Binge eating and drinking in early adulthood fundamentally changes the way neurons in the brain communicate. Scientists believe this is equivalent to a failure in a car’s gas pedal, which requires more pressure to be applied to “start”. Additionally, it remains unchanged for decades, increasing the risk of developing Alzheimer’s disease later in life. There’s not much that can be done about the past, but early intervention and treatment that targets this area of the brain may help.
Researchers at the University of Pennsylvania (Pennsylvania State University) have found that binge drinking in your 20s can cause lasting dysregulation that resembles the deficits in neural communication seen in people with cognitive decline. I discovered that. This was true for both male and female brains.
“Previous research has shown that binge drinking has an immediate effect on the brain, but we had no idea whether the changes would last for a long time or whether they would reverse over time.” said Nikki Crowley, assistant professor and director. from the Pennsylvania State Neuroscience Institute. “We are interested in understanding whether binge drinking in early adulthood can have lasting effects that are not apparent until later in life, even if one has stopped drinking for very long periods of time. This allows us to consider the impact of alcohol on an individual’s overall health from the perspective of the individual’s entire life history.”
In this study, the researchers had mice perform a “spontaneous” binge-drinking regimen in cycles. In this study, animals were given ethanol diluted in water and then removed from water on the fourth day to simulate binge drinking. Blood alcohol levels of ethanol increased when given in the dark. The control group was housed separately and underwent the same therapy with water only.
This process was repeated for four weeks on mice that were eight weeks old, equivalent to early adulthood in humans. He then returned to the water for 9 to 12 months, reaching middle age, or in human terms, his late 30s to mid-40s.
“Although mice have shorter lifespans than humans, they otherwise share many of the same physiology and can be used as models to address important public health questions faster than humans. ,” Crowley said. “We can also perform experiments in a controlled laboratory environment, which allows us to examine what is happening mechanistically at the cellular and molecular level, a depth not possible with human research. In this case, we can understand the effects that alcohol has on the brain on its own, without taking into account any of the social stress or environmental factors that humans are dealing with.”
They then exposed middle-aged mice to whole-cell patch-clamp electrophysiology, showing how this early-life binge affects signaling molecules (neurotransmitters) between two types of neurons, specifically pyramidal cells and GABAergic neurons. We investigated whether it would have such an effect.
“Pyramidal neurons are excitatory neurons found throughout the brain, and are abundant in the prefrontal cortex. GABAergic neurons act like an accelerator pedal in the brain, promoting activity; “Sex neurons are inhibitory neurons that act like brakes,” Dr. Crowley said. “To perform complex cognitive tasks, it is important that the accelerator and brake are balanced and flexible, but this balance can be disrupted for a variety of reasons, including neurodegenerative diseases such as Alzheimer’s disease and related dementias. We know it’s possible. We wanted to know if alcohol consumption was a potential cause.”
What they discovered was that even with long periods of abstinence, the effects of early binge drinking sessions were still seen in these particular neurons, particularly in their reduced ability to transmit information to each other. .
“The intrinsic excitability of pyramidal neurons, a measure of how easily neurons can talk to other neurons, was altered in a way that made communication difficult,” Crowley said. “You can think of it like how hard you need to press the gas pedal to get your car moving. Drinking changes this threshold, so more pressure is required. It wasn’t that easy for neurons to get involved.”
Additionally, the “go” neurotransmitter glutamate was found to more actively signal GABAergic neurons. This is a dysregulated behavior that is also seen in the cognitive decline associated with dementia.
“In our studies in mice, we found that we could detect the negative effects of binge drinking on neuronal regulation even after six months of abstinence, which is approximately several decades in human years,” Crowley said. said. “While some neuronal changes return to normal when you stop drinking, there are some long-term effects of heavy drinking in young adults.”
However, everything is not doom and gloom here. These findings will make it easier for researchers to target these neurons in order to enhance their functions. The research team is looking into using the protein somatostatin to repair the damage caused by heavy alcohol consumption.
“These studies provide insight into how alcohol, as a pharmacological agent, chronically alters brain signaling in the aging brain even after long periods of abstinence,” the researchers wrote in their paper. , providing important biological and mechanistic insights.” “A promising avenue for future research and potential treatment exploration would be to correlate neurophysiological changes seen after midlife alcohol exposure with behavioral measures of cognitive decline.”
The study was published in the journal Neurobiology of Aging.
Source: Pennsylvania State University
