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Until law, GLP-1 drugs were used to treat diabetes, obesity and even the recent evidences suggest that it could as well be used to treat chronic kidney problems. There is yet another research, published in JAMA Psychiatry on February 25, titled Once-Weekly Semaglutide in Adults With Alcohol Use Disorder: A Randomized Clinical Trial that explores if GLP-1 receptor agonist semaglutide reduce alcohol consumption and cravings in adults with alcohol use disorder.
The research was conducted over a period of 9 weeks, where in the randomized clinical trial, the participants who were administered semaglutide, it led to reductions in some but not all measures of weekly consumptions. It also reduced weekly alcohol and craving related to placebo, and also led to a greater relative reduction in cigarettes per day.
The research also found that weekly injections of semaglutide, which is the active ingredient in weight loss drugs like Wegovy also helped reduce cravings in people with alcohol use disorder.
The lead author Christian Hendershot said that these findings will help in developing new approaches to treat alcoholism. "Two drugs currently approved to reduce alcohol consumption aren't widely used. The popularity of Ozempic and other GLP-1 receptor agonists increases the chances of broad adoption of these treatments for alcohol use disorder," said Hendershot in news release by the University of Southern California's Institute for Addiction Research, where he is the director.
The study is government-funded research and was funded by the National Institute on Alcohol Abuse and Alcoholism, part of the National Institutes of Health.
The study was small, and took in account for only 48 adults over two months, thus experts say that it is not yet clear how safe these drugs are for people who do not need to lose weight. Though the results do add up with the evidence form animal studies on drugs like Ozempic and Wegovy on how it helps manage cravings, not just for food, but also for tobacco and alcohol. Scientists are also studying these drugs on smokers, people with opioid addiction and cocaine users.
Co-author Dr Klara Klein of the University of North Carolina at Chapel Hill who treats people with obesity and diabetes said, "This is such promising data. And we need more of it. We frequently will hear that once people start these medications that their desire to drink is very reduced, if not completely abolished."
The GLP-1 receptor agonists work by mimicking hormones GLP-1 in the gut and brain that regulates appetite and feelings of fullness. This response is what helps one lose weight, and what helps one curb their craving for alcohol. These drugs that mimic the functioning of your brain, which is responsible to tell your body when to stop consuming, are the same hormones that tell your body about other kinds of consumptions, including alcohol. Therefore by consuming the weight loss drugs one can treat alcohol use disorder.
However, the researchers have pointed out on the limited data on the research and have suggested to continue using the three approved drugs by the National Institute on Alcohol Abuse and Alcoholism and Substance Abuse and Mental Health Services Administration, namely, Disulfiram, Naltrexone, and Acamprosate to treat alcohol use disorder until large studies confirm these findings.
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Stanford University scientists have grown lab-made human brain tissue inside mice, successfully creating a new kind of animal model whose constitution is the closest to those of humans. This could help researchers study brain development and neurological diseases in living organisms with a lot more accuracy.
The study, published in Nature recently, discusses mice whose cerebral cortex was largely replaced by human brain tissue grown from stem cells.
The human tissue expanded to occupy more than 90% of the space available for the mouse cortex and formed connections with the animals' nervous systems successfully.
The researchers call them xenocortical mice. The breakthrough could provide scientists with a way to study human neurons in a living brain, something that cannot be done directly in people and is difficult to reproduce using conventional laboratory models.
The researchers first genetically engineered mice so that most of the cells destined to form their cerebral cortex and hippocampus would not develop. This created space for human brain tissue.
Then they transplanted human cortical organoids, three-dimensional structures made from human stem cells, into the brains of newborn mice.
The organoids were able to grow rapidly inside the animals. In successful transplants, the human tissue expanded nearly five-fold over a period of three months and eventually occupied more than 90% of the available cortical space.
The human cells also developed different types of neurons and formed connections with the mouse brain and, in some cases, extended nerve fibres into the spinal cord. It is important to note that these are not mice with an entirely human brain.
The animals still have a mouse nervous system, including their sensory organs and deeper brain structures. What has been humanised is the cortex, the outer part of the brain involved in functions including perception, learning, and complex information processing.
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One of the biggest problems in neuroscience is that findings in mice do not always translate to humans.
Human brain organoids grown in laboratory dishes have helped researchers study development and disease, but they lack many features of a living brain. They do not receive normal sensory information or interact with muscles and other organs. Putting human neural tissue inside a living animal provides that missing environment.
The Stanford researchers tested the model by exposing the mice to a temporary lack of oxygen. The human cortical cells showed significant damage, and the animals developed movement and coordination problems. This provided a way to observe how developing human neural tissue responds to an injury inside a living organism.
The researchers say the approach could eventually help investigate conditions including cerebral palsy, epilepsy, autism, schizophrenia and other neurodevelopmental or neurological disorders, while also providing a platform for testing potential treatments.
The experiment also raises difficult ethical questions. As scientists become increasingly capable of integrating human neural tissue into animals, researchers must consider whether increasingly sophisticated brain models could acquire unexpected characteristics or alter animal welfare.
The Stanford team sought outside ethical review of the work. Experts have emphasised that there is currently no evidence that these mice possess human-like consciousness, but they also argue that ethical oversight will become important as these models become more complex.
