Proteins form the building blocks of life, but when they form unusual clumps inside the brain, they raise an alarm that something isn’t right.

A classic example is Lewy bodies (LBs), abnormal clumps composed of the protein α-synuclein, which are considered biomarkers of neurodegenerative diseases such as Parkinson’s disease (PD) and dementia.

A recent study in Communications Biology by a team of Indian researchers examined how Parkinson’s disease–specific variants of α-synuclein behave. Under normal conditions, α-synuclein is largely inert and selective because its sticky, hydrophobic core remains hidden. However, disease-related chemical changes in PD-specific αSyn variants expose the core, turning the protein reactive.

This change allows the protein to trap other cellular proteins early on, driving the formation and growth of LBs in nerve cells—a cascade of events that may trigger Parkinson’s disease.

Based on their observations of molecular pathways, the researchers suggested a new model for Lewy body formation, the Multifactorial Random Disorder Model. These new insights might inform future approaches to prevent or slow LB formation in PD.

The promiscuous protein

LBs are notorious for disrupting brain function, depending on where they appear. When found in the brainstem, they interfere with vital processes, leading to symptoms such as depression, sleep disturbances, unstable blood pressure, and bowel or bladder problems.

If they form in the substantia nigra—a key region of the midbrain—they trigger the classic movement symptoms, such as tremor at rest, slowed movement, and muscle stiffness, which are associated with Parkinson’s disease.

Almost 9 decades after LBs were first identified in 1912, researchers found that the mutations in the protein α-synuclein played a central role in their formation.

The protein is commonly found in neurons and consists of three main parts: a charged front region, a sticky middle section that can drive clumping, and a tail. The strictly middle part is responsible for unwanted protein aggregation, but under normal conditions, it’s quite choosy and doesn’t bind to every protein available.

Studies show that disease-related changes in the cellular environment—such as shifts in ion concentrations or pH—can disrupt these protective interactions, exposing the protein’s sticky core.

Even though α-synuclein is a driving force, it isn’t the only protein LBs are made of. However, most existing models focus only on how α-synuclein clumps together and fail to clarify the molecular steps by which disease-specific forms of α-synuclein drive Lewy body formation.

The researchers in this study used E. coli bacteria to produce different versions of the α-synuclein protein, including healthy and disease-linked variants, some truncated at the C-terminus and others chemically tagged at a specific position (phosphorylation at S129). They conducted a range of tests, including protein aggregation, binding interactions, and protein folding, to examine how the different variants behaved.

They found that while the healthy versions showed no interest in interacting with the 22 different cellular proteins added to the reaction mixture by the researchers, the disease-linked variants bound with high affinity to almost all of them. They behaved like molecular decoys, nonselectively capturing nearby proteins and membrane organelles.

These findings led the team to propose an alternative model for how Parkinson’s disease may progress in the brain.

The new Multifactorial Random Disorder Model suggests that highly reactive, truncated forms of α-synuclein kickstart the process by grabbing nearby cellular components and forming the dense core of a Lewy body. As the structure grows, phosphorylated forms of the protein accumulate at the periphery, helping the Lewy body grow over time.

Understanding the molecular mechanisms behind Lewy body formation can bring us closer to more effective therapies for combating Parkinson’s disease, a condition that impacts millions of lives worldwide.

Researchers out of Spain and Italy report a globally pooled Internet Gaming Disorder prevalence of 6.1% among adults ages 18–35. Internet Gaming Disorder is considered a condition for further study in DSM-5-TR, with official classification in ICD-11.

Gaming problems often get viewed as an adolescent concern, while evidence indicates growing vulnerability in young adults. Late adolescents and young adults tend to show higher levels of depression, anxiety, and stress, along with lower self-esteem, compared to healthy regular gamers.

ICD-11 includes three core diagnostic features, including inability to control gaming behavior, increasing priority given to gaming over other activities, and persistent gaming behavior despite negative consequences, present for a minimum of 12 months.

ICD-11 includes three core diagnostic features, including inability to control gaming behavior, increasing priority given to gaming over other activities, and persistent gaming behavior despite negative consequences, present for a minimum of 12 months.

Prior meta-analyses place prevalence in the general population from 3.05% to 6.7%, with variation across age groups and across countries or continents. Estimates for children and adolescents range from 1% to 9%, with an adolescent estimate of 4.6%.

