A simple blood test could reveal Alzheimer’s risk 10 years before symptoms

 A simple blood test could help identify people at increased risk of Alzheimer's-related cognitive decline years before they experience any noticeable problems with memory or thinking. In a large international study, researchers found that older adults with very high levels of a particular blood biomarker faced a 38% chance of developing cognitive impairment within five years. Over 10 years, the estimated risk rose to 78%, although the longer-term findings were based on substantially less data.

The findings offer new insight into the potential of blood tests to predict future cognitive problems in people who currently show no signs of impairment. The research was led by scientists at the Mass General Brigham Neuroscience Institute and involved teams working across three continents. The results were presented at the Alzheimer's Association International Conference and simultaneously published in JAMA.

The study focused on phosphorylated tau 217 (p-tau217), a blood biomarker associated with Alzheimer's disease. A test measuring this marker recently received federal clearance, raising hopes that blood testing could make Alzheimer's detection more accessible. However, an important question has remained: Can these tests reliably predict whether someone with normal cognitive function will eventually develop symptoms?

Blood Test Reveals Cognitive Decline Risk Years in Advance

To investigate, researchers combined information from six observational studies and clinical trials conducted in North America, Japan, and Australia. Together, these studies included 2,684 older adults who showed no signs of cognitive impairment when they entered the research.

At enrollment, participants provided blood samples that were analyzed for p-tau217. They also underwent positron emission tomography (PET) brain scans, allowing researchers to establish baseline measurements of brain health. Annual follow-up assessments were then used to monitor changes in memory, thinking, and other cognitive abilities.

The combined data covered an unusually long period. Some participants entered one of the studies as early as 2004, while the most recent follow-up assessments took place in 2025.

Across the studies, approximately 478 participants eventually developed cognitive impairment. When researchers compared these outcomes with the original blood test results, they found a strong relationship between higher p-tau217 levels and the likelihood of future cognitive problems.

Among people with very high biomarker levels, the estimated probability of developing cognitive impairment reached 38% within five years. By 10 years, that figure increased to 78%. However, the researchers emphasized that substantially fewer observations were available for the 10-year period and beyond, making those longer-term predictions less certain.

A Powerful Alzheimer's Predictor Beyond Genetics and Brain Scans

One of the most important findings was that p-tau217 provided information about future cognitive decline beyond what could be explained by other established risk factors.

The biomarker remained significantly associated with cognitive impairment even after researchers accounted for amyloid-beta plaques, which are abnormal protein deposits in the brain that can be detected with PET imaging. Its predictive value also extended beyond known genetic risk factors (such as APOE4).

This suggests that a relatively simple blood test could eventually provide doctors with additional information when estimating an individual's likelihood of developing cognitive difficulties.

"This is a critical step toward better understanding what p-tau217 can tell us about a person's risk for cognitive impairment," said lead author Rachel F. Buckley, PhD, a cognitive neuroscientist with the Mass General Brigham Neuroscience Institute. "What really sets this work apart is that it estimates an individual's level of risk for cognitive impairment. We harmonized data across six cohorts, creating a large and varied data set, and still found consistent results showing how p-tau217 informs risk over time."

Rather than simply identifying biological changes associated with Alzheimer's, the research helps estimate how those changes translate into the probability of developing symptoms over a specific period.

Why Alzheimer's Blood Tests Are Not Yet Recommended for Healthy People

Despite the promising results, the researchers caution that blood tests are not currently recommended for routine Alzheimer's risk screening in people without symptoms.

One major reason is that preventive treatments capable of changing the course of the disease have not yet been established for otherwise healthy individuals identified as being at elevated risk.

"We do not yet have disease-modifying treatments for people who find out they are at high risk for developing cognitive impairment due to Alzheimer's disease, which is why we don't recommend currently available blood tests for asymptomatic individuals. Today, our medical advice would remain the same regardless of test results: exercise regularly, maintain a healthy diet, and prioritize sleep and overall wellness," said senior and corresponding author Reisa Sperling, MD, a neurologist with the Mass General Brigham Neuroscience Institute. "But the preventive care landscape could change rapidly if ongoing trials of disease-modifying therapies prove beneficial. In the future, these tests could help identify those who might benefit most from these treatments. Our long-term goal is to get us to where cholesterol testing is in predicting your risk of a heart attack."

