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  • Study links parental death to higher bullying risk in teens, with rural girls most affected

    Losing a parent or primary caregiver is one of the most disruptive events a child can face, and new research suggests it may also change how young people are treated at school. A large survey-based study found higher odds of bullying victimization among youth who experienced parental death.

    The study, led by researchers at Boston University School of Public Health and collaborators in China, analyzed responses from about 21 000 children aged 10 to 17. It was published in the Journal of Affective Disorders and drew on data collected between 2019 and 2021 in southwestern China.

    Who faced the biggest rise?

    Researchers reported that the link between bereavement and bullying varied by age, sex, the parent who died, and where children lived. Adolescents aged 13 to 17, girls, and students in rural areas showed the highest increases in reported bullying after a parent’s death.

    Maternal death was associated with a higher bullying risk specifically among boys in the sample, a pattern the authors said may reflect a uniquely protective role of maternal support for sons. The study emphasizes that family disruption can affect social behavior, confidence, and peer relationships during sensitive developmental periods.

    What the survey data showed

    In the study group, nearly 3 percent of participants reported experiencing a parental death. More than 15 percent said they were being bullied at school, highlighting how common peer victimization remains across adolescence.

    While most parental deaths captured in the dataset occurred before COVID-19 became widespread, global estimates indicate the pandemic left millions of children bereaved. Separate international analyses have estimated that more than 8 000 000 children worldwide lost a parent or primary caregiver due to pandemic-related causes.

    Support that lasts beyond the funeral

    The researchers argue that support for bereaved children should be long-term and tailored, combining emotional care with help navigating peer dynamics. They pointed to counseling, engagement of remaining caregivers or extended family, and school programs adjusted to developmental stage and cultural context.

    The study also calls for schools to train staff to recognize grief-related vulnerability and to strengthen overall school climate. Creating an inclusive environment, the authors suggested, may reduce bullying risk and help bereaved students regain stability as their needs evolve.

  • Parkinson’s trial tests dopamine stem cell implants at USC, offering a closer look at brain repair

    Parkinson’s trial tests dopamine stem cell implants at USC, offering a closer look at brain repair

    Doctors at Keck Medicine of USC have begun implanting dopamine-producing stem cells into the brains of people with Parkinson’s disease, as part of an early-stage clinical trial designed to assess safety and feasibility. The approach aims to replace nerve cells lost to the disorder and restore dopamine production at its source.

    Parkinson’s is a progressive neurological condition best known for tremor, stiffness and slowed movement, but it can also affect sleep, mood and cognition. In the United States, more than 1 000 000 people are living with Parkinson’s, and roughly 90 000 new cases are diagnosed each year, according to public health estimates.

    Why dopamine loss matters

    The disease is closely tied to the gradual death of dopamine-producing neurons, which disrupts signals that help coordinate movement. Standard treatments, including levodopa and other medications, can reduce symptoms, but they do not reliably stop the underlying neurodegeneration.

    The new strategy attempts to address that core deficit by placing replacement cells directly into brain circuits involved in motor control. Researchers say that if transplanted cells survive and produce dopamine in a regulated way, patients could see more stable symptom control than medication alone can provide.

    How the stem cell procedure works

    The trial uses induced pluripotent stem cells, or iPSCs, which are created by reprogramming adult cells back into a flexible state that can be guided to become specific cell types. In this study, the cells are engineered to mature into dopamine-producing neurons intended to integrate into the brain.

    During surgery, clinicians create a small opening in the skull and use imaging guidance to deliver the cells into the basal ganglia, a region central to movement regulation. Participants are monitored closely after implantation for complications such as infection and abnormal involuntary movements, known as dyskinesia.

    What researchers will watch next

    The multi-site U.S. study plans to enroll 12 people with moderate to moderate-severe Parkinson’s disease, with follow-up in the first 12 to 15 months focused heavily on safety signals. Researchers also plan longer observation, up to five years, to evaluate durability and potential longer-term risks.

    The investigational therapy, called RNDP-001, is produced by Kenai Therapeutics, and the FDA has granted the study fast-track designation, a process meant to speed development for serious conditions with unmet need. Even with that designation, researchers caution that larger trials would be required to determine whether the implants provide consistent, meaningful clinical benefit.