Gaming can have consequences

Delayed timing for financial independence, stable relationships, and starting a family lines up with a slower, more gradual move into adult roles. Young adulthood can include ongoing developmental change plus major transitions in education, work, and social life, and that combination can leave some people more vulnerable to using gaming as a coping mechanism during that period.

In the study, “Prevalence of Internet gaming disorder in young adults: a systematic review and meta-analysis,” published in Addictive Behaviors, researchers conducted a systematic review and meta-analysis to estimate the global prevalence of Internet Gaming Disorder among young adults and identify moderators linked to variability.

Database searches used the Web of Science Core Collection, Scopus, and PsycInfo, plus manual reference list searches that drew on prior systematic reviews and meta-analyses. Analytical samples from 93 studies included 149,601 participants ages 18–35, with an average age of 23.53 years (standard deviation of 6.28). 51.22% were female.

Prevalence estimates in primary samples ranged from 0% to 63% with a pooled prevalence of 6.1%. Gamer-only samples showed a pooled prevalence of 8.1% while mixed samples including gamers and non-gamers reached 5.47%.

Shifting numbers between studies

Different screening tools produced different prevalence estimates. Higher prevalence estimates appeared in samples assessed with the Internet Gaming Disorder Scale and DSM-5 criteria than in samples assessed with the Internet Gaming Disorder Test-10. Mixed samples showed lower prevalence estimates in samples assessed with the Game Addiction Scale than in samples assessed with the Internet Gaming Disorder Scale.

Larger sample sizes produced lower prevalence estimates in the full set of samples and in mixed samples. Trends suggested lower prevalence when there was a higher proportion of women in the samples, but the difference was non-significant.

The researchers conclude that strategies aimed at prevention and mental health interventions tailored to this age group are needed.

A national clinical trial led by the Alliance for Clinical Trials in Oncology has found that abemaciclib, an oral cancer drug, may slow tumor growth in patients with aggressive meningiomas that have specific genetic mutations. This primary analysis of Alliance A071401 is published in Nature Medicine.

Meningiomas, tumors that grow in the membranes that surround the brain and spinal cord, are the most common primary brain tumors. While most are benign or treatable, aggressive meningiomas with mutations in genes like NF2 and alterations in the CDK pathway can be fatal. Options are extremely limited for patients whose meningiomas are considered cancerous and return or continue to grow after surgery and radiation therapy.

“Patients with recurrent or progressive high-grade meningiomas have historically had very few treatment options, and most prior trials of medical therapy have been disappointing,” said senior author Priscilla Brastianos, MD, a neuro-oncologist with the Mass General Brigham Cancer Institute and co-chair of the Alliance Neuro-Oncology Committee.

Noting that the trial was the first national study to enroll patients based on mutational testing, Dr. Brastianos said that the research “shows that genomically driven trials for patients with meningioma are feasible and that targeted therapy may improve outcomes for patients with specific genetic mutations.”

The Alliance A071401 trial followed patients with grade 2 or 3 meningiomas whose tumors carried NF2 mutations or CDK pathway alterations. All patients evaluated had previously received surgery, radiation therapy, or both. Patients received an average number of nine cycles of abemaciclib, a CDK inhibitor that is currently approved for certain breast cancers.

Of the first 24 patients treated with abemaciclib, 58% had high-grade tumors that didn’t progress within the six months after they started therapy. There was no control arm in the study, due to the lack of standard treatment options available for patients with high-grade tumors after surgery and radiation. However, these results compare favorably to previous studies that found that on average, 0–29% of patients with grade 2 or 3 meningiomas had cancer that wasn’t progressing within six months from the time they started their experimental treatment.

In the Alliance A071401 trial, the median progression-free survival was 10 months, and the median overall survival was 29 months. Side effects were similar to what patients taking CDK inhibitors for other cancers experience. Common side effects included diarrhea, fatigue, headache, and nausea/vomiting. About a quarter of patients had a severe side effect (grade 3 or grade 4) that was possibly or likely related to treatment.

“We are encouraged by these exciting results, but we still have more work ahead of us to improve treatments for this understudied patient population,” said Dr. Brastianos.

