Researchers have discovered a gene that regulates alcohol consumption and when faulty can cause excessive drinking. They have also identified the mechanism underlying this phenomenon.
The study showed that normal mice show no interest in alcohol and drink little or no alcohol when offered a free choice between a bottle of water and a bottle of diluted alcohol.
However, mice with a genetic mutation to the gene Gabrb1 overwhelmingly preferred drinking alcohol over water, choosing to consume almost 85% of their daily fluid as drinks containing alcohol - about the strength of wine.
The consortium of researchers from five UK universities – Newcastle University, Imperial College London, Sussex University, University College London and University of Dundee – and the MRC Mammalian Genetics Unit at Harwell, funded by the Medical Research Council (MRC), Wellcome Trust and ERAB, publish their findings today in Nature Communications.
Dr Quentin Anstee, Consultant Hepatologist at Newcastle University, joint lead author said: “It’s amazing to think that a small change in the code for just one gene can have such profound effects on complex behaviours like alcohol consumption.
“We are continuing our work to establish whether the gene has a similar influence in humans, though we know that in people alcoholism is much more complicated as environmental factors come into play. But there is the real potential for this to guide development of better treatments for alcoholism in the future.”
Identifying the gene for alcohol preference
Working at the MRC Mammalian Genetics Unit, a team led by Professor Howard Thomas from Imperial College London introduced subtle mutations into the genetic code at random throughout the genome and tested mice for alcohol preference. This led the researchers to identify the gene Gabrb1 which changes alcohol preference so strongly that mice carrying either of two single base-pair point mutations in this gene preferred drinking alcohol (10% ethanol v/v - about the strength of wine), over water.
The group showed that mice carrying this mutation were willing to work to obtain the alcohol-containing drink by pushing a lever and, unlike normal mice, continued to do so even over long periods. They would voluntarily consume sufficient alcohol in an hour to become intoxicated and even have difficulty in coordinating their movements.
The cause of the excessive drinking was tracked down to single base-pair point mutations in the gene Gabrb1, which codes for the beta 1 subunit, an important component of the GABAA receptor in the brain. This receptor responds to the brain’s most important inhibitory chemical messenger (GABA) to regulate brain activity. The researchers found that the gene mutation caused the receptor to activate spontaneously even when the usual GABA trigger was not present.
These changes were particularly strong in the region of the brain that controls pleasurable emotions and reward, the nucleus accumbens, as Dr Anstee explains: “The mutation of the beta1 containing receptor is altering its structure and creating spontaneous electrical activity in the brain in this pleasure zone, the nucleus accumbens. As the electrical signal from these receptors increases, so does the desire to drink to such an extent that mice will actually work to get the alcohol, for much longer than we would have expected.”
Professor Howard Thomas said: “We know from previous human studies that the GABA system is involved in controlling alcohol intake. Our studies in mice show that a particular subunit of GABAA receptor has a significant effect and most importantly the existence of these mice has allowed our collaborative group to investigate the mechanism involved. This is important when we come to try to modify this process first in mice and then in man.”
Leading to a treatment for alcohol addiction
Initially funded by the MRC, the 10-year project aimed to find genes affecting alcohol consumption. Professor Hugh Perry, Chair of the MRC’s Neurosciences and Mental Health Board, said: “Alcohol addiction places a huge burden on the individual, their family and wider society. There’s still a great deal we don’t understand about how and why consumption progresses into addiction, but the results of this long-running project suggest that, in some individuals, there may be a genetic component. If further research confirms that a similar mechanism is present in humans, it could help us to identify those most at risk of developing an addiction and ensure they receive the most effective treatment.”
Most colleges require students to go through some sort of alcohol education program. When I was a freshman in college, I was required to play a video game that involved helping Franklin the frog navigate through various college parties without succumbing to alcohol poisoning. (Easy, Frank — remember to hydrate).
