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Using a custom-built tool to analyze electrical activity from neurons, researchers at Brown University have identified a brain-based biomarker that could be used to predict whether mild cognitive impairment will develop into Alzheimer’s disease.

“We’ve detected a pattern in electrical signals of brain activity that predicts which patients are most likely to develop the disease within two and a half years,” said Stephanie Jones, a professor of neuroscience affiliated with Brown’s Carney Institute for Brain Science who co-led the research. “Being able to noninvasively observe a new early marker of Alzheimer’s disease progression in the brain for the first time is a very exciting step.” 

The findings were published in Imaging Neuroscience.

Working with collaborators at the Complutense University of Madrid in Spain, the research team analyzed recordings of brain activity from 85 patients diagnosed with mild cognitive impairment and monitored disease progress over the next several years. The recordings were made using magnetoencephalography, or MEG – a noninvasive technique to record electrical activity in the brain – while patients were in a resting state with their eyes closed.

Most methods for studying MEG recordings compress and average the detected activity, making it difficult to interpret at the neuronal level. Jones and other researchers at Brown pioneered a computational tool, called the Spectral Events Toolbox, that reveals neuronal activity as discrete events, showing exactly when and how often activity occurs, how long it lasts and how strong or weak it is. The tool has become widely used and has been cited in more than 300 academic studies.

Using the Spectral Events Toolbox, the team looked at brain activity events in patients with mild cognitive impairment, occurring in the beta frequency band –– a frequency that has been implicated in memory processing, making it important to study in Alzheimer’s disease, according to Jones. They discovered distinct differences in the beta events of the participants who developed Alzheimer’s disease within two and a half years, in comparison with those who did not.

Two and a half years prior to their Alzheimer’s disease diagnosis, patients were producing beta events at a lower rate, shorter in duration and at a weaker power. To our knowledge, this is the first time scientists have looked at beta events in relation to Alzheimer’s disease.”

Danylyna Shpakivska, the Madrid-based first author of the study

Spinal fluid and blood biomarkers can identify the presence of toxic beta amyloid plaques and tau tangles –– proteins that build up in the brain and are thought to contribute to Alzheimer’s disease symptoms. A biomarker from brain activity itself represents a more direct method of assessing how neurons respond to this toxicity, said David Zhou, a postdoctoral researcher in Jones’ lab at Brown who will lead the next phase of the project.

Jones envisions that the Spectral Events Toolbox could be used by clinicians to diagnose Alzheimer’s disease before it progresses. 

“The signal we’ve discovered can aid early detection,” Jones said. “Once our finding is replicated, clinicians could use our toolkit for early diagnosis and also to check whether their interventions are working.”

Meanwhile, Jones and her team will move into a new phase of research, funded by a Zimmerman Innovation Award in Brain Science from the Carney Institute. 

“Now that we’ve uncovered beta event features that predict Alzheimer’s disease progression, our next step is to study the mechanisms of generation using computational neural modeling tools,” Jones said. “If we can recreate what’s going wrong in the brain to generate that signal, then we can work with our collaborators to test therapeutics that might be able to correct the problem.”

The research was supported by the National Institutes of Health, including the Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative, in addition to funding from agencies in Spain. 

The World Health Organization (WHO) announces the reclassification of hepatitis D as cancerous, emphasizing the urgent need for the elimination of viral hepatitis, according to an official news release. The agency calls on governments to act amid a growing public health crisis.

Viral hepatitis is highly prevalent across the globe, affecting nearly 300 million people and claiming the lives of over 1.3 million each year. Hepatitis is a viral infection that can be acute or chronic, depending on the specific type. For chronic infections, symptom management is the standard of care. However, vaccines can help prevent infection with viral hepatitis.^1,2

“Every 30 seconds, someone dies from a hepatitis-related severe liver disease or liver cancer. Yet we have the tools to stop hepatitis,” Tedros Adhanom Ghebreyesus, MD, WHO Director-General, said in an official news release.¹

There are 5 types of hepatitis viruses. They include³:

• Hepatitis A: Caused by the hepatitis a virus (HAV); contracted from consuming contaminated food or water
• Hepatitis B: Caused by hepatitis B virus (HBV); most common liver infection in the world; often acute but can be chronic
• Hepatitis C: Spreads through shared needles or syringes; more likely to be chronic
• Hepatitis D: Caused by the hepatitis D virus (HDV); most common in those with hepatitis B
• Hepatitis E: Caused by the hepatitis E virus (HEV); typically resolves without treatment; treatment required for pregnant individuals

All types of hepatitis are associated with acute liver infection; however, only hepatitis B, C, and D can lead to chronic infections with a higher risk of liver cirrhosis, failure, or cancer. According to the authors of the study’s findings, hepatitis D is associated with a 2- to 6-fold higher risk of liver cancer compared with hepatitis B.¹

The WHO’s announcement stems from the International Agency for Research on Cancer’s (IARC) reclassification of hepatitis D as carcinogenic, supported by data from a study published in The Lancet Oncology. The study assessed the carcinogenic potential of HDV, human cytomegalovirus (HCMV), and Merkel cell polyomavirus (MCPyV).^4,5

HDV is a single-stranded RNA virus that depends on the presence of the hepatitis B virus for replication and infection. HCMV, a member of the beta-herpesvirus family, is commonly transmitted via bodily fluids and can be passed from mother to fetus during pregnancy. MCPyV is a widely circulating virus typically acquired during early childhood through direct contact and is known to persist on the skin as part of the normal virome.⁵

The WHO’s classification of hepatitis D as carcinogenic marks a pivotal moment in the global fight against viral hepatitis. With mounting evidence linking HDV to significantly elevated cancer risk, health leaders are urging swift policy action, expanded access to hepatitis B vaccination, and stronger surveillance systems. As the burden of viral hepatitis continues to grow—despite the availability of effective prevention tools—experts stress that eliminating hepatitis is not only possible but also essential to reducing liver cancer worldwide.

REFERENCES

1. WHO urges action on hepatitis, announcing hepatitis D as carcinogenic. WHO. July 28, 2025. Accessed August 4, 2025. https://www.who.int/news/item/28-07-2025-who-urges-action-on-hepatitis-announcing-hepatitis-d-as-carcinogenic

2. Global viral hepatitis. CDC. July 25, 2025. Accessed August 4, 2025. https://www.cdc.gov/hepatitis/global/index.html

3. What is viral hepatitis? Cleveland Clinic. March 27, 2025. Accessed August 4, 2025. https://my.clevelandclinic.org/health/diseases/4245-hepatitis-viral-hepatitis-a-b–c#overview

4. Karagas M, Kaldor J, Michaelis M, et al. Carcinogenicity of hepatitis D virus, human cytomegalovirus, and Merkel cell polyomavirus. The Lancet Oncology. June 27, 2025. doi: 10.1016/S1470-2045(25)00403-6

5. IARC Monographs evaluation of the carcinogenicity of hepatitis D virus, human cytomegalovirus, and Merkel cell polyomavirus. International Agency for Research on Cancer. June 27, 2025. Accessed August 4, 2025. https://www.iarc.who.int/news-events/iarc-monographs-evaluation-of-the-carcinogenicity-of-hepatitis-d-virus-human-cytomegalovirus-and-merkel-cell-polyomavirus/

For decades, medical professionals debated whether a common antiviral medication used to treat flu in children caused neuropsychiatric events or if the infection itself was the culprit.

Now researchers at Monroe Carell Jr. Children’s Hospital at Vanderbilt have debunked a long-standing theory about oseltamivir, known as Tamiflu.

According to the study, published in JAMA Neurology, oseltamivir treatment during flu episodes was associated with a reduced risk of serious neuropsychiatric events, such as seizures, altered mental status and hallucination.

“Our findings demonstrated what many pediatricians have long suspected, that the flu, not the flu treatment, is associated with neuropsychiatric events,” said principal investigator James Antoon, MD, PhD, MPH, assistant professor of Pediatrics in the Division of Pediatric Hospital Medicine at Monroe Carell. “In fact, oseltamivir treatment seems to prevent neuropsychiatric events rather than cause them.”

Key points:

• Influenza itself was associated with an increase in neuropsychiatric events compared to children with no influenza, regardless of oseltamivir use.
• Among children with influenza, those treated with oseltamivir had about 50% reduction in neuropsychiatric events.
• Among children without influenza, those who were treated with oseltamivir prophylactically had the same rate of events as the baseline group with no influenza.