    Stem cell and cell-replacement approaches are an active area of Parkinson’s research worldwide, reflecting a broader push to move beyond symptom relief toward disease-modifying strategies. For now, the USC-led effort adds closely watched clinical data on whether implanted dopamine neurons can be delivered safely and function as intended in patients.

  • Chimpanzee call combinations hint at language roots: What a major Taï Forest study found

    New research based on years of field recordings suggests wild chimpanzees can combine calls in ways that shift or expand meaning, a trait long seen as central to human language. The findings challenge the idea that complex, rule-like vocal communication is uniquely human.

    Scientists studied thousands of vocalisations from three chimpanzee groups in Taï National Park in Côte d’Ivoire. They analysed how the meanings of 12 call types changed when paired into 16 different two-call combinations across many everyday situations.

    How chimpanzees change call meaning

    The researchers report four main patterns that alter meaning when calls are combined, including compositional pairings that add information. Other combinations appear to clarify context, helping narrow a call’s meaning depending on what follows.

    The study also describes non-compositional, idiom-like combinations, where two familiar calls together convey a meaning that is not a simple sum of the parts. That kind of structure resembles a key feature of human language, where fixed phrases can carry distinct meanings.

    Why the context matters

    Previous work on primate call combinations has often focused on narrow scenarios such as predator alerts, with only a small number of known combinations. In Taï, the team found a broader and more flexible set of pairings used across feeding, travelling, social bonding and other contexts.

    Because chimpanzees and bonobos are humans’ closest living relatives, the results feed into a larger debate about language evolution. The authors argue these combinatorial abilities may have deeper evolutionary roots than once assumed, though they also note more comparative research is needed.

    What this means for language origins

    The findings do not mean chimpanzees use human-like grammar, but they do suggest vocal communication can be more generative in great apes than previously documented. That could shift how scientists frame the early building blocks that eventually supported human language.

    Researchers also warn that long-term fieldwork is becoming harder as human pressures grow on wild chimpanzee populations. Continued observation in natural habitats, they argue, is essential to map the full range of great ape communication.

  • New Alzheimer’s study points to subtle brain blood flow changes as an early warning sign

    New Alzheimer’s study points to subtle brain blood flow changes as an early warning sign

    Small shifts in how blood moves through the brain and how brain cells receive oxygen may be closely connected to the risk of Alzheimer’s disease. That is the conclusion of new research from the Mark and Mary Stevens Neuroimaging and Informatics Institute (Stevens INI) at the Keck School of Medicine of USC.

    The study, published in Alzheimer’s and Dementia: The Journal of the Alzheimer’s Association, examined older adults both with and without cognitive impairment. Researchers found that simple, noninvasive measures of brain blood flow and oxygen levels were linked to well known signs of Alzheimer’s, including amyloid plaque buildup and shrinkage of the hippocampus, the part of the brain that plays a central role in memory. The results suggest that the health of the brain’s blood vessels may influence the disease process early on and could help flag people at risk before noticeable symptoms develop.

    “Amyloid and tau are often considered the primary players in Alzheimer’s disease, but blood flow and oxygen delivery are also critical,” said Amaryllis A. Tsiknia, lead author of the study and USC PhD candidate. “Our results show that when the brain’s vascular system functions more like it does in healthy aging, we also see brain features that are linked to better cognitive health.”

    Noninvasive Tools to Measure Brain Circulation

    To study these changes, the team relied on two painless techniques that can be used while a person rests quietly. Transcranial Doppler ultrasound tracks how quickly blood travels through the brain’s major arteries. Near infrared spectroscopy evaluates how effectively oxygen reaches brain tissue near the surface of the cortex.

    Researchers then applied advanced mathematical modeling to combine these readings into overall indicators of cerebrovascular function. These indicators reflect how well the brain adjusts blood flow and oxygen delivery in response to natural fluctuations in blood pressure and carbon dioxide.

    Vascular Health Linked to Amyloid and Memory Centers

    Participants whose vascular indicators more closely resembled those of cognitively healthy adults tended to have lower amyloid levels and a larger hippocampus. Both features are associated with reduced Alzheimer’s risk.

    “These vascular measures are capturing something meaningful about brain health,” said Meredith N. Braskie, PhD, senior author of the study and assistant professor of neurology at the Keck School of Medicine. “They appear to align with what we see on MRI and PET scans that are commonly used to study Alzheimer’s disease, providing important information about how vascular health and standard brain measures of Alzheimer’s disease risk may be related.”

