Laut einer neuen Studie an Mäusen kann Komasaufen als junger Erwachsener Jahrzehnte später dauerhafte Hirnschäden verursachen, indem er die Art und Weise, wie die Neuronen des Gehirns kommunizieren, grundlegend verändert und möglicherweise das Risiko erhöht, später im Leben an Alzheimer zu erkranken.

I’ve linked to the news release in the post above. In this comment, for those interested, here’s the link to the peer reviewed journal article:

https://www.sciencedirect.com/science/article/pii/S0197458024001726

From the linked article:

Binge drinking as a young adult causes permanent brain damage decades on

Binge drinking in early adult years fundamentally changes how the brain’s neurons communicate, in what scientists equate to a faulty gas pedal in a car that needs more pressure applied to “go.” What’s more, it remains unchanged for decades, raising the risk of developing Alzheimer’s disease later in life. While there’s not much we can do about the past, it may help earlier intervention and treatment to target this area of the brain.

The University of Pennsylvania (Penn State) researchers found that binge drinking in your 20s can result in permanent dysregulation that resemble the faulty neuronal information transmission seen in people with cognitive decline. It was the same in both male and female brains.

“Pyramidal neurons are excitatory neurons found throughout the brain, and heavily in the prefrontal cortex; they act like the gas pedal for the brain and encourage activity, whereas GABAergic neurons are inhibitory neurons that act like the brakes,” Crowley said. “It’s important for the gas and the brakes to be balanced and flexible to execute complicated cognitive tasks, and we know this balance can go awry for various reasons – including in neurodegenerative diseases like Alzheimer’s disease and related dementias. We wanted to know if alcohol consumption could be a potential cause of that.”

What they found was that even with long periods of abstinence, the impact of early-years binge drinking sessions could still be seen in these specific neurons, particularly in their compromised ability to relay information to each other.

What’s more, the “go” neurotransmitter glutamate was found to be more actively signaling to GABAergic neurons – a dysregulated behavior that is also seen in dementia-related cognitive decline.