There are also important limitations to the research. Although the investigators brought together data from multiple studies and geographic regions, the participants may not fully represent the broader population. This potential selection bias could affect how well the findings apply to other groups.

In addition, the analysis focused on predicting cognitive impairment over relatively limited periods rather than estimating a person's lifetime risk. Researchers say larger, more representative studies and longer follow-up periods will be needed to confirm the findings and improve the precision of individual risk predictions.

Could Blood Tests Help Prevent Alzheimer's Before Symptoms Begin?

The greatest potential benefit of this approach may emerge as scientists develop treatments designed to slow or prevent Alzheimer's-related cognitive decline before noticeable symptoms develop.

Several clinical trials are already investigating whether disease-modifying therapies can benefit people who have biological signs of Alzheimer's but have not yet experienced cognitive impairment. If those treatments prove effective, blood biomarkers such as p-tau217 could help identify individuals most likely to benefit from early intervention.

Such an approach could eventually make Alzheimer's prevention more similar to cardiovascular prevention, where cholesterol measurements help doctors estimate future heart attack risk and determine who may benefit from treatment.

For now, the blood test offers researchers a way to identify higher-risk individuals who may be suitable candidates for prevention studies.

"Today, p-tau217 can help identify people at high risk for future Alzheimer's dementia for participation in prevention trials," said Sperling. "As these trials move forward, individualized estimates, including the biomarker's prognostic value, could guide earlier treatment and monitoring decisions."

Authorship: In addition to Sperling and Buckley, Mass General Brigham authors include Diana L. Townsend, Colin J. Birkenbihl, Madison Cuppels, Gillian T. Coughlan, Mabel T. Seto, Jane A. Brown, Michael J. Properzi, Merle C. Hönig, Annie Li, Aaron P. Schultz, Jasmeer Chhatwal, Hyun-Sik Yang, Steven Arnold, Pia Kivisäkk, Brian Healy, Jorge Garcia Condado, Wai-Ying Wendy Yau, Michelle Farrell, Rebecca E. Amariglio, Dorene M. Rentz, Kathryn V. Papp, and Keith A. Johnson. Additional authors include Bryan D. James, Sid O'Bryant, Robert A. Rissman, Melissa Petersen, Jessica Z. K. Caldwell, Tobey Betthauser, Julie Elisabeth Oomens, Maria Carrigan, Sterling C. Johnson, Oliver Langford, Ron Brookmeyer, Timothy J. Hohman, Michael Donohue, and Paul S. Aisen.

Source: Sciencedaily

Scientists use sound waves to deliver a new attack on deadly brain cancer

 Scientists at the University of Virginia Comprehensive Cancer Center have developed a promising experimental strategy for treating glioblastoma, the most common and aggressive malignant brain tumor in adults. The new approach could help overcome some of the biggest obstacles that have limited the effectiveness of existing brain cancer treatments.

The research team, led by UVA's Roger Abounader, MD, PhD, identified tiny genetic molecules known as "microRNAs" that can interfere with several genes responsible for the development and growth of glioblastoma. To deliver these molecules into the brain, the researchers combined specialized nanoparticles, focused ultrasound and microscopic bubbles. Together, these technologies offer a way to temporarily cross the brain's protective barrier, which normally prevents many treatments from reaching brain tumors and other neurological conditions.

"This new approach could help target numerous molecules that promote cancer growth, including those for which no drugs exist, at the same time to achieve better therapies," said Abounader, a professor at UVA's School of Medicine in the Department of Microbiology, Immunology and Cancer Biology, as well as its Comprehensive Cancer Center and Center for RNA Science and Medicine. "We are hoping to translate our findings into future clinical trials for patients with glioblastoma and other brain tumors."

Why Glioblastoma Is So Difficult to Treat

Glioblastoma is the most common malignant brain tumor in adults and one of the most aggressive forms of cancer. It claims more than 13,000 lives in the United States each year. One reason it is so difficult to treat is that cancer cells spread into surrounding healthy brain tissue, making it nearly impossible for surgeons to remove the entire tumor.

Another major challenge is the brain's natural "blood-brain barrier." This protective system helps shield the brain from harmful substances, including toxins and infectious agents. Unfortunately, it also blocks many drugs that could otherwise be used to attack brain cancer.