    The researchers also observed that people diagnosed with mild cognitive impairment or dementia showed weaker vascular function compared to cognitively normal participants. This finding supports the view that declining blood vessel health in the brain is part of the broader Alzheimer’s disease continuum.

    “These findings add to growing evidence that Alzheimer’s involves meaningful vascular contributions in addition to classic neurodegenerative changes,” said Arthur W. Toga, PhD, director of the Stevens INI. “Understanding how blood flow and oxygen regulation interact with amyloid and brain structure opens new doors for early detection and potentially prevention.”

    Potential for Earlier and Broader Screening

    Compared with MRI and PET imaging, these methods are less costly and easier to perform. They do not involve injections, radiation exposure, or demanding tasks for patients. That simplicity could make them useful for large scale screening or for individuals who are unable to undergo more intensive brain imaging.

    The authors caution that the findings represent a single snapshot in time and do not establish cause and effect. Ongoing long term studies are tracking participants to see whether shifts in these vascular measures can predict future cognitive decline or response to treatment.

    “If we can track these signals over time, we may be able to identify people at higher risk earlier and test whether improving vascular health can slow or reduce Alzheimer’s-related brain changes,” Tsiknia said.

    About the Study

    In addition to Tsiknia and Braskie, the study’s other authors are Peter S. Conti, Rebecca J. Lepping, Brendan J. Kelley, Rong Zhang, Sandra A. Billinger, Helena C. Chui and Vasilis Z. Marmarelis.

    This work was supported by the Office of The Director, National Institutes of Health, under Award Number S10OD032285, and by the National Institute on Aging [R01AG058162].

  • NYU study maps a prefrontal naming network, offering new clues to why word retrieval can fail

    Scientists at New York University have mapped a brain network linked to naming and word retrieval, a core function that can break down after stroke, traumatic brain injury, or neurodegenerative disease. The work helps explain why some people can name an object they see but struggle to find words in everyday conversation.

    The study, published in Cell Reports, points to a left-lateralized network involving the dorsolateral prefrontal cortex and nearby frontal regions. Researchers say the findings refine how neuroscience understands the step-by-step process of turning meaning into spoken words.

    How researchers mapped naming circuits

    The team analyzed electrocorticography recordings, a method that measures brain activity directly from the cortical surface during clinical monitoring. Data came from 48 neurosurgical patients, allowing unusually precise timing and localization of language-related signals.

    Using computational clustering, the researchers identified two partially overlapping systems involved in naming. One system tracked semantic processing, linking words to meaning and responding to how expected a word was within a sentence.

    Auditory naming highlights dorsal hub

    A second system was tied to articulatory planning and speech production, showing activity patterns that were less dependent on whether words were presented visually or through sound. This network was centered more ventrally in frontal and precentral regions associated with speech motor planning.

    The results also revealed a ventral-to-dorsal gradient across the prefrontal cortex, with a dorsal frontal area emerging as a key hub for mapping sounds to meaning in auditory contexts. The authors argue this dorsal prefrontal contribution has been underappreciated in earlier models.

    Why the findings matter clinically

    Clinicians frequently see anomia, the difficulty of retrieving words, in patients with focal brain damage and in conditions such as primary progressive aphasia. By separating semantic integration from articulatory planning, the study may help guide more targeted assessments and rehabilitation strategies.

    The work could also inform brain-computer interface research aimed at restoring communication, by clarifying which neural signals best reflect the intent to name a concept. While the authors caution that translation to devices and therapies will take time, the map provides a clearer target for future studies.

  • UCLA study suggests accelerated TMS may ease treatment-resistant depression in five days, but follow-up timing matters

    UCLA study suggests accelerated TMS may ease treatment-resistant depression in five days, but follow-up timing matters

    Researchers at UCLA Health say an accelerated form of transcranial magnetic stimulation, or TMS, may deliver comparable symptom relief for some people with treatment-resistant depression in just five days. The approach aims to reduce the practical burden of the standard schedule, which typically requires daily weekday visits over six to eight weeks.