Other universities require students to watch educational videos or take online quizzes about appropriate alcohol use.These one-time interventions do work, but their effect tends to wear off as the school year progresses, according to a recent study.
Stony Drunk!Steve hitting on Tony and Tony just realizing maybe Steve was into him
Tony’s first reaction to Steve Rogers leaning against Tony for support is to look him over his shoulder at Natasha to ask, “Is he okay?”
Because this isn’t normal. The serum should combat any mortal alcohol in his system as Thor phrases. Not that Tony doesn’t know about Thor bringing his own moonshine along and sharing. Asgardian food and drink are a mystery and Tony can’t help but wonder if they’re safe for them to have. Thor seems not to be too concerned but Tony doesn’t know how much of human physiology Thor truly knows about, not to undermine the guy who plays dumb like a champ.
Natasha looks amused at the question. “He’ll sleep it off just fine. Let him enjoy it.” And she proves to be no further help than that. Even keeping Sam at bay, Tony notices.
Strangely enough Steve looks comfortable where he is leaning on Tony, with more weight than Tony can keep holding up without it ending with them both on the floor.
“Can we sit, big guy?” Tony asks and is surprised when Steve groans out a protest. He ends up needing to manhandle as much as Steve allows, because Tony isn’t doing that on his own much as his pride hates to admit to it.
The sit or fall rather gracelessly onto the sofa. Steve encroaches on Tony’s space. Tony doesn’t mind so much, he doesn’t mind physical contact but he is still mildly concerned about Steve’s lethargic movement and need for proximity with Tony himself.
One of Steve’s hands it holding onto Tony’s and he’s staring at their hands. Fingers brushing almost ticklishly against Tony’s rougher, scarred hands. Steve just keeps touching, stroking over his fingers, around the what Tony always considered knobby knuckles or kneading at his palm. It’s nice and would be relaxing if Steve didn’t seem a little out of it like he does.
“Tony.” Steve’s voice is almost sleepy.
Steve doesn’t answer right away. He’s quiet long enough that Tony actually thinks he might have forgotten he said anything to begin with. Given his inebriated state it’s not exactly a surprise.
Instead Steve is leaning close enough Tony can feel a few warm puffs of breath. There is a trace of something sweet, like honey, with each.
“ ‘m tired. Should come to bed with me.”
It’s low and soft but the words are clear enough to short circuit Tony’s brain. Steve is hovering even closer and for several sudden frantic beats of his heart Tony thinks Steve is going to kiss him. He gets so close and Tony isn’t sure if he’s relieved or disappointed when Steve’s head instead ends up on his shoulder.
Either way it’s a little overwhelming. Not made any better by the way Steve paws at him and seems to have planned to settle in with Tony. Steve’s bulk is getting heavier and heavier, and the breath against his neck makes Tony shiver. Hair starting to stand on end Tony slips under Steve’s weigh to end up under him, surrounded by the warmth he gives off. Or that might be due to the revolving idea in Tony’s head that hasn’t quite taken root just yet.
Tony might need to seriously consider the possibility that Steve was into him.
Tony also desperate needed to call Rhodey as soon as possible. Because Tony wasn’t stupid enough not to know how completely screwed he was.
Alcohol consumption affects the brain in multiple ways, ranging from acute changes in behavior to permanent molecular and functional alterations. The general consensus is that in the brain, alcohol targets mainly neurons. However, recent research suggests that other cells of the brain known as astrocytic glial cells or astrocytes are necessary for the rewarding effects of alcohol and the development of alcohol tolerance. The study, first-authored by Dr. Leonardo Pignataro, was published in the February 6th issue of the scientific journal Brain and Behavior.
“This is a fascinating result that we could have never anticipated. We know that astrocytes are the most abundant cell type in the central nervous system and that they are crucial for neuronal growth and survival, but so far, these cells had been thought to be involved only in brain’s support functions. Our results, however, show that astrocytes have an active role in alcohol tolerance and dependence,” explains Dr. Pignataro.