Two separate studies suggest that minor lifestyle changes can lead to a longer life. One Norwegian-led team estimated that adding five min/day of moderate-to-vigorous intensity physical activity and reducing daily sedentary time by 30 min/day might prevent a proportion of deaths under high-risk and population-based approaches.

Another analysis from an Australian-led group links small combined gains in sleep, physical activity, and diet quality with added years of lifespan and healthspan.

Physical inactivity has been estimated to cause 7–9% of global mortality. Self-reported physical activity can be inaccurate, with device-measured data offering a different basis for linking movement patterns to mortality. Threshold-based estimates that assume benefits start only after meeting activity recommendations leave uncertainty around smaller gains that fall below that target.

Sleep, physical activity, and nutrition shape all-cause mortality and noncommunicable disease risk. Separate attention to each behavior can miss behavior patterns that shift together in daily life.

Deaths averted with small shifts

In the study, “Deaths potentially averted by small changes in physical activity and sedentary time: an individual participant data meta-analysis of prospective cohort studies,” published in The Lancet, Norwegian researchers conducted an individual participant data meta-analysis to estimate the proportion of deaths preventable from five-min and 10-min increases in moderate-to-vigorous intensity physical activity and 30-min and 60-min reductions in daily sedentary time.

Five minutes a day of more moderate-to-vigorous intensity physical activity was associated with deaths preventable under two prevention strategies: 6% of all deaths might be preventable if the least active participants exercised for five minutes a day; 10% of all deaths might be preventable if all participants except the most active engaged.

Thirty minutes a day less sedentary time was also associated with fewer preventable deaths; 3% of all might be preventable if just the least-active were more active; 7.3% of deaths if all but the already most active engaged.

In the study, “Minimum combined sleep, physical activity, and nutrition variations associated with lifeSPAN and healthSPAN improvements: a population cohort study,” published in eClinicalMedicine, Australian researchers used a prospective cohort to determine the minimum combined improvements in sleep, moderate-to-vigorous physical activity, and diet quality associated with longer lifespan and healthspan.

Optimal sleep, physical activity, and diet quality were associated with added years. Sleep of 7.2–8.0 hours a day, more than 42 minutes a day of moderate-to-vigorous physical activity, and a diet quality score of 57.5–72.5 were associated with 9.35 additional years of lifespan.

Minimum combined changes linked to smaller gains used minute-level and point-level shifts. Five minutes a day more sleep, 1.9 minutes a day more moderate-to-vigorous physical activity, and a 5-point increase in diet quality score were associated with one additional year of lifespan. Twenty four minutes a day more sleep, 3.7 minutes a day more moderate-to-vigorous physical activity, and a 23-point increase in diet quality score were associated with 4.0 additional years of healthspan.

Where the results point

Both teams framed small, realistic shifts as aligning with meaningful gains. One set of estimates tied a few minutes a day of more moderate-to-vigorous intensity physical activity and less sedentary time to shares of deaths potentially preventable.

Another set of estimates tied modest concurrent gains in sleep, physical activity, and diet quality to added years of lifespan and healthspan.

New research co-led by Indiana University School of Medicine scientists has exposed a vulnerability in acute myeloid leukemia by identifying the blood cancer’s reliance on a specific signaling pathway involved in the body’s inflammation response. Their preclinical evidence suggests that blocking this pathway with a new drug compound can weaken acute myeloid leukemia during critical stages, paving the way for more effective and targeted treatments for this hard-to-treat disease.

According to the National Cancer Institute, the five-year survival rate for AML is only 32.9%, and about 22,000 new cases were reported in 2025. Acute myeloid leukemia (AML) is known for being treatment-resistant and having a high relapse rate.

“AML is a challenging blood cancer because a small population of cells, known as leukemia stem cells, can survive chemotherapy and later regenerate the disease,” said Tzu-Chieh (Kate) Ho, Ph.D., assistant research professor of pediatrics at the IU School of Medicine and a lead author of the study. “Our research goal was to understand the critical mechanisms these leukemia stem cells rely on at both diagnosis and relapse, and to identify potential therapeutic targets.”