    TMS is a noninvasive brain stimulation therapy that uses magnetic pulses to target regions involved in mood regulation. It is commonly offered when patients do not improve after multiple antidepressant trials, and it has become a widely used option in outpatient psychiatric care.

    A five-by-five TMS schedule

    In the study, clinicians compared a compressed protocol known as 5×5, meaning five sessions per day for five consecutive days, with a conventional six-week course. The analysis included 175 patients, with 40 receiving the accelerated format and 135 receiving standard treatment.

    Both groups saw significant reductions in depression symptoms, and overall outcomes were not meaningfully different between schedules. The findings were published in the Journal of Affective Disorders, and the authors noted the results could expand access for patients who struggle to attend weeks of appointments.

    Why follow-up may change results

    One key observation was that some patients in the accelerated group did not appear to improve immediately after the five-day course ended. When assessed again two to four weeks later, those individuals showed substantial improvement, with depression scores falling by an average of 36%.

    That pattern suggests end-of-week assessments may underestimate the benefit of accelerated TMS for certain patients. The researchers said timing could be important when clinicians and patients decide whether a short course is working.

    What the study did not prove

    The researchers cautioned that the comparison was not a randomized clinical trial, meaning patients were not randomly assigned to the accelerated or standard schedule. They also reported that the traditional course performed better on some longer-term measures, underscoring the need for larger controlled trials.

    Even so, the team argues that a shorter TMS pathway could help more eligible patients start and complete care, especially those facing transportation, work, or caregiving barriers. Further research is expected to refine who benefits most, and whether booster sessions after a short course improve durability.

  • Autism communication study finds no effectiveness gap, pointing to a mismatch in styles

    A new study suggests autistic and non-autistic people can communicate information just as effectively, challenging a common assumption that autism inherently limits social connection. Researchers say many real-world difficulties may stem from mismatched communication styles rather than reduced social ability.

    The research was led by the University of Edinburgh and tested how accurately information was passed along between 311 participants. The team assessed groups made up entirely of autistic people, entirely of non-autistic people, and mixed groups.

    How the communication test worked

    In the experiment, the first participant heard a short story from a researcher and then retold it to the next person in a chain. Each person repeated what they remembered, and the final participant recalled the story aloud.

    Researchers scored how much information was retained at each step to measure communication effectiveness. They found no meaningful differences in accuracy between autistic-only, non-autistic-only, and mixed groups.

    Preference, not performance, stood out

    After the task, participants rated how comfortable the interaction felt, including how friendly, easy, or awkward it seemed. Autistic participants tended to prefer learning from other autistic people, while non-autistic participants often preferred interacting with non-autistic peers.

    The study supports the idea that communication challenges frequently arise when autistic and non-autistic people interact without shared expectations. The authors argue the results add weight to viewing autistic communication as a difference in style, not a deficit.

    Dr Catherine Crompton of the University of Edinburgh said the findings could help shift attention away from attempts to fix autistic communication. She added that reducing misconceptions and improving mutual understanding could help create more inclusive spaces.

  • NYU Study Links Aging Anxiety to Faster Biological Aging in Women, with Health Worries Playing the Biggest Role

    NYU Study Links Aging Anxiety to Faster Biological Aging in Women, with Health Worries Playing the Biggest Role

    Worrying about getting older, particularly fears of future health decline, may be tied to faster biological aging in women, according to new research from NYU School of Global Public Health. The study connects aging anxiety with changes in epigenetic markers measured in blood.

    Researchers analyzed data from 726 women in the Midlife in the United States study, combining survey responses with laboratory measures. They focused on whether subjective anxiety about aging aligned with objective indicators of cellular aging.

    How biological aging was measured

    The team used two widely cited epigenetic clocks to assess aging biology, including DunedinPACE, which estimates the pace of aging, and GrimAge2, which is designed to capture accumulated biological risk. Higher anxiety scores were associated with faster aging on DunedinPACE.

    The clearest link involved worries about age-related health problems rather than concerns about appearance or fertility. Researchers suggested health fears may be more persistent over time, potentially making them more relevant to longer-term stress biology.

    Why the link may matter

    Accelerated epigenetic aging has been associated in prior research with higher risk of age-related disease and earlier functional decline, though it is not a diagnosis on its own. The NYU findings add to evidence that psychological stressors can correlate with measurable biological changes.