The team of researchers from Columbia and Yale Universities analyzed how alcohol exposure changes gene expression in astrocyte cells and identified gene sets associated with stress, immune response, cell death, and lipid metabolism, which may have profound implications for normal neuronal activity in the brain. “Our findings may explain many of the long-term inflammatory and degenerative effects observed in the brain of alcoholics,” says Dr. Pignataro. “The change in gene expression observed in alcohol-exposed astrocytes supports the idea that some of the alcohol consumed reaches the brain and that ethanol (the active component of alcoholic beverages) is locally metabolized, increasing the production free radicals that react with cell components to affect the normal function of cells. This activates a cellular stress response in the cells in an attempt to defend from this chemical damage. On the other hand, the body recognizes these oxidized molecules as "foreign objects” generating an immune response against them that leads to the death of damage cells. This mechanism can explain the inflammatory degenerative process observed in the brain of chronic alcoholics, allowing for the development of different and novel therapeutically approaches to treat this disease" added Dr. Pignataro.
The consequences of alcohol on astrocytes revealed in this study go far beyond what happens to this particular cell type. Astrocytes play a crucial role in the CNS, supporting normal neuronal activity by maintaining homeostasis. Therefore, alcohol changes in gene expression in astrocytes may have profound implications for neuronal activity in the brain.
These findings will help scientists better understand alcohol-associated disorders, such as the brain neurodegenerative damage associated with chronic alcoholism and alcohol tolerance and dependence. “We hope that this newly discovered role of astrocytes will give scientists new targets other than neurons to develop novel therapies to treat alcoholism,” Leonardo Pignataro concluded.
A team of UC San Francisco researchers has found that a tiny segment of genetic material known as a microRNA plays a central role in the transition from moderate drinking to binge drinking and other alcohol use disorders.
Previous research in the UCSF laboratory of Dorit Ron, PhD, Endowed Chair of Cell Biology of Addiction in Neurology, has demonstrated that the level of a protein known as brain-derived neurotrophic factor, or BDNF, is increased in the brain when alcohol consumed in moderation. In turn, experiments in Ron’s lab have shown, BDNF prevents the development of alcohol use disorders.
In the new study, Ron and first author Emmanuel Darcq, PhD, a former postdoctoral fellow now at McGill University in Canada, found that when mice consumed excessive amounts of alcohol for a prolonged period, there was a marked decrease in the amount of BDNF in the medial prefrontal cortex (mPFC), a brain region important for decision making. As reported in the October 21, 2014 online edition of Molecular Psychiatry, this decline was associated with a corresponding increase in the level of a microRNA called miR-30a-5p.
MicroRNAs lower the levels of proteins such as BDNF by binding to messenger RNA, the molecular middleman that carries instructions from genes to the protein-making machinery of the cell, and tagging it for destruction.
Ron and colleagues then showed that if they increased the levels of miR-30a-5p in the mPFC, BDNF was reduced, and the mice consumed large amounts of alcohol. When mice were treated with an inhibitor of miR-30a-5p, however, the level of BDNF in the mPFC was restored to normal and alcohol consumption was restored to normal, moderate levels.
“Our results suggest BDNF protects against the transition from moderate to uncontrolled drinking and alcohol use disorders,” said Ron, senior author of the study and a professor in UCSF’s Department of Neurology. “When there is a breakdown in this protective pathway, however, uncontrolled excessive drinking develops, and microRNAs are a possible mechanism in this breakdown. This mechanism may be one possible explanation as to why 10 percent of the population develop alcohol use disorders and this study may be helpful for the development of future medications to treat this devastating disease.”
One reason many potential therapies for alcohol abuse have been unsuccessful is because they inhibit the brain’s reward pathways, causing an overall decline in the experience of pleasure. But in the new study, these pathways continued to function in mice in which the actions of miR-30a-5p had been tamped down—the mice retained the preference for a sweetened solution over plain water that is seen in normal mice.
