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  • Loss of Smell May Signal Early Alzheimer’s: New Study Points to an Immune Trigger

    Loss of Smell May Signal Early Alzheimer’s: New Study Points to an Immune Trigger

    A subtle decline in the sense of smell could be among the earliest detectable changes linked to Alzheimer’s disease, potentially emerging well before clear memory problems. New research from Germany suggests the shift may be driven by the brain’s immune cells damaging key odor-processing connections.

    The study, led by scientists at the German Center for Neurodegenerative Diseases (DZNE) and Ludwig Maximilian University of Munich, focuses on microglia, immune cells that help maintain brain health. Researchers report that in early Alzheimer’s, microglia may begin dismantling nerve fibers needed for normal smell perception.

    How the brain’s smell circuit changes

    The team examined communication between the olfactory bulb, which processes odor signals, and the locus coeruleus, a brainstem region involved in sensory regulation and other core functions. Long nerve fibers from the locus coeruleus help tune activity in the olfactory bulb, supporting normal smell processing.

    According to the researchers, early Alzheimer’s-related alterations make these fibers appear abnormal to microglia. In response, microglia break down the connections, which could help explain why smell deficits can appear early in the disease course.

    An eat-me signal on neurons

    The study points to changes in the nerve fiber membrane as a likely trigger. A molecule called phosphatidylserine, typically kept on the inner side of the cell membrane, was observed on the outside, where it can act as an immune cue.

    Microglia are known to respond to this kind of signal during normal synaptic pruning, a process that removes unused or impaired connections. The researchers suggest that in early Alzheimer’s, abnormal neuron activity may prompt this membrane shift, leading microglia to remove fibers that are still needed.

    Evidence from mice, tissue, and PET scans

    To support the mechanism, the scientists combined results from Alzheimer’s-like mouse models with analyses of human brain tissue and PET imaging data from people diagnosed with Alzheimer’s or mild cognitive impairment. Together, these lines of evidence point to immune-driven damage occurring at an early stage.

    The findings also connect to a growing push for earlier diagnosis, as newer Alzheimer’s treatments are generally aimed at earlier phases of the disease. Researchers say a better understanding of smell-related changes could help identify people who should receive further testing before cognitive symptoms become pronounced.

    Smell loss can have many causes, including aging, infections, allergies, and other neurological conditions, so it is not a stand-alone diagnostic sign. Still, the study strengthens the case that changes in olfaction may offer a practical early clue worth taking seriously in Alzheimer’s research and clinical follow-up.

  • New MS remyelination drugs move closer to trials as K102 and K110 show promise in repairing nerve damage

    New MS remyelination drugs move closer to trials as K102 and K110 show promise in repairing nerve damage

    Multiple sclerosis (MS) is a long-term autoimmune condition that affects over 2.9 million people around the world. In MS, the immune system mistakenly attacks the myelin sheath, a protective layer that insulates nerve fibers. This damage interrupts communication between the brain and body, leading to symptoms such as numbness, tingling, vision problems, and paralysis.

    Although existing treatments can help reduce inflammation, there are still no approved therapies that protect neurons or rebuild the damaged myelin sheath. Scientists have now made significant progress toward that goal with support from the National Multiple Sclerosis Society. Their work has led to the discovery of two compounds capable of promoting remyelination, the process of repairing the myelin coating on nerve fibers.

    The study, published in Scientific Reports, was led by Seema Tiwari-Woodruff, a professor of biomedical sciences at the University of California, Riverside, School of Medicine, and John Katzenellenbogen, a professor of chemistry at the University of Illinois Urbana-Champaign (UIUC). The research was funded through two National MS Society initiatives: a standard investigator-initiated grant and the organization’s Fast Forward program, which accelerates commercialization of promising research.

    “Our work represents more than a decade of collaboration, with the last four years focused on identifying and optimizing new drug candidates that show strong potential to treat MS and possibly other neurological diseases involving demyelination,” Tiwari-Woodruff said.

    With this support, the team launched a drug development program that has since been licensed by Cadenza Bio, Inc. Backed by investor funding, the company has continued advancing the research and is preparing for clinical testing of what could become a first-of-its-kind treatment for people with MS.

    From discovery to development

    This new work builds on earlier studies involving a compound called indazole chloride, which had shown promise in promoting myelin repair and regulating immune responses in mouse models of MS. However, indazole chloride lacked the chemical properties and patent potential required for clinical and commercial use, Tiwari-Woodruff explained.