Current treatment generally begins with surgery to remove as much of the tumor as possible. Patients then receive radiation therapy and chemotherapy to help control the remaining cancer and extend survival. Despite these efforts, glioblastoma remains exceptionally difficult to manage.

The UVA researchers are pursuing a different strategy. Instead of relying on drugs that target individual cancer-related processes, their approach uses microRNAs, small pieces of genetic material capable of suppressing the activity of multiple problematic genes at the same time.

By disrupting several genes that help glioblastoma grow and survive, the treatment could potentially slow or even stop tumor growth. This ability to target multiple cancer-driving mechanisms is especially important because combining several conventional cancer drugs can produce harmful side effects. In addition, many of the molecules involved in cancer growth cannot currently be targeted by available medications.

Using Ultrasound to Deliver Cancer-Fighting Molecules

Getting these genetic molecules into the brain presents another major challenge. To overcome it, Abounader's team uses focused ultrasound guided by magnetic resonance imaging (MRI), allowing researchers to direct sound waves precisely toward the intended area.

The ultrasound works with tiny "microbubbles" to temporarily open the blood-brain barrier. This creates a brief opportunity for nanoparticles carrying the microRNAs to pass through the barrier and enter the brain, where they can act on genes involved in tumor growth.

The researchers tested this approach in laboratory experiments and animal models of glioblastoma. Their findings showed that the microRNA treatment slowed tumor growth and helped the animals survive longer.

Although these results are encouraging, the strategy remains experimental and will require additional research before it can be evaluated in human patients. Abounader believes the findings provide an important early indication that the technology could eventually benefit people with glioblastoma and potentially those with other types of cancer.

"This approach could have broad applications for several brain and other human diseases," Abounader said. "We and many others are intensively working to lighten the burden of cancer, and hopefully also completely cure it, but this requires a continued investment in cancer and medical research."

UVA Expands Focused Ultrasound Cancer Research

UVA Health has been at the forefront of focused ultrasound research since the technology's early development. Over the years, its scientists have built an extensive research program investigating how precisely directed sound waves might be used to treat a wide range of medical conditions.

Recognizing the technology's potential in cancer care, UVA partnered with the Charlottesville-based Focused Ultrasound Foundation to establish the Focused Ultrasound Immuno-Oncology (FUSION) Center. It is the first center in the world devoted specifically to investigating how focused ultrasound can be combined with cancer immunotherapy. Researchers believe this combination could lead to major advances in cancer treatment during the 21st century.

The effort also supports the broader missions of UVA Comprehensive Cancer Center and UVA's Paul and Diane Manning Institute of Biotechnology, both of which are working to improve care through new medical discoveries.

UVA Comprehensive Cancer Center is among just 57 cancer centers nationwide to receive the National Cancer Institute's prestigious "comprehensive" designation. The recognition reflects its excellence in cancer research and patient care.

The Manning Institute was established to speed the discovery and development of new medicines and potential cures for some of the most difficult diseases. Its work is supported by a statewide clinical trials network designed to make emerging treatments more accessible to patients as they move through research and testing.

Study Findings and Research Support

Abounader and his colleagues published their experimental approach and initial laboratory findings in JCI, the Journal of Clinical Investigation. The study is open access and can be read free of charge.

The research team included Shekhar Saha, Ying Zhang, Myron K. Gibert Jr., Collin Dube, Farina Hanif, Elizabeth Qian Xu Mulcahy, Sylwia Bednarek, Yunan Sun, Pawel Marcinkiewicz, Xiantao Wang, Gijung Kwak, Ahsan H. Polash, Haolin Li, Kadie Hudson, Manikarna Dinda, Tapas Saha, Matthew McCord, Fadila Guessous, Nichola Cruickshanks, Rossymar Rivera Colon, Lily Dell'Olio, Rajitha Anbu, Wenjie Liu, Songy Choi, Benjamin Kefas, Pankaj Kumar, Alexander L. Klibanov, David Schiff, Jung Soo Suk, Justin Hanes, Jamie Mata, Markus Hafner and Abounader. The researchers reported having no financial interest in the work.

Funding came from the National Institutes of Health's National Cancer Institute through grants U01 CA220841 and P30 CA044579, along with the NIH's National Institute of Neurological Disorders and Stroke through grants R01 NS122222 and R21 NS122136. Additional support was provided by a UVA Comprehensive Cancer Center pilot grant, a Schiff Foundation grant, the Ben and Catherine Ivy Foundation, and the Focused Ultrasound Foundation.