This result has significant implications for future treatments, Ron said. “In searching for potential therapies for alcohol abuse, it is important that we look for future medications that target drinking without affecting the reward system in general. One problem with current alcohol abuse medications is that patients tend to stop taking them because they interfere with the sense of pleasure.”
AkaKuro 34? Also, do you take any pairings or is there something you won't write?
Thank you for being patient! Doing these in order is tough, haha.
As far as what pairings I’ll take, I’m pretty much okay with any, unless it’s unethical (I don’t do incest or statutory) And if I receive a pairing I don’t particularly care for, I will still do my best to make it enjoyable for the reader. For example, I don’t actually ship AkaKuro (because I LOVE KagaKuro and AkaFuri) but I’m not so against it that I won’t write it. I like both characters. Okay, sorry, I went on forever, haha.
Oh, and I’m up for writing more than KnB and Free! I also really like Haikyuu!! and Yowamushi Pedal. So, I wouldn’t mind getting some requests in those fandoms~
This takes place in the future and other pairings appear (AoKise, MidoTaka) I hope you enjoy!! (Warning: Drunken shenanigans)
*~* #34 “If you keep looking at me like that we won’t make it to a bed.” *~*
Kuroko Tetsuya was always level-headed. Cool. Calm.
Until tonight, that is.
It was all Aomine’s fault, Akashi
had decided. He was the one who had
suggested they go out for drinks after dinner, while the redhead was content to
enjoy a nice meal with his former teammates.
Kise was to blame, as well. He had dragged them all to his favorite
So, while the blond took turns
singing with Shuutoku’s point guard, the rest of them were left to eat, drink
and/or be merry.
“Tetsu, your cup is empty again,”
Aomine laughed raucously, pouring some of his drink into the shadow’s cup. “C’mon,
Now, normally, Kuroko would reply
with a stoic: ‘And just what are we
But tonight, he smiled, face
flushed, and happily lifted his glass to clink it against the taller man’s.
“Wow, I’ve never seen Kuro-chin
drunk before,” Murasakibara mused, adding another empty tapas plate to the ever-growing
pile in front of him.
“Shouldn’t you do something about
this, Akashi?” Midorima adjusted his glasses, eyebrows raised in expectation.
“Perhaps you should be more
concerned with your beau,” Akashi jutted
his chin forward. The bespectacled man
turned and nearly crushed the lucky item in his hand. Takao and Kise, who had been singing a duet
into the same microphone, had evidently gotten to close and were now kissing
sloppily in front of the karaoke machine.
“Takao!” the green-haired man
grabbed his boyfriend by the back of the shirt and pulled him off of the blond.
“Wassa matta, Shinchi?” And then he laughed. “Ha ha, I said ‘Shinchi’!”
Yes, that was a perfect example of how
their night was going.
Midorima dragged Takao home after
that. Aomine, who had sobered up after belatedly
realizing his boyfriend had been making out with another man, followed suit,
promising quite the punishment when they got home. Kise didn’t seem to mind as he happily
skipped – stumbled – after the tanned man.
This left Akashi, Kuroko and
“Do you need help with Kuro-chin?”
the tallest asked.
“My condo isn’t far from here,” the
redhead steadied the man next to him, pulling Kuroko’s arm over his shoulder to
keep him upright. “Thanks for the offer.”
“Be careful,” he waved and walked
toward the train station.
The walk home was a challenge.
“Maybe I should have asked for
help,” Akashi lamented as he practically carried Kuroko up the stairs to the
lobby. “Tetsuya, get a hold of yourself.”
“Sorry, Akashi-kun,” he bowed and
then nearly took a tumble.