“Taken together, these three findings do not support the theory that oseltamivir increases the risk of neuropsychiatric events,” said Antoon. “It’s the influenza.”

The team reviewed the de-identified data from a cohort of children and adolescents ages 5-17 who were enrolled in Tennessee Medicaid between July 1, 2016, and June 30, 2020.

During the four-year period, 692,295 children, with a median age of 11 years, were included in the study cohort. During follow-up, study children experienced 1,230 serious neuropsychiatric events (898 neurologic and 332 psychiatric).

The clinical outcomes definition included both neurologic (seizures, encephalitis, altered mental status, ataxia/movement disorders, vision changes, dizziness, headache, sleeping disorders) and psychiatric (suicidal or self-harm behaviors, mood disorders, psychosis/hallucination) events.

“The 2024-2025 influenza season highlighted the severity of influenza-associated neurologic complications, with many centers reporting increased frequency and severity of neurologic events during the most recent season,” said Antoon. “It is important for patients and families to know the true risk-benefit profile of flu treatments, such as oseltamivir, that are recommended by the American Academy of Pediatrics.”

“These flu treatments are safe and effective, especially when used early in the course of clinical disease,” added senior author Carlos Grijalva, MD, MPH, professor of Health Policy and Biomedical Informatics at Vanderbilt University Medical Center.

Investigators hope the findings will provide reassurance to both caregivers and medical professionals about the safety of oseltamivir and its role in preventing flu-associated complications.

The study was funded by the National Institutes of Health (grants K23AI168496, K24AI148459 and P50HD106446).

Source:

Vanderbilt University Medical Center

Have you ever wondered why some people who drink alcohol develop serious liver problems while others don’t? A study from University of Louisville researchers published in May in Toxicological Sciences suggests that the answer might be hidden in everyday sources such as drinking water, food packaging or even non-stick cookware.

Scientists at UofL, along with colleagues from Boston University and the University of Massachusetts Lowell, have identified perfluorooctane sulfonate (PFOS) as a potential environmental factor that worsens alcohol-associated liver disease.

PFOS is a man-made chemical belonging to the group known as per- and polyfluoroalkyl substances (PFAS), often referred to as “forever chemicals” because they do not readily break down in the environment or the human body. These substances have been used for decades in products such as non-stick cookware, water-resistant clothing, fast-food packaging, stain-resistant carpets and upholstery, and firefighting foams. Their extensive use has led to widespread contamination in the environment. Recent data from National Health and Nutrition Examination Survey show that PFAS can be detected in approximately 95% of Americans, sparking increasing concern about their long-term health effects.

At the same time, alcohol consumption remains a significant global health issue. According to the World Health Organization, alcohol contributes to nearly 3 million deaths worldwide each year, and its consumption continues to rise globally. In the U.S. alone, excessive alcohol use is responsible for approximately 95,000 deaths annually, making it one of the leading causes of preventable death and a major contributor to liver disease.

“Given the increasing prevalence of alcohol consumption and the widespread presence of PFAS in the environment, many individuals who drink alcohol may be inevitably exposed to these persistent pollutants. This makes it critically important to study how combined exposures to alcohol and environmental chemicals like PFOS might influence liver health,” said Matthew Cave, UofL professor of medicine and publication co-author.

Although it is well known that both alcohol and PFOS cause liver damage individually, little has been understood about their combined effects until now. Recent studies have shown that only about 35% of heavy drinkers develop severe forms of liver disease, indicating that additional factors such as genetics, sex, microbiome and environmental exposures may contribute to individual susceptibility.

“This work helps explain why two people with similar alcohol consumption may experience very different liver outcomes,” said Frederick Ekuban, assistant professor of medicine at UofL and first author of the study. “Environmental exposures like PFOS may be the missing link.”

Using animal models, the researchers simulated real-world exposures to both alcohol and PFOS. The study showed that co-exposure to alcohol and PFOS significantly increased fat accumulation and markers of liver damage, as well as clear signs of disrupted metabolism and activation of genes and pathways predicted to be associated with oxidative stress and cancer development.