Source: ScienceDaily

Common pesticide linked to 2.5 times the risk of Parkinson’s disease

 A pesticide used for decades in agriculture may be linked to a much greater risk of Parkinson's disease, and scientists have uncovered a possible explanation for how it damages the brain.

Researchers at UCLA Health found that people with long-term residential exposure to chlorpyrifos, a widely used pesticide, had more than 2.5 times the risk of developing Parkinson's disease compared with those who were not exposed. Laboratory experiments also revealed how the chemical can interfere with the brain's ability to remove damaged proteins, leading to the loss of nerve cells essential for controlling movement.

The study, published in Molecular Neurodegeneration, goes beyond identifying a connection between pesticide exposure and Parkinson's. By examining what happens inside affected brain cells, the researchers uncovered a biological mechanism that could eventually provide new ways to protect the brain from damage.

A Common Pesticide With a Troubling Link to Parkinson's

Parkinson's disease affects nearly one million Americans. The progressive neurological condition gradually damages brain cells involved in movement, often causing tremors, muscle stiffness, slowed movement, and difficulties with coordination.

One of the defining features of Parkinson's is the loss of neurons that produce dopamine. This chemical messenger allows nerve cells to communicate and helps the brain coordinate smooth, controlled movements. As dopamine levels decline, the brain becomes less capable of regulating those movements.

Although inherited genetic factors can influence who develops Parkinson's, researchers have increasingly focused on environmental exposures that may also contribute to the disease. Pesticides are of particular interest because some chemicals used to kill insects or other agricultural pests can also interfere with biological processes in the nervous system.

Chlorpyrifos has been used extensively in agriculture for decades. Its residential use was banned in the United States in 2001, and agricultural applications faced additional restrictions in 2021. However, the pesticide remains in use on many crops in the United States and continues to be widely applied in other countries.

Because exposure may have occurred years before symptoms appeared, understanding the potential long-term effects of chlorpyrifos is particularly important. Identifying specific chemicals associated with Parkinson's could help researchers develop prevention strategies and determine whether previously exposed individuals might benefit from additional neurological monitoring.

Researchers Find More Than Double the Parkinson's Risk

To investigate the connection, UCLA scientists examined information from 829 people diagnosed with Parkinson's disease and 824 people without the condition. All participants were enrolled in the university's long-running Parkinson's Environment and Genes study, which investigates how environmental exposures and inherited factors influence Parkinson's risk.

The researchers combined California's detailed pesticide application records with participants' residential and workplace address histories. This allowed them to estimate how much chlorpyrifos individuals may have encountered over time based on where they lived and worked.

The results revealed a striking association. People with prolonged residential exposure to chlorpyrifos had more than 2.5 times the risk of Parkinson's disease compared with those who had no such exposure.

Although this population analysis could not establish that the pesticide directly caused Parkinson's, the researchers took an additional step to investigate whether chlorpyrifos could produce the kinds of brain damage seen in people with the disease.

How the Pesticide Damages Brain Cells

The team exposed mice to chlorpyrifos in aerosol form for 11 weeks. The inhalation approach was designed to resemble a common way people may encounter pesticides in the environment.

The exposed mice developed movement difficulties and lost neurons responsible for producing dopamine. This was particularly significant because the degeneration of these same nerve cells is a central feature of Parkinson's disease.

The researchers also detected inflammation in the animals' brains, along with abnormal accumulations of a protein called alpha-synuclein.

Under normal conditions, alpha-synuclein is found in nerve cells and plays a role in their functioning. However, the protein can accumulate in abnormal clumps that are closely associated with Parkinson's disease. These deposits are a major focus of research into why certain brain cells gradually deteriorate.

Together, the findings showed that chlorpyrifos exposure could reproduce several important characteristics of Parkinson's in laboratory animals, strengthening the biological evidence behind the human population findings.

Scientists Uncover a Breakdown in the Brain's Cleanup System

The researchers then turned to zebrafish to investigate exactly how chlorpyrifos harms neurons. These small fish are frequently used in neuroscience research because they allow scientists to study biological processes involved in nerve cell development and survival.

Their experiments pointed to a disruption in autophagy, a natural cellular maintenance process that helps remove damaged proteins and other unwanted material.