“No matter,” Akashi sighed. “Let’s get you into bed, okay?” They made it to the elevator and halfway down the hallway before Kuroko fell over, taking Akashi with him. “Oww…”
Crimson eyes opened to see a
flushed Kuroko beneath him, icy blue eyes clouded and breaths coming out in
pants. Kuroko’s tongue darted out to
lick his lips and Akashi homed in on the pink appendage. Suddenly, Akashi’s mind began to wander. He wondered just what that tongue tasted like. Vanilla came to mind.
“Akashi-kun,” Kuroko’s voice drew
him from his thoughts. “If you keep
looking at me like that, we won’t make it to a bed.” Akashi felt his face heat up.
“W-What?” he asked, eyes wide.
“If you keep staring at me, we’ll
never make it to your apartment,” Kuroko blinked up at him. “And I’m starting to get sleepy.”
“Ah, right,” Akashi swallowed and
cleared his throat.
Never again would he condone
drinking at their get-togethers.
THE dangers of drinking too much are well known. But how much is too much? To find out, Agnieszka Kalinowski and Keith Humphreys of Stanford University in California scoured the globe for countries whose governments have defined the size of a “standard drink” or set guidelines for low-risk consumption. They found there isn’t a whole lot of agreement. Among the 37 nations polled, the size of a standard drink varies by 250%, the team reports in the scientific journal Addiction. Britain and Iceland, for instance, have a typical tipple defined as just 8 grams of alcohol, while for Austrians the standard is set at a dizzying 20 grams. In some places, such as Switzerland, the recommendations are vague, with a standard drink estimated to be somewhere between 10 and 12 grams. Luxembourg, on the other hand, pins it precisely at 12.8 grams.
Note: I started this fic back in september but have since had time to reflect on the story I’d like to tell. I have made the decision to rewrite/rework what I already have and then write to it’s completion. If it sounds familiar, that’s why. (Warnings for this chapter are in the tags)
Ian was getting ready for another long night when he
heard his phone ringing from across the room.
With one leg in and one leg out of the pair of pants he was trying to
pull on, Ian hopped over to his dresser before his phone stopped ringing. He
didn’t recognize the number and figured it was one of his regulars. He brought the phone up to his ear, slightly
out of breathe from his effort, answered with a “Hello?”
He heard rustling coming from the other end followed
by a series of expletives coming from a voice he had hadn’t heard in months.
Do you ever wake up with a raging hangover and picture the row of brain cells that you suspect have have started to decay? Or wonder whether that final glass of wine was too much for those tiny cells, and pushed you over the line?
Well, it’s true that alcohol can indeed harm the brain in many ways. But directly killing off brain cells isn’t one of them.
The brain is made up of nerve cells (neurons) and glial cells. These cells communicate with each other, sending signals from one part of the brain to the other, telling your body what to do. Brain cells enable us to learn, imagine, experience sensation, feel emotion and control our body’s movement.
Alcohol’s effects can be seen on our brain even after a few drinks, causing us to feel tipsy. But these symptoms are temporary and reversible. The available evidence suggests alcohol doesn’t kill brain cells directly.
There is some evidence that moderate drinking is linked to improved mental function. A 2005 Australian study of 7,500 people in three age cohorts (early 20s, early 40s and early 60s) found moderate drinkers (up to 14 drinks for men and seven drinks for women per week) had better cognitive functioning than non-drinkers, occasional drinkers and heavy drinkers.
But there is also evidence that even moderate drinking may impair brain plasticity and cell production. Researchers in the United States gave rats alcohol over a two-week period, to raise their alcohol blood concentration to about 0.08. While this level did not impair the rats’ motor skills or short-term learning, it impacted the brain’s ability to produce and retain new cells, reducing new brain cell production by almost 40%. Therefore, we need to protect our brains as best we can.
Excessive alcohol undoubtedly damages brain cells and brain function. Heavy consumption over long periods can damage the connections between brain cells, even if the cells are not killed. It can also affect the way your body functions. Long-term drinking can cause brain atrophy or shrinkage, as seen in brain diseases such as stroke and Alzheimer’s disease.
