Liquor Impacting Brain Activity (Credit-Freepik)
Many of us believe that we are great drinkers and that alcohol does not affect us as much. People who are able to drink without showing any sign of inebriation are known as social drinkers. In short, they are not addicted to alcohol but will not turn down the opportunity to have a good time! While it may seem like it doesn’t affect you, new studies suggest that it is just an illusion, even if you have high tolerance, alcohol affects your cognitive and motor functions more than you think.
The study reveals the below implications and techniques:
Think of it as the foundation for your brain's performance. When brain conductivity is high, information flows smoothly, and that helps your brain in rapid processing and response. On the other hand, low conductivity can hinder cognitive function, leading to slower thinking, impaired memory, and difficulties with coordination.
A study conducted at the Neuroscience Research Australia (NeuRA) and UNSW Science unveiled a startling connection between alcohol consumption and brain conductivity.
While many people brush off the effects of alcohol as temporary changes in behaviour, the reality is much more complex. Beyond the obvious impacts on coordination and judgment, alcohol significantly alters brain function. Alcohol dramatically slowed down brain activity, especially in areas responsible for decision-making, planning, and physical coordination. This decline was so significant that it resembled the brain changes seen in normal ageing. This means even one drink could temporarily accelerate the ageing process of your brain.
The implications of this research are far-reaching. It provides compelling evidence that alcohol consumption has a direct and measurable impact on brain function. The discovery that alcohol can significantly reduce brain conductivity opens new avenues for understanding the neurocognitive effects of alcohol abuse and dependence. While you may not feel like alcohol is affecting you and you have a high tolerance, it most definitely changes and affects your decision-making abilities and impulse control.
Furthermore, the MRI technique employed in the study could be a valuable tool for assessing the impact of other substances on the brain and for developing interventions to mitigate alcohol-related brain damage.
Credit: UCSF
Drug-resistant superbug Candida auris (C. auris) has now been detected in 27 US states. According to the latest data from the US Centers for Disease Control and Prevention (CDC), 3,437 clinical cases have been reported through July 25.
The figure is about 1,000 fewer than the 4,290 cases reported during the same period last year.
C. auris is a deadly fungus that primarily poses a concern for people who are hospitalised or in long-term care facilities. The total number of clinical cases has increased since the pathogen was first detected in the US in 2016, the CDC said.
While the rate of increase has slowed in recent years, C. auris remains a “critical public health threat.”
First discovered in Japan in 2009, the pathogen can live silently on the skin but can become deadly when it reaches the bloodstream. It kills about 3,000 patients in US hospitals and long-term care facilities each year.
Now, a new study published in the journal Science has revealed why the deadly superbug can be so difficult to remove from the skin once it takes hold.
Researchers at the University of California, San Francisco (UCSF) found that C. auris actively rewires the skin’s immune system to protect itself, taking refuge in hair follicles where current therapies cannot reach it.
“Candida auris colonizes skin way better than most other fungi, setting it up to invade once the immune system is weakened,” said Dean Merrill, a dermatologist, UCSF professor and first author of the study.
“The big clinical problem is that we have no effective way to remove it from the skin,” he added.
To understand why C. auris persists on the skin unlike other fungi, researchers compared it with Candida albicans, a common fungus that the skin and immune system normally clear quickly.
In mice, C. auris was found to persist by taking refuge in hair follicles.
While C. albicans activated an immune signal called IL-17, which helps renew the skin’s surface and strengthen antifungal defenses, allowing the infection to be cleared, C. auris, triggered interferon gamma, a signal more commonly associated with viral infections.
The fungus achieved this by remodeling its outer cell wall to expose more of a molecule called chitin. This prompted immune cells to release interferon gamma around the hair follicle.
The interferon gamma then blocked the skin’s antifungal defenses, including IL-17. It also slowed the natural replacement of cells in the hair follicle, causing older, damaged cells to accumulate and creating a niche where C. auris could flourish.
The findings reveal potential targets for preventing C. auris from persisting on the skin.
One possible approach could involve drugs that shift the immune response away from interferon gamma and toward IL-17, which drives the skin’s normal antifungal clearing process.
Another possibility could be drugs that block chitin, potentially preventing the fungus from amplifying interferon gamma signals, Merrill said.
More broadly, the researchers say the findings offer a new way of understanding how microbes can quietly coexist with humans before becoming dangerous.
Credit: AI
The Democratic Republic of Congo’s (DRC) Ebola outbreak may have been spreading for months before health authorities officially declared it, raising new questions about why the early warning signs were missed.
According to the World Health Organization (WHO), genetic sequencing indicates that the current outbreak began as early as February 2026, while the DRC officially declared the outbreak on May 15. By then, the virus had already had time to spread through communities in eastern DRC.
The outbreak is being caused by the Bundibugyo virus, a rare Ebola species for which there is currently no approved vaccine or specific course of treatment.
One of the major reasons why the current Ebola outbreak expanded within a short period of time was that it not immediately recognised.
Some early patients were reportedly treated for malaria or typhoid, illnesses that can initially cause symptoms such as fever, weakness, vomiting and diarrhoea. Early testing also focused on the more common Zaire strain of Ebola, delaying recognition of Bundibugyo virus.