    Working with UIUC chemists Katzenellenbogen and Sung Hoon Kim, who created new versions of the molecule, Tiwari-Woodruff’s group, led by recent UC Riverside graduate Micah Feri, screened more than 60 analogs of indazole chloride. From this effort, they identified two standout candidates, K102 and K110. Both showed better safety, efficacy, and drug-like characteristics in tests using mice and human cells.

    Among the two, K102 emerged as the leading candidate. It not only stimulated myelin repair but also helped regulate immune activity, a critical balance for MS therapies. The compound also performed well in human oligodendrocytes — cells responsible for producing myelin — derived from induced pluripotent stem cells, suggesting the results could translate effectively from animal studies to human disease.

    Normally, oligodendrocyte precursor cells develop into mature myelin-producing cells that repair nerve insulation. In MS, this repair process often breaks down, leading to lasting nerve damage. A compound like K102 that can restore myelin could help improve nerve signal transmission and potentially limit long-term disability.

    “K110 is also a strong candidate,” Tiwari-Woodruff said. “It has slightly different central nervous system effects and may be better suited for other conditions like spinal cord injury or traumatic brain injury, so we’re keeping it in the pipeline.”

    From bench to biotech

    Tiwari-Woodruff and Katzenellenbogen credit the National MS Society’s Fast Forward program as a turning point. Fast Forward accelerates the commercialization of promising therapies by promoting academic-industry partnerships. The highly competitive grant enabled Tiwari-Woodruff and Katzenellenbogen to generate sufficient data to license the rights to Cadenza Bio to develop K102 and K110. The patents are jointly held by UCR and UIUC, with an exclusive, worldwide licensing agreement in place between the universities and Cadenza Bio.

    “This project has been a good example of how long-standing academic collaborations can lead to real-world applications,” Katzenellenbogen said. “Our shared goal was always to take a promising idea and develop it into a therapy that could help people with MS. We’re finally getting close to that reality.”

    Initially, UCR’s Office of Technology Partnerships collaborated with UIUC to seek patent protection. Grace Yee, assistant director of technology commercialization at UCR, said the joint efforts of UCR, UIUC, and the National MS Society advocated for and promoted the technology to investors and industry for commercial development.

    “Our entrepreneurs-in-residence also helped advise the project, so the team was able to develop materials and messaging to highlight the project’s commercial value,” she said. “When investors expressed interest in the technology, UCR and UIUC helped them understand how the technology addresses an unmet need in treating MS. These efforts led to the licensing agreement with Cadenza Bio.”

    Elaine Hamm, chief operating officer at Cadenza Bio, said she and Carol Curtis, cofounder of Cadenza Bio, were impressed by the possibility of moving from slowing axon damage to repairing axon damage.

    “This is the future we want to build,” Hamm said. “It is why we licensed the technology, and why we are excited to move it forward to patients in need.”

    More than a decade in the making

    Tiwari-Woodruff and Katzenellenbogen have worked together for more than 12 years. Tiwari-Woodruff’s move from UCLA to UCR in 2014, she said, turned out to be a pivotal decision.

    “The support from UCR — from leadership to infrastructure — has been extraordinary,” Tiwari-Woodruff said. “None of this would’ve been possible without that backing. Funding for academic labs like mine and John’s is crucial. This is selfless work, driven by a deep love of science and commitment to human health.”

    Though the initial focus is MS, the team believes K102 and K110 could eventually be applied to other diseases involving neuronal damage, including stroke and neurodegeneration.

    Cadenza Bio is now advancing K102 through the necessary non-clinical studies required to support first-in-human clinical trials.

    “We’re hopeful that clinical trials can begin soon,” said Tiwari-Woodruff. “It’s been a long journey — but this is what translational science is all about: turning discovery into real-world impact.”

    The research was also supported in part by grants from the National Institutes of Health and Cadenza Bio.

    Tiwari-Woodruff, Katzenellenbogen, Kim, and Feri were joined in the research by Flavio D. Cardenas, Alyssa M. Anderson, Brandon T. Poole, Devang Deshpande, Shane Desfor, Kelley C. Atkinson, Stephanie R. Peterson, Moyinoluwa T. Ajayi, Fernando Beltran, Julio Tapia, and Martin I. Garcia-Castro of UCR; Kendall W. Nettles and Jerome C. Nwachukwu of The Scripps Research Institute, Florida; and David E. Martin and Curtis of Cadenza Bio, Oklahoma.