There is debate about whether permanent brain damage is caused directly or indirectly.
We know, for example, that severe alcoholic liver disease has an indirect effect on the brain. When the liver is damaged, it’s no longer effective at processing toxins to make them harmless. As a result, poisonous toxins reach the brain, and may cause hepatic encephalopathy (decline in brain function). This can result in changes to cognition and personality, sleep disruption and even coma and death.
Alcoholism is also associated with nutritional and absorptive deficiencies. A lack of Vitamin B1 (thiamine) causes brain disorders called Wernicke’s ncephalopathy (which manifests in confusion, unsteadiness, paralysis of eye movements) and Korsakoff’s syndrome (where patients lose their short-term memory and coordination).
So, how much alcohol is okay?
To reduce the lifetime risk of harm from alcohol-related disease or injury, the National Health and Medical Research Council recommends healthy adults drink no more than two standard drinks on any day. Drinking less frequently (such as weekly rather than daily) and drinking less on each occasion will reduce your lifetime risk.
To avoid alcohol-related injuries, adults shouldn’t drink more than four standard drinks on a single occasion. This applies to both sexes because while women become intoxicated with less alcohol, men tend to take more risks and experience more harmful effects.
For pregnant women and young people under the age of 18, the guidelines say not drinking is the safest option.
So while alcohol may not kill brain cells, if this myth encourages us to rethink that third beer or glass of wine, I won’t mind if it hangs around.
For individuals who drink before sleeping, alcohol initially acts as a sedative - marked by the delta frequency electroencephalogram (EEG) activity of Slow Wave Sleep (SWS) - but is later associated with sleep disruption. Significant reductions in EEG delta frequency activity and power also occur with normal development between the ages of 12 and 16; likewise this is a time when alcohol is commonly consumed for the first time, with dramatic increases in drinking occurring among collage-age individuals. A study of the effects of alcohol on sleep EEG power spectra in college students has found that pre-sleep drinking not only causes an initial increase in SWS-related delta power but also causes an increase in frontal alpha power, which is thought to reflect disturbed sleep.
“People likely tend to focus on the commonly reported sedative properties of alcohol, which is reflected in shorter times to fall asleep, particularly in adults, rather than the sleep disruption that occurs later in the night,” said Christian L. Nicholas, National Health & Medical Research Council Peter Doherty Research Fellow in the Sleep Research Laboratory at The University of Melbourne as well as corresponding author for the study.
“The reduction in delta frequency EEG activity we see across the ages is thought to represent normal brain maturational processes as the adolescent brain continues to develop to full maturity,” said Nicholas. “Although the exact function of non-Rapid Eye Movement (NREM) sleep, and in particular SWS, is a topic of debate, it is thought to reflect sleep need and quality; thus any disruption to this may affect the underlying restorative properties of sleep and be detrimental to daytime functioning.”
Nicholas and his colleagues recruited 24 participants (12 female, 12 male), healthy 18- to 21-year-old social drinkers who had consumed less than seven standard drinks per week during the previous 30 days. Each participant underwent two conditions: pre-sleep alcohol as well as a placebo, followed by standard polysomnography with comprehensive EEG recordings.
Results showed that alcohol increased SWS delta power during NREM. However, there was a simultaneous increase in frontal alpha power.
“For individuals researching sleep in the field of alcohol studies,” said Nicholas, “our findings indicate that care needs to be taken when interpreting increases in ‘visually scored’ SWS associated with alcohol consumption. Increases in SWS, which traditionally would be interpreted as a good thing, can be associated with more subtle changes indicating disrupted sleep, such as the increases we observed in alpha activity, which are revealed when more detailed micro-structural components of the sleep electroencephalogram are assessed.”
Nicholas explained that the increase in frontal alpha power that occurs as a result of pre-sleep drinking likely reflects a disruption of the normal properties of NREM slow wave sleep.