Study findings and drug development

In the study published in Leukemia, the researchers examined leukemia stem cells from AML patients during their diagnosis and relapse. They discovered that an inflammatory signaling pathway involved in the body’s immune system response—known as Interleukin-1 (IL-1) signaling—is significantly elevated at both stages. When the team used genetic approaches to reduce this signal in human AML cells, the cells formed fewer colonies and showed a diminished ability to reestablish leukemia.

The researchers also developed a new drug-like compound, UR241-2, designed to block the key proteins found in the IL-1 signaling pathway. In preclinical models, the compound impaired leukemia stem cells while largely sparing healthy blood-forming cells and significantly reduced leukemia levels in the mice. Their findings suggest that targeting this pathway could strengthen current AML treatments like chemotherapy and reduce the risk of relapse.

“Our studies indicate that IL-1 signaling is not a random feature, but rather a fundamental survival mechanism that persists across different stages of AML and can be targeted,” said Reuben Kapur, Ph.D., director of the IU School of Medicine Herman B Wells Center for Pediatric Research and co-author of the study. “This opens up exciting possibilities for developing therapies that are more effective and more precise.”

Future directions and clinical implications

UR241-2 is still in early preclinical development, but similar drugs are already being tested in clinical trials for other cancers and immune-related diseases, suggesting a promising path toward eventually evaluating this compound for AML.

“Future AML treatments may incorporate our strategy alongside standard chemotherapy as an approach to reduce relapse risk,” Ho said. “We hope these approaches will ultimately help improve treatment outcomes and long-term prognosis for patients with AML.”

Ho and Kapur are also researchers in the Wells Center’s Hematologic Malignancies and Stem Cell Biology Program and the IU Melvin and Bren Simon Comprehensive Cancer Center.

Researchers have developed a wearable, comfortable and washable device called Revoice that could help people regain the ability to communicate naturally and fluently following a stroke, without the need for invasive brain implants.

The device, whose development was led by researchers at the University of Cambridge, uses a combination of ultra-sensitive sensors and artificial intelligence to decode speech signals and emotional cues to allow people with post-stroke speech impairment to communicate naturally.

The Revoice device, worn as a soft and flexible choker, captures the wearer’s heart rate and tiny vibrations from throat muscles, and uses those signals to reconstruct intended words and sentences in real time.

The signals from the device are processed by two AI agents: one reconstructs words from fragments of silently mouthed speech, while the other interprets emotional state and contextual information, such as the time of day or weather conditions, to expand short phrases into complete, expressive sentences.

In a small trial with five patients with dysarthria, a common type of post-stroke speech impairment, the device achieved a word error rate of 4.2% and a sentence error rate of just 2.9%. Unlike existing assistive speech technologies, which often require slow letter-by-letter input, eye tracking or brain implants, the Revoice device provides seamless real-time communication, turning just a few mouthed words into full, fluent sentences.

Potential impact and ongoing research

Their results, reported in the journal Nature Communications, could not only have implications for stroke rehabilitation, but could also help support people with conditions such as Parkinson’s and motor neuron disease.

The researchers are currently planning a clinical study in Cambridge for native English-speaking dysarthria patients to assess the viability of the system, which they are hoping to launch this year.

About half of people develop dysarthria, or dysarthria in combination with aphasia, following a stroke. Dysarthria is a physical condition that causes weakness in the muscles of the face, mouth and vocal cords. It affects people in different ways, but often causes an inability to speak clearly, slurred or slow speech, or speaking in short, disjointed bursts rather than full sentences.

“When people have dysarthria following a stroke, it can be extremely frustrating for them, because they know exactly what they want to say, but physically struggle to say it, because the signals between their brain and their throat have been scrambled by the stroke,” said Professor Luigi Occhipinti from Cambridge’s Department of Engineering, who led the research.

“That frustration can be profound, not just for the patients, but for their caregivers and families as well.”

Current therapies and device development

Most stroke patients with dysarthria work with a speech therapist to regain their ability to communicate, primarily through repetitive word drills, where patients repeat words or phrases back to the speech therapist. Typical recovery time varies from a few months to a year or more.

“Patients can generally perform the repetitive drills after some practice, but they often struggle with open-ended questions and everyday conversation,” said Occhipinti.

“And as many patients do recover most or all of their speech eventually, there is not a need for invasive brain implants, but there is a strong need for speech solutions that are more intuitive and portable.”