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The death of a 16-year-old San Francisco boy has sparked concerns about the arrival of cychlorphine, a synthetic opioid that experts describe as 10 times more potent than fentanyl.
Dante Paul Lacourte died at his home on April 7 after taking drugs that contained cychlorphine. His death was the first confirmed cychlorphine-related overdose reported in San Francisco. The drug had already been linked to dozens of deaths elsewhere in the US.
The case has led to four arrests till now. San Francisco police said they seized more than 20,000 counterfeit pills, along with firearms, during searches connected to the investigation into the teenager's death.
Cychlorphine is a synthetic opioid that has crept up in the illicit drug supply in the last few years. It was first identified in the US in 2024 and belongs to a growing group of highly potent synthetic opioids.
The White House's Office of National Drug Control Policy warned in April that cychlorphine could be “up to ten times more potent than fentanyl” and linked it to 55 deaths across the US between 2025 and 2026. Tennessee has recorded the largest number of confirmed deaths so far.
Fentanyl is already notorious for being an extremely powerful opioid. Cychlorphine adds another layer of risk to an illicit drug supply that is already difficult to predict.
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Cychlorphine can be mixed into other drugs or pressed into counterfeit prescription pills, meaning someone may believe they are taking a familiar medication when the tablet actually contains a much more powerful opioid.
This was one of the concerns highlighted in the San Francisco case. Police said counterfeit pills had been seized from earlier, unrelated investigations and subsequently tested positive for cychlorphine, suggesting the drug was already circulating through multiple sources.
Another problem with cychlorphine is detection. Fentanyl test strips do not detect cychlorphine, so a negative fentanyl test does not mean a drug is free from cychlorphine.
Like other powerful opioids, cychlorphine can suppress the central nervous system and slow or stop breathing.
Its high potency means very small amounts can potentially produce profound opioid effects.
Experts say the drug also increases the risk that a person could move rapidly from intoxication to life-threatening respiratory depression.
Naloxone, commonly known as Narcan, can reverse opioid overdoses, but the response to these extremely potent synthetic opioids can be complicated.
The New York Times reported that multiple doses of Narcan may be needed to reverse cychlorphine's effects, while people responding to an overdose may have only one or two doses available.
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San Francisco health officials say the emergence of cychlorphine shows how quickly the illicit drug supply can change.
Daniel Tsai, director of the San Francisco Department of Public Health, said, “What we see now with cyclorphine, a new category of synthetic opioids potentially 10 times more potent than fentanyl, of course, it’s a great cause for concern.”
He also stressed that the safest way to avoid the risk is not to take counterfeit pills or illicit drugs. San Francisco is now working on wastewater surveillance that could help detect cychlorphine and other novel drugs before they are identified through an overdose death.
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The Ebola Bundibugyo virus outbreak in the Democratic Republic of the Congo (DRC) is showing early signs of slowing in some areas, WHO Director-General Tedros Adhanom Ghebreyesus said on Wednesday.
Speaking at a hybrid press briefing, Tedros said there were “encouraging signs” that the response was gaining ground, while warning that the epidemic continues to grow and cause deaths.
“We are now starting to see encouraging signs that we are gaining ground.”
According to Tedros, transmission is declining in some of the worst-affected parts of Ituri province.
Other signs of progress include:
Not yet. Tedros stressed that the “epidemic continues to grow, and continues to kill.”
More than 7,200 cases and over 3,500 deaths have been reported across seven provinces.
Although transmission has declined in parts of Ituri, it is falling from a high level. In the past week alone, around 300 new cases and 160 deaths were reported from Ituri, accounting for nearly half the national total, the WHO chief said.
In North Kivu, meanwhile, cases are rising rapidly. Over the past two weeks, the number of weekly cases has almost doubled, from about 100 to more than 200.
“The area is so vast that it is hard to speak of a single epidemic. It is many outbreaks, in many places. We must get the response right in every one of them,” Dr Tedros said.
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Last week, Congolese Health Minister Samuel Roger Kamba said transmission of the Bundibugyo virus had declined, with daily cases falling from about 120 at the peak in mid-August to around 80.
“We are fighting a very dangerous virus that is killing many of our people. Today, we can say that the outbreak is under control,” he said.
“At one point, we were recording about 120 cases per day; today, we’re seeing about 80 per day. So the number of new cases is decreasing every day.”
Kamba said 10 of the 62 affected health zones had reported no new cases for more than 22 days. Six health zones had gone more than 42 days without a new case, while four had gone more than 21 days without one.
He described the figures as “encouraging” but stressed that people must remain fully mobilized and not lower their guard.
The outbreak, caused by the rare Bundibugyo virus, was declared by the WHO on May 15. It is the DRC’s 17th Ebola outbreak since the virus was first identified in 1976.
It is also the second-deadliest Ebola outbreak on record, behind the West African outbreak that lasted from 2014 to 2016.
Clinical trials of vaccines and treatments against the Bundibugyo virus are ongoing. The DRC also received more than 70,000 doses of the Ervebo vaccine last month. Ervebo is approved for protection against the more common Zaire Ebola virus.
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