“Similar increases in alpha-delta activity, which are associated with poor or unrefreshing sleep and daytime function, have been observed in individuals with chronic pain conditions,” he said. “Thus, if sleep is being disrupted regularly by pre-sleep alcohol consumption, particularly over long periods of time, this could have significant detrimental effects on daytime wellbeing and neurocognitive function such as learning and memory processes.”
Alcohol is not a sleep aid, said Nicholas. “The take-home message here is that alcohol is not actually a particularly good sleep aid even though it may seem like it helps you get to sleep quicker. In fact, the quality of the sleep you get is significantly altered and disrupted.”
Bacteria in the gastrointestinal tract fulfill many vital functions and are critical for digestion. Yet, these same bacteria can induce strong inflammatory responses by the immune system if they penetrate the gut and enter the bloodstream.
Although acute inflammation is a natural response to protect the body, chronic or systemic inflammation is linked to numerous disorders and diseases. Prior research has established the involvement of inflammatory processes in the development of psychiatric disorders, including major depression and alcohol dependence, but the origins of such inflammation have remained unclear.
Now, researchers at Université Catholique de Louvain in Belgium, led by senior authors Dr. Philippe de Timary and Dr. Peter Stärkel, have found that inflammatory pathways are stimulated in alcohol-dependent patients by bacteria that escape the gut barrier, which correlated with alcohol craving. They report their findings in the current issue of Biological Psychiatry.
“In this study, we established a link between alcohol consumption, craving and activation of pro-inflammatory cytokines which contribute to a systemic inflammatory status in alcohol-dependent patients,” said Stärkel.
To conduct this work, they recruited 63 actively-drinking alcohol-dependent patients who underwent testing both before and after alcohol detoxification. That data was compared with testing from 14 healthy volunteers.
When patients were exposed to alcohol, the researchers found that the inflammatory response originated from gut-derived bacterial products that crossed the gut barrier, which in turn, activated specific inflammatory pathways in blood mononuclear cells.
Prior to undergoing detoxification, the observed inflammation correlated with both alcohol consumption and alcohol craving among the alcohol-dependent patients. Following detoxification, some, but not all, of the altered inflammatory processes were either partially or fully recovered.
“This establishes a new concept where events having their origin at peripheral sites in the body could modify central brain mechanisms that ultimately influence behaviour in alcohol dependence,” Stärkel explained.
Dr. John Krystal, Editor of Biological Psychiatry, commented, “This study suggests that there may be a link between inflammatory processes that develop when gut barriers to bacteria break down and risk for continued heavy drinking among people with alcohol use disorders. The findings suggest that it might be helpful to protect and restore gut integrity and to reduce inflammation when helping patients recover from alcohol use disorders.”
Stärkel agreed, adding, “The study does not only open new areas for research but also identifies new targets for developing novel treatment and management approaches for alcohol dependence. Targeting the gut-brain axis either at the level of the gut itself or at the level of effector cells such as blood mononuclear cells in order to influence behaviour could become a potential option in the care of alcohol-dependent patients.”
Maternal alcohol consumption during pregnancy has detrimental effects on fetal central nervous system development. Maternal alcohol consumption prior to and during pregnancy significantly affects cognitive functions in offspring, which may be related to changes in cyclin-dependent kinase 5 because it is associated with modulation of synaptic plasticity and impaired learning and memory. Prof. Ruiling Zhang and team from Xinxiang Medical University explored the correlation between cyclin-dependent kinase 5 expression in the hippocampus and neurological impairments following prenatal ethanol exposure, and found that prenatal ethanol exposure could affect cyclin-dependent kinase 5 and its activator p35 in the hippocampus of offspring rats. These findings, which reported in the Neural Regeneration Research (Vol. 8, No. 18, 2013), propose new insights into the mechanisms underlying the role of ethanol exposure in central nervous system injuries, and provide a new strategy for treating the consequences of prenatal ethanol exposure.