Chronischer Alkoholkonsum verändert die Expression von Genen im Endocannabinoidsystem in wichtigen Gehirnregionen tiefgreifend und wirkt sich auf Bereiche aus, die an Belohnung, Impulskontrolle und Entscheidungsfindung beteiligt sind
https://in.umh-csic.es/en/articulos/endocannabinoid-system-gene-expression-in-mesocorticolimbic-brain-regions-of-individuals-with-alcohol-use-disorder-a-descriptive-study/
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> In this context, the study focused on analysing the neurobiological mechanisms associated with alcohol use disorder by examining post-mortem brain tissue from individuals who had consumed alcohol chronically for an average of 35 years. Specifically, the researchers investigated changes in the endocannabinoid system, which is closely linked to reward and addiction mechanisms
>By comparing samples from individuals with alcohol use disorder with those from non-addicted individuals, the team observed a marked imbalance in the expression of several endocannabinoid system genes. In particular, they detected a strong increase in the CB1 receptor: expression of the gene encoding this receptor rose by 125% in the prefrontal cortex and by 78% in the nucleus accumbens. “This receptor is closely involved in the reinforcement of addictive behaviours and the risk of relapse”, notes researcher María Salud García Gutiérrez, first author of the study.
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>In contrast, expression of the CB2 receptor gene was reduced by approximately 50% in both regions. “Since the CB2 receptor plays neuroprotective and anti-inflammatory roles, its reduction suggests an impairment of the brain’s defence mechanisms against alcohol-induced damage”, explains the researcher.
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>Another striking finding was the alteration of the GPR55 receptor, known as an ‘orphan’ receptor because for years its natural ligand was unknown. The researchers found higher levels of GPR55 in the prefrontal cortex, with a 19% increase, but significantly lower levels in the nucleus accumbens, with a 51% reduction. This study is the first to document changes in this gene in humans with alcohol use disorder.
> In addition, the team observed changes in the enzyme FAAH, which is responsible for degrading anandamide, an endocannabinoid produced by the nervous system that influences anxiety and pleasure. In individuals with alcoholism, FAAH gene expression was lower in the prefrontal cortex but 24% higher in the nucleus accumbens, potentially altering the availability of these regulatory substances.
>**According to the authors, these findings help to better understand why the brains of people with alcohol use disorder show increased vulnerability to relapse and reduced executive control. Identifying which components of the endocannabinoid system are altered, and in which brain regions, opens the door to new, more specific and personalised therapeutic targets.**
[Endocannabinoid system gene expression in mesocorticolimbic brain regions of individuals with alcohol use disorder: A descriptive study – García‐Gutiérrez – Addiction – Wiley Online Library](https://onlinelibrary.wiley.com/doi/10.1111/add.70293)
For once they aren’t just stating the obvious, they’re actually getting into the rather interesting mechanisms of what makes the obvious happen.
so alcoholics cant handle weed either right? p
Or, equally likely, is that people with alcohol use disorder (AUD) express endocannabinoid genes differently, which may account for why they become addicted while others do not.