WHO’s own assessment had already identified an unusual cluster of severe illness and deaths in the Mongbwalu health zone in Ituri Province by early May. A subsequent investigation covering April 15 to May 13 identified 246 suspected cases and 65 deaths across three health zones.
Geographical disadvantage was also one of the reasons. Ituri is affected by armed conflict, population displacement and poor road access. Health workers have faced shortages of protective equipment, while some facilities have struggled because of workers' strikes.
Also read: Nova Scotia's Ebola Trial: Why Is Canada Testing A Vaccine When It Has No Outbreak?
The Ebola outbreak in DRC continues to grow at a rapid pace. The latest government figures cited by WHO and international media show about 4,200 confirmed Ebola cases and at least 1,900 deaths in DRC.
WHO Regional Director for Africa Mohamed Janabi described the situation bluntly: “We are chasing the virus, the virus is ahead of us.”
WHO Director-General Tedros Adhanom Ghebreyesus has also warned that the outbreak is moving faster than the response, with cases doubling in some hotspots. He wrote on on X that “the outbreak is spreading faster than our scale up of the response”, adding that new cases had doubled in some hotspots over the previous week.
Ebola becomes considerably harder to contain once transmission moves beyond identifiable limits. Unlike respiratory viruses, Ebola primarily spreads through contact with infected bodily fluids and contaminated materials. But when patients are not recognised early, they can unknowingly expose others, healthcare workers and caregivers.
Also read: FDA Approves Moderna's First mRNA Flu Vaccine, Marking A Milestone In Influenza Prevention
One of the major challenges in this outbreak is that around 60–70% of new cases are reportedly occurring outside known contact chains, making traditional contact tracing much harder. The current outbreak has also unfolded in crowded urban and displacement settings, rather than remaining confined to an isolated rural location.
The 2014–2016 West African Ebola epidemic was officially declared in March 2014, although the first human case was later traced back to December 2013. That outbreak eventually led to more than 11,000 deaths.
The WHO is now pushing to accelerate the response, including clinical trials of the Ervebo vaccine, which is licensed against the Zaire strain but may offer some protection against Bundibugyo. Researchers are also developing vaccines specifically targeting Bundibugyo virus.
mRNA-1469 is an investigational vaccine developed using Moderna's messenger RNA (mRNA) platform, the same technology used in its COVID-19 vaccine. The vaccine builds on the company's broader research into filoviruses, the family of viruses that includes Ebola.
Credit: AI
A new experimental menopause drug has shown promising results in reducing hot flashes, with the company reporting an 83% reduction in moderate-to-severe episodes in a mid-stage clinical trial.
Shares of Canadian biotechnology company AbCellera surged nearly 40% on Monday after it announced positive results for ABCL635, an experimental non-hormonal treatment for moderate-to-severe vasomotor symptoms associated with menopause.
The Phase 2 study involved 92 women. After four weeks, women who received a single 600-mg dose of ABCL635 experienced an 83% reduction in the frequency of moderate-to-severe hot flashes, equivalent to 8.8 fewer episodes per day from baseline. The placebo group reported a 33% reduction, or 3.5 fewer episodes per day.
The treatment also improved the severity of symptoms, sleep and women's overall assessment of their improvement, according to the company.
The most commonly reported side effects, however, included headache, fatigue and reactions at the injection site.
ABCL635 takes a different approach from hormone replacement therapy (HRT). It is a non-hormonal antibody treatment that targets the neurokinin 3 receptor, or NK3R, a protein involved in the brain's regulation of body temperature.
During menopause, falling estrogen levels can disrupt the activity of a group of brain cells known as KNDy neurons. This can make the body's temperature-control system overly sensitive, triggering hot flashes. By blocking NK3R signaling, ABCL635 is designed to help restore that balance.
Also read: Lifestyle Genetics And Hormones: Understanding The Interplay Of Risk Factors For Ovarian Cancer
One of the drug's potential advantages is its dosing. ABCL635 is being developed as a long-acting, once-monthly injection, rather than a daily pill.
AbCellera's chief medical officer Sarah Noonberg said the approach could appeal to women already accustomed to self-injecting medicines and could potentially improve adherence compared to daily dosing.
When the Phase 2 programme began, Noonberg said: “Menopausal symptoms can have a profound impact on quality of life,” adding that the company wanted to assess whether ABCL635 could offer women a safe and effective non-hormonal alternative.
However, the drug is still experimental and has not been approved for clinical use. AbCellera said additional 12-week trial data are expected later this year, which will provide a better picture of how long the benefits last and how the treatment performs over a longer period.
The drug development comes as non-hormonal menopause treatments are gaining popularity. FDA-approved options already include drugs targeting neurokinin pathways, including Astellas' Veozah and Bayer's Lynkuet, giving women alternatives when hormone therapy is unsuitable or not preferred.
Hot flashes, also known as vasomotor symptoms, are among the most common symptoms of menopause. The Menopause Society says up to 80% of women experience hot flashes or night sweats at some point during the menopause.
A hot flash can begin suddenly, often as an intense wave of heat across the face, neck and chest. It may be followed by sweating, chills, dizziness, anxiety or racing heartbeat. When these episodes happen during sleep, they are known as night sweats.
Frequent hot flashes can repeatedly interrupt sleep, leaving women irritable and fatigued the next day. Poor sleep can then affect concentration, mood and daily functioning, creating a cycle in which one menopause symptom amplifies another.
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