Publications by authors named "Marion M Friske"

Currently available clinical treatments on alcohol use disorder (AUD) exhibit limited efficacy and new druggable targets are required. One promising approach to discover new molecular treatment targets involves the transcriptomic profiling of brain regions within the addiction neurocircuitry, utilizing animal models and postmortem brain tissue from deceased patients with AUD. Unfortunately, such studies suffer from large heterogeneity and small sample sizes.

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  • Alcohol use disorder (AUD) may lead to accelerated biological aging, which is linked to increased health risks, particularly through inflammation and changes in DNA related to brain function.
  • The study examined various biological age markers in brain and blood samples from individuals with and without AUD, revealing significant links between certain markers and accelerated aging specifically in certain brain regions and blood samples.
  • Findings indicated that while some age markers suggested accelerated aging in individuals with AUD, others showed no significant relationship, highlighting the complexity of biological aging in substance use disorders.
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  • Cocaine use disorder (CUD) leads to significant changes in the brain, with suspected involvement of epigenetic factors, but most research so far has focused on animal studies rather than humans.
  • This study analyzed DNA methylation in the brains of individuals with and without CUD, finding 20 differentially methylated regions (DMRs) linked to gene activity related to drug behavior.
  • Although no direct epigenome-wide significance was found for any particular gene, a trend of accelerated biological aging was observed in CUD individuals, suggesting potential long-term impacts of the disorder on brain health.
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During the COVID-19 pandemic, many potential risk groups have been identified, such as those with obesity, diabetes, preexisting organ injuries, and several other conditions. Smoking is the most reported substance use disorder linked to increased COVID-19 hospitalization rate and disease severity. In relation to smoking, we discuss the impairment of the innate and the adaptive immune systems as being among the main potential reasons for increased COVID-19 infection risk and severity.

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Background: Chronic alcohol consumption and alcohol use disorder have a tremendous impact on the patient's psychological and physiological health. There is evidence that chronic alcohol consumption influences SARS-CoV2 infection risk, but so far, the molecular mechanism underlying such an effect is unknown.

Methods: We generated the expression data of SARS-CoV2 infection-relevant genes (Ace2, Tmprss2, and Mas) in different organs in rat models of chronic alcohol exposure and alcohol dependence.

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Alcohol Use Disorder (AUD) is a major contributor to global mortality and morbidity. Postmortem human brain tissue enables the investigation of molecular mechanisms of AUD in the neurocircuitry of addiction. We aimed to identify differentially expressed (DE) genes in the ventral and dorsal striatum between individuals with AUD and controls, and to integrate the results with findings from genome- and epigenome-wide association studies (GWAS/EWAS) to identify functionally relevant molecular mechanisms of AUD.

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(1) Background: Epigenome-wide association studies (EWAS) in peripheral blood have repeatedly found associations between tobacco smoking and aberrant DNA methylation (DNAm), but little is known about DNAm signatures of smoking in the human brain, which may contribute to the pathophysiology of addictive behavior observed in chronic smokers. (2) Methods: We investigated the similarity of DNAm signatures in matched blood and postmortem brain samples ( = 10). In addition, we performed EWASs in five brain regions belonging to the neurocircuitry of addiction: anterior cingulate cortex (ACC), Brodmann Area 9, caudate nucleus, putamen, and ventral striatum ( = 38-72).

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Alcohol use disorder (AUD) is closely linked to the brain regions forming the neurocircuitry of addiction. Postmortem human brain tissue enables the direct study of the molecular pathomechanisms of AUD. This study aims to identify these mechanisms by examining differential DNA-methylation between cases with severe AUD (n = 53) and controls (n = 58) using a brain-region-specific approach, in which sample sizes ranged between 46 and 94.

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