  • Study of the hippocampus suggests newborn brains start densely wired, then prune connections for sharper memory

    Study of the hippocampus suggests newborn brains start densely wired, then prune connections for sharper memory

    The hippocampus, a brain region essential for forming memories and mapping space, may develop in a way that challenges the long-held idea of the mind as a blank slate. New research from the Institute of Science and Technology Austria suggests key memory circuits begin life with unusually dense wiring that is later trimmed and refined.

    In a study published in Nature Communications, scientists examined how a major hippocampal network changes after birth in mice. The team focused on CA3 pyramidal neurons, cells widely seen as central to storing and retrieving memories.

    How the CA3 circuit develops

    Using patch-clamp recordings and high-resolution imaging, researchers compared the CA3 network across early postnatal stages, adolescence, and adulthood. The methods allowed them to measure tiny electrical signals and map how strongly neurons were connected at different ages.

    The results pointed to an early-life circuit that is highly connected and seemingly random, followed by a gradual shift toward fewer but more organized links. Rather than adding connections over time, the network became more efficient by losing many of its initial ones.

    Pruning may boost memory efficiency

    Lead researcher Peter Jonas said the pattern fits a pruning model in which the system starts full and then becomes streamlined. The researchers argue that an initially exuberant network could help the hippocampus quickly integrate different kinds of sensory information into usable memories.

    If the brain started with far fewer built-in links, the team notes, neurons would first need more time to find and connect to each other, potentially slowing early information processing. The study adds to broader evidence that brain development often involves overproduction of connections followed by activity-dependent pruning.

    While the work was conducted in mice, the hippocampus is highly conserved across mammals, making the findings relevant to ongoing debates about how genetics and experience shape learning. The authors say future research will need to clarify what signals drive which connections are kept or removed, and how this process relates to memory performance.

  • Ancient Lead Exposure and a Key Gene: New Clues to Why Modern Humans Outpaced Neanderthals

    Ancient Lead Exposure and a Key Gene: New Clues to Why Modern Humans Outpaced Neanderthals

    What made the modern human brain so different from that of our extinct relatives, such as Neanderthals? Researchers at the University of California San Diego School of Medicine, along with an international team, have discovered that ancient hominids, including early humans and great apes, came into contact with lead far earlier than previously believed — up to two million years before modern humans began mining it. This long-term exposure may have influenced how early brains evolved, possibly hindering language and social development in all but modern humans, who possess a unique protective genetic variant. The findings were published in Science Advances on October 15, 2025.

    The team examined fossilized teeth from 51 hominids found across Africa, Asia, and Europe. The samples included both modern and archaic humans such as Neanderthals, early human ancestors like Australopithecus africanus, and extinct great apes including Gigantopithecus blacki.

    Lead traces were present in 73% of the fossils studied, with 71% of modern and archaic human samples showing contamination. Fossils of G. blacki dating back 1.8 million years revealed the highest levels of acute exposure.

    It was previously thought that humans began facing significant lead exposure only in recorded history, especially during the Roman era, when lead pipes were used for water systems, and later during the Industrial Revolution. Lead pollution declined only after the late twentieth century.

    “We stopped using lead in our daily lives when we realized how toxic it is, but nobody had ever studied lead in prehistory,” said corresponding author Alysson Muotri, Ph.D., professor of pediatrics and cellular & molecular medicine at UC San Diego School of Medicine, associate director of the Archealization Center, and director of the Sanford Integrated Space Stem Cell Orbital Research Center.

    To the researchers’ surprise, teeth from people born in the mid-twentieth century (the 1940s through the 1970s), when exposure to leaded gasoline and paint was widespread, showed similar lead patterns to ancient human fossils.

    The scientists suggest that ancient humans and their relatives might have encountered lead through their search for water, much like the Romans did later in history.

    “One possibility is that they were looking for caves with running water inside,” Muotri said. “Caves contain lead, so they were all contaminated. Based on the tooth enamel studies, it started very early in infancy.”

    Lead exposure disrupts brain growth and function, impairing intelligence and emotional regulation.

    Faced with this evidence, Muotri and his team began to question how modern humans managed to thrive despite such toxic conditions during their evolutionary past.