In short, the study demonstrates that PFOS exposure can significantly worsen liver damage when combined with alcohol consumption. While this research used high levels of alcohol to understand the underlying mechanisms, the findings reveal important biological pathways that warrant further investigation across different drinking patterns.

The research team also found that PFOS interferes with the liver’s ability to manage fats, disrupts its natural protective and repair systems and activates pathways that promote liver injury.

“While the liver typically has a remarkable capacity to recover from alcohol-induced stress, PFOS appears to push that resilience beyond its limits, resulting in compounded and more severe damage,” said Jennifer Schlezinger professor of environmental health at Boston University and co-author of the publication.

Perhaps most concerning, the team discovered that 60% of all PFOS exposure ended up concentrated in the liver, exactly where alcohol damage occurs.

Ongoing research at UofL is examining how other PFAS compounds may interact with alcohol, whether males and females respond differently to these exposures and what the long-term consequences of combined exposures might be. The team is also exploring whether targeted therapies can be developed to prevent or mitigate this type of liver damage.

Although more studies are needed, people can take practical steps now to limit their exposure to PFAS. These include:

• Choose stainless steel or cast-iron cookware instead of non-stick pans
• Use water filters, especially in areas near industrial zones
• Avoid stain-resistant treatments on furniture and carpets
• Reduce consumption of packaged fast foods and microwave popcorn.
• Select household products with PFAS-free labels

Given that liver disease affects millions of Americans and is becoming more prevalent worldwide, the findings of this research support growing calls for stronger regulation and oversight of persistent chemical contaminants. By better understanding the hidden interactions between environmental toxicants and lifestyle behaviors, scientists and policymakers may be better equipped to prevent and treat liver disease.

Opioids like morphine are widely used in medical practice due to their powerful pain-relieving effects. However, they carry the risk of serious adverse effects such as respiratory depression and drug dependence. For this reason, Japan has strict regulations in place to ensure that these medications are prescribed only by authorized physicians.

In the United States, however, the opioid OxyContin was once prescribed frequently triggering a surge in the misuse of synthetic opioids such as fentanyl. As a result, the number of deaths caused by opioid overdose surpassed 80,000 in 2023, escalating into a national public health crisis now referred to as the “opioid crisis”.

Opioids may soon have a rival, however. A team of researchers at Kyoto University has recently discovered a novel analgesic, or pain reliever, which exerts its effect through an entirely different mechanism. Clinical development of their drug ADRIANA is currently underway as part of an international collaborative effort.

“If successfully commercialized, ADRIANA would offer a new pain management option that does not rely on opioids, contributing significantly to the reduction of opioid use in clinical settings,” says corresponding author Masatoshi Hagiwara, a specially-appointed professor at Kyoto University.

The research team was first inspired by substances that mimic noradrenaline, which is released in life-threatening situations and activates α2A-adrenoceptors to suppress pain. However, these pose a high risk of cardiovascular instability. After observing noradrenaline levels and α2B-adrenoceptors, the team hypothesized that selectively blocking α2B-adrenoceptors could elevate noradrenaline levels, leading to activation of α2A-adrenoceptors and resulting in pain relief without causing cardiovascular instability.

To identify selective inhibitors of α2B-adrenoceptors and measure the activity of individual α2-adrenoceptor subtypes, the researchers employed a novel technology known as the TGFα shedding assay and conducted compound screening leading to their discovery of the world’s first selective α2B-adrenoceptor antagonist.

After success in administering the compound to mice and conducting non-clinical studies to assess its safety, physician-led clinical trials were conducted at Kyoto University Hospital. Both the Phase I trial in healthy volunteers and the Phase II trial in patients with postoperative pain following lung cancer surgery yielded highly promising results.

Building on these outcomes, preparations are now underway for a large-scale Phase II clinical trial in the United States, in collaboration with BTB Therapeutics, Inc, a Kyoto University-originated venture company.

As Japan’s first non-opioid analgesic, ADRIANA has the potential not only to relieve severe pain for patients worldwide but could also play a meaningful role in addressing the opioid crisis — a pressing social issue in the United States — and thus contribute to international public health efforts.

“We aim to evaluate the analgesic effects of ADRIANA across various types of pain and ultimately make this treatment accessible to a broader population of patients suffering from chronic pain,” says Hagiwara.