Autophagy functions much like an internal recycling system. Cells use it to break down worn-out or defective components so that potentially harmful material does not accumulate. This process is especially important for neurons, many of which must remain functional throughout a person's lifetime.

When chlorpyrifos interfered with this cleanup system, damaged material accumulated inside neurons, contributing to their deterioration.

The researchers also made an encouraging discovery. When they restored the cellular cleanup process or removed synuclein protein in their experiments, the neurons were protected from damage.

This finding suggests that the pesticide's harmful effects may depend partly on a biological pathway that researchers could potentially target with future treatments.

A Potential New Strategy for Protecting Against Parkinson's

The discovery raises the possibility of developing therapies that strengthen the brain's cellular cleanup mechanisms and help protect vulnerable neurons. Such treatments might eventually prove useful for people exposed to chlorpyrifos or other pesticides that disrupt similar processes.

However, the protective effects have so far been demonstrated in laboratory models. Additional research will be needed to determine whether enhancing autophagy can prevent or reduce pesticide-related brain damage in humans.

Scientists also want to investigate whether other commonly used pesticides interfere with the same cellular mechanisms. Although chlorpyrifos use has declined in the United States, many people were exposed before restrictions were introduced, and related agricultural chemicals remain widely used.

The findings could also help identify people with a history of substantial pesticide exposure who may benefit from closer neurological monitoring. Earlier recognition of possible changes in brain function could become increasingly important as researchers work toward treatments that slow or prevent Parkinson's progression.

Dr. Jeff Bronstein, professor of Neurology at UCLA Health and the study's senior author, emphasized the importance of identifying a particular chemical rather than treating all pesticides as a single category.

"This study establishes chlorpyrifos as a specific environmental risk factor for Parkinson's disease, not just pesticides as a general class," said Dr. Jeff Bronstein.

"By showing the biological mechanism in animal models, we've demonstrated that this association is likely causal. The discovery that autophagy dysfunction drives the neurotoxicity also points us toward potential therapeutic strategies to protect vulnerable brain cells."

Source: Sciencedaily

Scientists discover a surprising brain benefit of eating peanuts every day

 Eating peanuts every day may offer surprising benefits for the aging brain. Researchers at Maastricht University Medical Center in the Netherlands have found that regularly consuming unsalted, skin-roasted peanuts can improve how certain brain regions respond to insulin in older adults. The findings come from the Institute of Nutrition and Translational Research in Metabolism (NUTRIM) and were published in the peer-reviewed journal Food & Function.

Although insulin is best known for regulating blood sugar, it also plays an essential role in the brain. It helps nerve cells grow, survive, and communicate with one another, supporting memory and other cognitive abilities. Healthy insulin signaling may also help protect against processes associated with Alzheimer's disease.

After participants consumed peanuts daily for 16 weeks, researchers observed improved insulin responsiveness in a group of brain regions in the right hemisphere. These included portions of the lingual gyrus, hippocampus, parahippocampal gyrus, and posterior cingulate gyrus, all of which contribute to memory-related processes.

"The hormone insulin plays an important role in the brain, where it supports memory and other cognitive processes. As people age, the brain may become less responsive to insulin, which has been linked to age-related cognitive decline," says Dr. Peter Joris, the study's senior author and an associate professor in the Department of Nutrition and Movement Sciences, NUTRIM, Maastricht University Medical Center. "Our study found that daily peanut consumption beneficially affected insulin responsiveness in memory-related brain regions in older adults. These findings suggest that enhanced regional brain insulin responsiveness may contribute to the cognitive benefits of unsalted, skin-roasted peanut intake."

Daily Peanuts Linked to Better Memory and Brain Blood Flow

The study included 31 healthy adults between the ages of 60 and 75. During the peanut consumption phase, participants ate 60 grams (approximately two servings) of peanuts each day for 16 weeks. Researchers used a randomized, controlled crossover trial, a rigorous study design that allowed them to compare the effects of eating peanuts with those of avoiding them.

The new findings build on earlier research by Joris published in 2025. That investigation found that consuming peanuts for 16 weeks increased overall cerebral blood flow (CBF) by 3.6% and improved verbal memory performance by 5.8%.

Cerebral blood flow measures how much blood circulates through the brain, carrying oxygen and nutrients that brain cells need to function properly. It is an important indicator of the health of the brain's blood vessels. Those earlier results appeared in the peer-reviewed journal Clinical Nutrition.