Occhipinti and his colleagues developed the Revoice device as such a solution. The sensors in the device capture subtle vibrations from the throat to detect speech signals and decode emotional states from pulse signals—a simplified but effective proxy. The device also uses an embedded lightweight large language model (LLM) to predict full sentences, so only uses minimal power.

Trial results and future directions

Working with colleagues in China, the researchers carried out a small trial with five stroke patients with dysarthria, as well as 10 healthy controls. In the study, participants wore the device and mouthed short phrases. By nodding twice, they could choose to expand those phrases into sentences using the embedded LLM.

In one example, “We go hospital” became “Even though it’s getting a bit late, I’m still feeling uncomfortable. Can we go to the hospital now?” The sensors in the Revoice device inferred that the wearer was feeling frustrated due to their elevated heart rate, and that it was getting late at night. The LLM was able to use this data to expand three mouthed words into a full sentence.

Participants in the study reported a 55% increase in satisfaction, showing that the device could be a promising development to help stroke patients regain their ability to communicate.

Although extensive clinical trials will be required before the device can be made widely available, the researchers hope that future versions of the device will include multilingual capabilities, a broader range of emotional states and fully self-contained operation for everyday use.

“This is about giving people their independence back,” said Occhipinti. “Communication is fundamental to dignity and recovery.”

Researchers at Mass General Brigham and Karolinska Institutet have identified a new method to predict asthma exacerbations with a high degree of accuracy. The study is published in Nature Communications.

Asthma is one of the world’s most common chronic diseases, affecting over 500 million people. Asthma exacerbations—commonly known as asthma attacks—are a major cause of disease morbidity and health care costs.

Despite the prevalence of asthma, clinicians currently lack reliable biomarkers to identify which patients are at high risk for future attacks. Current methods often fail to distinguish between stable patients and those prone to severe exacerbations.

The study analyzed data from three large asthma cohorts totaling over 2,500 participants, backed by decades of electronic medical records. Researchers used a high throughput approach called metabolomics to measure small molecules in the blood of individuals with asthma.

They identified an important relationship between two classes of metabolites, sphingolipids and steroids, and asthma control. Specifically, they identified that sphingolipid to steroid ratios could predict exacerbation risk over a 5-year period. In some cases, the model could differentiate the time-to-first exacerbation between high- and low-risk groups by nearly a full year.

Implications for asthma care

“One of the biggest challenges in treating asthma is that we currently have no effective way to tell which patient is going to have a severe attack in the near future,” says Jessica Lasky-Su, Associate Professor at the Channing Division of Network Medicine at Mass General Brigham and Harvard Medical School.

“Our findings solve a critical unmet need. By measuring the balance between specific sphingolipids and steroids in the blood, we can identify high-risk patients with 90% accuracy, allowing clinicians to intervene before an attack occurs.”

The team discovered that while individual metabolite levels provided some insight, the ratio between sphingolipids and steroids was the most powerful predictor of future health.

“We found that the interaction between sphingolipids and steroids drives the risk profile. This ratio approach is not only biologically meaningful but also analytically robust, making it highly suitable for development into a practical, cost-effective clinical test, says Craig E. Wheelock, Principal Researcher at the Institute of Environmental Medicine at Karolinska Institutet.”

Next steps and future research

The researchers believe these findings represent a significant step toward precision medicine for asthma. A clinical assay based on these ratios could be easily implemented in standard laboratories, helping doctors identify patients who appear stable but have underlying metabolic imbalances.

However, the researchers emphasize that the results need to be validated further before the test can be used in clinical practice. Among other things, more studies on asthma patients, including direct clinical trials and cost-effectiveness analyses are required.

Taking acetaminophen during pregnancy does not increase the risk of autism, attention-deficit hyperactivity disorder (ADHD), or intellectual disability among children. That is according to the most rigorous analysis of the evidence to date, published in The Lancet Obstetrics, Gynecology & Women’s Health, and led by researchers from City St George’s, University of London.

Researchers conducted a systematic review and meta-analysis of 43 existing studies to determine whether acetaminophen was safe to use in pregnancy or not. This was in response to public concerns following claims back in September 2025 that suggested taking acetaminophen during pregnancy might impact the neurodevelopment of those children and increase their risk of autism.

