate alcohol and drug abuse in vulnerable individuals carrying specific genetic risk factors, hence producing the final risk for alcohol- and substance-use disorders development. The nature of these genes remains to be fully determined, but studies indicate their direct or indirect relation to the stress hypothalamo-pituitary-adrenal (HPA) axis and/or reward systems. Over the past decade, clock genes have been revealed to be key-players in influencing acute and chronic alcohol/drug effects. In parallel, the influence of chronic stress and stressful life events in promoting alcohol and substance use and abuse has been demonstrated. Furthermore, the reciprocal interaction of clock genes with various HPA-axis components, as well as the evidence for an implication of clock genes in stress-induced alcohol abuse, have led to the idea that clock genes, and Period genes in particular, may represent key genetic factors to consider when examining gene × environment interaction in the etiology of addiction. The aim of the present review is to summarize findings linking clock genes, stress, and alcohol and substance abuse, and to propose potential underlying neurobiological mechanisms.

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“…Overall, these human genetic studies pinpointed an important role for PER2 in alcohol drinking. How PER2 and other clock‐related genes are regulated by alcohol or impact alcohol response or drinking behavior has received increasing attentions in particular with the use of mouse models (Davis et al., ; Partonen, ). One possible mechanism is that Per2 in mouse may control glutamate transport and accumulation in the brain (Spanagel et al., ).…”

Section: Discussionmentioning

confidence: 99%

Brain Imaging‐Guided Analysis Reveals DNA Methylation Profiles Correlated with Insular Surface Area and Alcohol Use Disorder

Zhao

Zheng

2019

Alcoholism Clin & Exp Res

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Background: Alcohol use disorder (AUD) is a wide-spread, heritable brain disease, but few studies have linked genetic variants or epigenetic factors to brain structures related to AUD in humans, due to many factors including the high-dimensional nature of imaging and genomic data.Methods: To provide potential insights into the links among epigenetic regulation, brain structure, and AUD, we have performed an integrative analysis of brain structural imaging and blood DNA methylome data from 52 AUD and 58 healthy control (HC) subjects collected in the Nathan Kline Institute-Rockland Sample.Results: We first found that AUD subjects had significantly larger insular surface area than HC in both left and right hemispheres. We then found that 7,827 DNA methylation probes on the HumanMethylation450K BeadChip had significant correlations with the right insular surface area (false discovery rate [FDR] < 0.05). Furthermore, we showed that 44 of the insular surface area-correlated methylation probes were also strongly correlated with AUD status (FDR < 0.05). These AUD-correlated probes are annotated to 36 protein-coding genes, with 16 genes (44%) having been reported by others to be related to AUD or alcohol response, including TAS2R16 and PER2. The remaining 20 genes, in particular ARHGAP22, might represent novel genes involved in AUD or responsive to alcohol.Conclusions: We have identified 36 insular surface area-and AUD-correlated protein-coding genes that are either known to be AUD-or alcohol-related or not yet reported by prior studies. Therefore, our study suggests that the brain imaging-guided epigenetic analysis has a potential of identifying possible epigenetic mechanisms involved in AUD.

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Clock genes in human alcohol abuse and comorbid conditions

Cited by 34 publications

References 72 publications

Involvement of Activated Brain Stress Responsive Systems in Excessive and “Relapse” Alcohol Drinking in Rodent Models: Implications for Therapeutics

Involvement of Activated Brain Stress Responsive Systems in Excessive and “Relapse” Alcohol Drinking in Rodent Models: Implications for Therapeutics

Clock genes × stress × reward interactions in alcohol and substance use disorders

Brain Imaging‐Guided Analysis Reveals DNA Methylation Profiles Correlated with Insular Surface Area and Alcohol Use Disorder

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