How Scientists Measured the Effects of Peanuts on the Brain

One distinguishing feature of the NUTRIM research was its combination of a carefully controlled dietary intervention lasting several months with sophisticated brain imaging technology.

To examine changes in brain function, researchers used arterial spin labeling magnetic resonance imaging (ASL-MRI), a technique that measures blood flow in different regions of the brain. They evaluated insulin responsiveness by tracking changes in regional cerebral blood flow after insulin was administered through the nose.

The team also used abdominal MRI scans to measure fat accumulation in the liver, known as intrahepatic lipid (IHL) content. Cognitive abilities were assessed using the Cambridge Neuropsychological Test Automated Battery (CANTAB), a standardized collection of computerized tests.

Researchers believe several components of peanuts may contribute to their observed effects on brain health, rather than any single nutrient being responsible.

"Multiple nutrients present in peanuts, including unsaturated fats, dietary fiber, vitamins and minerals and bioactive phytochemicals, could potentially contribute to the observed brain benefits," says Joris. "Peanuts are also a good source of plant-based protein and are especially rich in L-arginine. L-arginine is a key precursor of nitric oxide (NO), which has been reported to facilitate learning and memory performance."

What Participants Ate During the 16-Week Study

To ensure participants consumed a consistent amount, researchers supplied premeasured packets of skin-roasted peanuts throughout the peanut intervention period.

Participants were instructed to eat their peanuts in the morning or afternoon, but they could choose how to incorporate them into their daily routine. They could consume the entire portion at once, divide it into smaller amounts throughout the day, or include the peanuts in their meals.

During the control phase, participants avoided peanuts entirely. After 16 weeks, they switched to the opposite study condition, allowing researchers to compare brain health measurements under both dietary approaches.

Source: ScienceDaily

Wearable ultrasound patch boosts REM sleep without drugs or surgery

 Researchers led by the University of Texas at Austin have created a soft wearable patch that improved REM sleep in real-world testing without medication or surgery. Known as NEUSLeeP, the device combines gentle ultrasound stimulation with electrodes that track brain activity as it happens. This allows the patch to influence deep areas of the brain involved in sleep while also monitoring the brain's response.

"This is the first time we've been able to noninvasively target deep brain regions involved in REM sleep, while simultaneously monitoring brain activity," said Kai Wing "Kevin" Tang, a recent UT biomedical engineering Ph.D. graduate who led the research effort. "Our skin-attached NEUSLeeP patch opens up new possibilities for understanding sleep and treating sleep disorders in home settings," added Huiliang "Evan" Wang, assistant professor in the Cockrell School of Engineering's Department of Biomedical Engineering, who supervised Tang's work and served as the principal investigator (PI) directing the overall project.

Wearable Patch Helps People Reach REM Faster

The researchers tested the technology in a study involving 28 people, with the results published in Nature Communications. On average, participants entered REM sleep 43 minutes sooner and remained in that stage for about 16 minutes longer.

The benefits were observed in both healthy sleepers and participants experiencing some sleep difficulties. Users also described the patch as comfortable and safe, and the study reported minimal adverse effects.

Possible Benefits for Stress and Emotional Health

Among healthy participants, NEUSLeeP stimulation also increased heart rate variability, which is commonly used as an indicator of the body's ability to respond to stress. Brain imaging revealed changes in circuits associated with emotion, raising the possibility that the technology could support mood regulation and psychological resilience.

"REM sleep is not just about dreaming -- it's about emotional reset and stress adaptation," explained Gregory Fonzo, assistant professor in the Dell Medical School's Department of Psychiatry and Behavioral Sciences and one of the project's co-PIs. "By enhancing REM, we may help people better cope with stress and improve their overall well-being."

REM sleep disruptions have been associated with depression, anxiety and post-traumatic stress disorder (PTSD). Current approaches to sleep problems, including medication and behavioral therapy, may cause side effects or may not directly address the underlying factors that interfere with REM sleep.

Future Trials for Insomnia, Depression and PTSD

The team plans to conduct larger studies to verify the initial results and evaluate whether NEUSLeeP could help people with PTSD, depression and chronic insomnia. The researchers also see potential uses in home sleep monitoring, neuroscience research and personalized sleep treatments.