    The authors emphasized that mental and physical health are often treated separately despite frequent overlap. They argued that addressing aging anxiety could be a meaningful, potentially modifiable factor in supporting healthier aging.

    Limits and what comes next

    The study captured a single point in time, so it cannot prove that anxiety causes faster aging. When researchers adjusted for health behaviors that can accompany anxiety, such as smoking and alcohol use, the statistical link weakened and was no longer significant.

    The team called for further research to clarify cause and effect, track changes over time, and identify which interventions might reduce harmful stress while supporting healthier coping. They also pointed to broader social pressures and caregiving burdens that can intensify midlife worries for women.

  • Study suggests recessive disease carriers face subtle Darwinian selection, challenging genetics textbooks

    New population-scale research suggests that people who carry single harmful variants in recessive disease genes are not always fully unaffected, as many genetics textbooks imply. Using health and reproductive data, the study finds small but measurable disadvantages that could shape how these variants persist over generations.

    Researchers analyzed genetic and life-outcome information from more than 300 000 participants in the UK Biobank, a major long-running resource for biomedical research. They focused on 1 900 genes linked to recessive disorders, where disease typically appears only when both gene copies are affected.

    On average, individuals carried about two potentially damaging variants across these recessive genes, the authors reported. As a group, carriers showed a slightly higher burden of medical diagnoses and a modest reduction in reproductive success, suggesting lower odds of passing these variants on.

    Signals strongest for disability genes

    The pattern was most pronounced for genes associated with intellectual disability, where carrier variants appeared less common than expected. The researchers also observed that carriers of these variants tended to spend fewer years in education, a signal consistent with subtle effects even in people who do not meet clinical thresholds.

    The findings build on earlier work showing many cases of intellectual disability arise from de novo mutations that occur spontaneously in a child rather than being inherited. Because each child typically acquires around 100 new mutations across the genome, rare but consequential changes can still emerge even if selection slowly reduces inherited risk variants.

    Evolution may still be at work

    The authors argue that these small carrier disadvantages are consistent with ongoing Darwinian selection in modern populations, operating through health and reproduction rather than survival alone. They also point to the possibility that social factors, including mate choice, could contribute, echoing Darwin’s later emphasis on sexual selection.

    Experts caution that the reported effects are modest and observed at the group level, meaning they may not predict outcomes for any single person. Still, the results may influence how genetic counseling, population genetics, and the long-term dynamics of disease variants are taught and studied.

  • AI-built molecular atlas maps Alzheimer’s brain beyond amyloid plaques, pointing to overlooked metabolic shifts

    AI-built molecular atlas maps Alzheimer’s brain beyond amyloid plaques, pointing to overlooked metabolic shifts

    Researchers at Rice University have created a label-free molecular atlas of the Alzheimer’s brain in an animal model, using laser-based imaging paired with artificial intelligence. The work aims to clarify how the disease emerges and spreads beyond what standard pathology typically captures.

    The study used hyperspectral Raman imaging, an advanced form of Raman spectroscopy that reads chemical fingerprints in tissue without dyes or fluorescent tags. By scanning brain slices at high resolution, the team generated a detailed chemical map designed to reflect the brain’s native state.

    What the imaging revealed

    Analysis indicated that Alzheimer’s-linked chemical changes were not limited to amyloid plaques. Instead, the alterations appeared across multiple brain regions, with uneven patterns that could help explain why symptoms develop gradually and differ between individuals.

    To handle the large dataset, the researchers applied both unsupervised and supervised machine learning methods. Unsupervised tools grouped tissue by molecular similarity, while supervised models helped distinguish Alzheimer’s-affected samples from controls across different regions.

    Metabolic signals in key regions

    Beyond protein-related pathology, the maps pointed to broader metabolic differences, including shifts in cholesterol and glycogen signals. The strongest contrasts were reported in brain regions central to memory and cognition, including the hippocampus and cortex.

    The authors argue that these molecular patterns support a wider view of Alzheimer’s as a disorder involving disrupted brain structure and energy balance, not only plaque formation. They say a whole-brain, label-free approach could help surface changes that targeted assays might miss.

    While the findings are based on an animal model and would need validation in human tissue, the researchers suggest the approach could eventually inform earlier detection strategies and more region-specific treatment research. The study was published in ACS Applied Materials and Interfaces with support from U.S. federal research funders.