The claims were based on earlier studies that reported small associations between acetaminophen in pregnancy and increased risks of autism. However, these were often based on studies prone to biases, including being limited by the type of data collected and not exploring comparisons between siblings to account for family history, which is vital information.

The team looked at 43 studies with the highest quality and most rigorous research methods and compared pregnancies where the mother had taken acetaminophen to pregnancies where they had not taken the drug.

They pooled the results of sibling comparison studies that compared siblings born to the same mother, where one pregnancy involved acetaminophen exposure and another did not. This design helps control for shared genetics, family environment and long-term parental characteristics that traditional studies cannot fully account for.

Across the sibling-comparison studies, data included 262,852 children assessed for autism, 335,255 for ADHD and 406,681 for intellectual disability. When compared to pregnancies with no exposure to acetaminophen, it was confirmed that taking acetaminophen in pregnancy was not linked to childhood autism, ADHD or intellectual disability.

Professor Asma Khalil, professor of obstetrics and maternal fetal medicine at City St George’s, University of London and consultant obstetrician, who led the study, said, “Our findings suggest that previously reported links are likely to be explained by genetic predisposition or other maternal factors such as fever or underlying pain, rather than a direct effect of the acetaminophen itself.

“The message is clear: Acetaminophen remains a safe option during pregnancy when taken as guided. This is important as acetaminophen is the first-line medication we recommend for pregnant women in pain or with a fever, and so they should feel reassured that they still have a safe option to relieve them of their symptoms.”

All studies were assessed for their quality based on the Quality In Prognosis Studies (QUIPS) tool that evaluates numerous factors in the way the research has been conducted to determine the risk of bias, another strength of this work. The lack of association between taking acetaminophen during pregnancy and the risk of the child having autism, ADHD or intellectual disabilities also remained in the studies deemed to be at low risk of bias (and therefore highest quality), and in those which had a longer follow-up period of over five years.

The authors note that a limitation of the current study was that it was not possible to analyze smaller groups in the studies with sibling comparisons based on which trimester of pregnancy acetaminophen was consumed in, sex of the baby or how often acetaminophen was taken, because too few of the existing studies reported these data.

Overall, the findings of the study support the recommendations made by major medical organizations worldwide. The researchers hope that this gold-standard review will put an end to any skepticism about using acetaminophen during pregnancy, as avoiding acetaminophen for significant pain or fever can expose both mother and baby to known risks, particularly untreated maternal fever.

Sexual desire is a fundamental part of being human and a driving force in many relationships, yet we still don’t fully understand why it varies so much from person to person.

In a large-scale study published in the journal Scientific Reports, researchers are giving us some answers. One of the most surprising findings is that men’s desire peaks in their late 30s and early 40s, not in their teens or 20s, as previously assumed.

Researchers from the University of Tartu in Estonia analyzed data from 67,334 adults in the Estonian Biobank. This is a massive repository that contains biological samples and lifestyle information of some of the country’s adult population. The samples in the study represented about 7% of the country’s adults, with participants aged 18 to 89 years.

Levels of desire

The study authors asked these individuals to rate their general level of sexual desire and then compared their answers with a range of background information. This included age, gender, sexual orientation and even their jobs and level of education.

“Our large study considered the individual and interactive roles of several demographic factors in sexual desire, including age, gender, sexual orientation, relationship status, number of children, recent childbirth, educational attainment, and occupation,” wrote the scientists in their paper.

“The findings showed that demographic factors alone—even without accounting for psychological or relational influences—explained 28% of the variance in sexual desire.”

In other words, nearly one-third of the difference between one person’s sexual desire and another’s can be predicted just by looking at basic facts such as age, gender and family.

Key differences

The study also revealed a few more insights into the ways our lives shape our sexual desire. While it tends to dip for everyone as they get older, which was already common knowledge, it drops much more steeply in women.

Another major factor affecting desire is having children, which affects men and women differently. For women, having more children was linked to a lower sexual desire, while men with larger families, on the other hand, reported higher levels of desire.

And who has the highest levels of desire? According to the data, people who identify as bisexual or pansexual.

By providing more details about sexual desire, the researchers hope it will reduce the sense of distress in those who feel as though there is something wrong with them when their desire changes. They also want relationship counselors to use the data to help people understand that shifts in desire are often a natural response to life stages and circumstances.