"Our vision is a future where patients with mental health disorders can optimize their sleep with a noninvasive and safe treatment," said Vincent Mysliwiec, M.D., a professor at UT Health San Antonio, a leading expert in sleep disorders, and another co-PI on the project. "This technology could help millions of people get the restorative sleep they need."

Researchers Move Toward Commercialization

The team is collaborating with Discovery to Impact, UT's commercialization unit, in an effort to move the technology toward the market. A patent application has also been filed for the device.

Other team members are William D. Moscoso-Barrera, Mengxia Yu, Mengmeng Yao, Jinmo Jeong, Ilya Pyatnitskiy, Anakaren Romero Lozano, Jiachen Wang, Ju-Chun Hsieh, Tony Sungjin Chae, Daniel Song, Julieta Garcia, Rithvik Mittapalli and Adam Bush of the Department of Biomedical Engineering; Benjamin Baird of the College of Natural Sciences' Department of Psychology; and Wynn Legon of Virginia Tech's Fralin Biomedical Research Institute.

Source: ScienceDaily

Depression may shut down the brain’s ability to make new neurons

 Most of the brain's roughly 100 billion neurons are produced before birth. However, the small number of new neurons that continue to form in the adult hippocampus may play an important role in protecting against depression, according to new research from Columbia University Vagelos College of Physicians and Surgeons.

The findings provide the first evidence that neurogenesis, the process of producing new neurons, stalls in the brains of adults with major depressive disorder. Researchers also identified molecular programs involved in controlling this process, offering potential clues for developing new treatments.

"Historically, depression was thought to be a disease of neurotransmitter deficiency, especially serotonin, but we now think that depression stems from multiple issues that affect our neurons' ability to adapt to stress and changing environments," says Maura Dupont, professor of psychiatry, who led the research.

"Without the ability to create new neurons, people with depression may not have the resilience to effectively adapt to the environment."

How New Neurons May Shape Memory and Emotion

The researchers focused on the hippocampus, a brain region that plays a major role in episodic memory and emotional responses to the environment. It is also one of the few areas of the adult brain that continues to generate new neurons.

Although the hippocampus is not the only brain region involved in depression, its influence over both memory and emotion has made it an important area of study. Researchers believe changes there may contribute to the tendency of people with depression to interpret experiences more negatively.

"The hippocampus is important for our ability to distinguish between similar but different memories and separate the emotional connotation of past memories and current events," Dupont says.

This ability is known as pattern separation. When it becomes impaired, individual memories and the emotions attached to them may become less distinct, allowing separate experiences to blend together.

"You may be out with a friend for lunch, but she's tired and doesn't talk much. With intact pattern separation, you remember this as a unique event. With impaired pattern separation, it becomes mixed with previous memories of feeling rejected, leading you to think, 'They're upset with me'," Dupont explains. "And I see this a lot in my patients, where they can only retrieve negative information from their memories."

Research in mice has shown that adult neurogenesis is necessary for pattern separation. A recent study involving patients with brain tumors, in whom neurogenesis was eliminated by radiation therapy directed at the hippocampus, suggests that the same relationship may exist in humans.

"It's important to emphasize that we do not yet know the complete mechanism, particularly in humans, but the newborn neurons seem to enhance pattern separation because they are especially responsive to new experiences and can be incorporated into new memory circuits more easily, allowing new memories to be stored separately from the old ones," Dupont says. "Turning neurogenesis back on may be a way to treat depression in some people by rewiring their hippocampus circuit."

Depression Affects More Than New Neuron Growth

The researchers found that the changes linked to depression extended well beyond neurogenesis. New neuron formation operates within a larger hippocampal circuit that stores episodic memories along with their emotional significance, and molecular disruptions appeared throughout that system.

The affected genes included those involved in building new connections between neurons, supporting communication among brain cells, supplying cellular energy, and moving materials within cells.

The trisynaptic circuit, the hippocampus's primary pathway for establishing new emotional memories, also displayed evidence of inflammation and cellular stress in people with depression.

To identify these changes, researchers studied nearly half a million brain cells collected from people with depression and control subjects shortly after each donor's death.

Using an array of recently developed techniques, the team measured the activity of every gene within individual cells and examined whether cellular proteins had been altered. This enormous dataset allowed researchers to see what individual cells were doing and determine exactly where affected cells were located within the hippocampal circuit.

Genes, Environment, and the Biology of Depression

The analysis revealed altered activity in several genes whose genetic variants have previously been associated with major depression.

Other disrupted genes showed epigenetic changes that may reflect the influence of environmental factors. Epigenetic mechanisms can adjust how strongly genes are turned on or off without altering the underlying DNA sequence.

"These are like dimmer switches that control how active genes are, and they are affected by life experiences such as stress, learning, aging, chemicals, etc.," Dupont says.

The diversity of molecular changes may also help explain why depression can look so different from one person to another.

"Overall, the wide range of effects we found could reflect different pathogenetic mechanisms, perhaps indicating that depression is not just one disease," she adds.

Researchers still have only a limited understanding of depression's underlying biology, according to Dupont. By defining the disorder more precisely at the cellular and molecular levels, studies like this one could eventually provide new targets for treatment.

Source: ScienceDaily

Children at risk for depression get “stuck” on sad faces

 A smile or a frown may reveal more than emotion alone. The faces that capture a child's attention could provide important clues about their mental health and how depression develops.

New research from Binghamton University, State University of New York, suggests that depression may influence how strongly children focus on emotional expressions such as happy or sad faces. The pattern appears to differ depending on whether a child has a family history of depression.

Researchers at the Mood Disorders Institute at Binghamton University study how depression develops in children and adolescents, with particular attention to how family history and emotional experiences may influence vulnerability over time. By identifying these patterns while children are still developing, scientists hope to better understand who may be at greater risk and eventually improve prevention strategies.

"Most of the vulnerabilities that we focus on are still developing during this time period," said Brandon Gibb, director of the Mood Disorders Institute and SUNY distinguished professor of psychology. "You can catch things as they're developing, rather than only studying them once they're already there and pretty stable."

Following Children's Attention Over Time

Earlier research has linked depression with greater attention to sad faces. However, those associations have generally been modest, and scientists have not been sure whether biased attention contributes to depression or develops because of it.

The Binghamton study was designed to investigate that question by tracking both depressive symptoms and attention patterns over time. According to the researchers, it is the first study to examine how changes in each may predict later changes in the other among children.

"The real novel piece is that we looked at these transactional relations," said Kelly Gair, a PhD student at Binghamton and lead author of the paper. "Between attentional biases and depressive symptoms, we looked at the way that they were mutually predicting one another across the time points, which is especially novel and hasn't been done before."

The research team, which also included Leslie A. Brick from the University of New Mexico, followed 242 children and their mothers for two years. Participants were assessed every six months.

During each visit, children viewed pairs of faces on a screen. One face showed a neutral expression, while the other displayed an emotion (happy, sad, or angry). Eye tracking technology measured which face held the child's attention and for how long.

Children in the study looked at faces conveying different emotions onscreen, and eye tracking technology recorded where their attention veered. Photo credit: NimStim Set of Facial Expressions (Tottenham et al., 2009).

Family History Changes the Pattern

The results suggest that increasing depressive symptoms do not affect every child's attention in the same way. Family history appeared to play an important role.

Among children whose mothers had a history of major depressive disorder, rising depressive symptoms were associated with greater attention to sad faces. In other words, as these children experienced more symptoms themselves, their attention became increasingly drawn toward expressions of sadness.

"For those who are already at risk, the more these children experience depression themselves, the more they lose their ability to pull their attention away from the sad things around them," Gibb said.

"We know that when you're depressed, it changes what you pay attention to," Gair said. "Our results suggest that these changes may be more long-lasting and may differ depending on family history. One thought is that for children of mothers with depression, who are exposed to more facial displays of sadness from interactions with their mom, these types of facial expressions become even more salient when they experience depression themselves, so their attention becomes increasingly stuck on sad expressions."

Happy Faces May Lose Their Pull

A different pattern emerged among children whose mothers had no history of depression.

When depressive symptoms increased in these children, they did not become more focused on sad expressions. Instead, they paid less attention to happy faces.

"In our lower-risk children, what seems to be happening is that experiences of depression are eroding a protective factor, which is how much they pay attention to happy faces," Gibb said.

The distinction suggests that depression may alter emotional attention through different pathways depending on a child's underlying level of familial risk. For some children, sadness may become increasingly difficult to ignore. For others, positive emotional signals may simply become less likely to capture their attention.

Source: ScienceDaily