    A tiny genetic change

    A gene known as neuro-oncological ventral antigen 1 (NOVA1) plays a major role in brain formation and synaptic development. Acting as a key regulator of neurodevelopment, NOVA1 helps determine how neural progenitor cells react to lead exposure, and disturbances in its activity are linked to neurological disorders.

    Nearly all modern humans carry a version of the NOVA1 gene that differs by a single DNA base pair from the version found in Neanderthals. Earlier work from Muotri’s group showed that swapping the modern NOVA1 with the older variant in miniature brain models, called organoids, caused dramatic changes in brain structure and connectivity.

    “Everything about the organoids is identical except for that genetic variant, allowing us to ask whether that specific mutation between us and Neanderthals is giving us any advantage,” said Muotri. The archaic variant accelerated brain maturation but resulted in less complexity over time. “If all humans have this newer mutation in all corners of the world, very strong genetic pressure must have selected for it in our species.”

    To test whether lead exposure might have shaped this genetic shift, the researchers created brain organoids with both the modern and ancestral NOVA1 variants, exposing them to lead and monitoring the growth of cortical and thalamic neurons.

    They found that lead changed NOVA1 activity in both types of organoids, influencing genes linked to conditions such as autism and epilepsy.

    However, only the archaic NOVA1 variant altered the activity of FOXP2, a gene crucial for speech and language. People with certain FOXP2 mutations struggle to form complex words and sentences.

    “These type of neurons related to complex language are susceptible to death in the archaic version of NOVA1,” said Muotri. “ The FOXP2 gene is identical between us and the Neanderthals, but it’s how the gene is regulated by NOVA1 that likely contributes to language differences.”

    Evolutionary implications

    The findings suggest that the acquisition of the modern NOVA1 variant may have protected us from the detrimental effects of lead, promoting complex language development and social cohesion. This could have given modern humans a significant evolutionary advantage over Neanderthals, even in the presence of lead contamination.

    Muotri believes these results have important implications for understanding how environmental stressors shaped brain development during human evolution. He speculates that lead exposure may have contributed to the extinction of Neanderthals around 40,000 years ago.

    “Language is such an important advantage, it’s transformational, it is our superpower,” said Muotri. “Because we have language, we are able to organize society and exchange ideas, allowing us to coordinate large movements. There is no evidence that Neanderthals could do that. They might have had abstract thinking, but they could not translate that to each other. And maybe the reason is because they never had a system to communicate that was as efficient as our complex language.”

    Understanding how NOVA1 gene variants can affect FOXP2 expression helps elucidate the relationship between lead contamination and brain development and also sheds light on neurological conditions related to language, including speech apraxia — a condition that makes it difficult to produce speech sounds correctly — and autism.

    The study’s co-authors included Janaina Sena de Souza, Sandra M. Sanchez-Sanchez, Jose Oviedo, University of California San Diego; Marian Bailey and Matthew Tonge at Southern Cross University; Renaud Joannes-Boyau, Southern Cross University and University of Johannesburg; Justin W. Adams, University of Johannesburg and Monash University; Christine Austin, Manish Arora, Icahn School of Medicine at Mount Sinai, Kira Westaway, Macquarie University; Ian Moffat, Flinders University and University of Cambridge; Wei Wang and Wei Liao, Anthropology Museum of Guangxi; Yingqi Zhang, Institute of Vertebrate Paleontology and Paleoanthropology; Luca Fiorenza, Monash University and Johann Wolfgang Goethe University; Marie-Helene Moncel, Museum National d’Histoire Naturelle; Gary T. Schwartz, Arizona State University; Luiz Pedro Petroski and Roberto H. Herai, Pontifícia Universidade Católica do Paraná; Jose Oviedo, University of Arizona; and Bernardo Lemos, Harvard T. H. Chan School of Public Health.

    The study was funded, in part, by the National Institutes of Health (grants R01 ES027981, P30ES023515, R01ES026033), the Australian Research Council (grant DP170101597), the National Science Foundation (grant BCS 0962564), and the The Leakey Foundation.

    Disclosures: Muotri is the co-founder of and has an equity interest in TISMOO, a company specializing in genetic analysis and human brain organogenesis. The terms of this arrangement have been reviewed and approved by the University of California San Diego in accordance with its conflict-of-interest policies.

  • Ozempic and other GLP-1 drugs tied to lower depression and anxiety in large Swedish study, raising new questions about mental health benefits

    Ozempic and other GLP-1 drugs tied to lower depression and anxiety in large Swedish study, raising new questions about mental health benefits

    Popular GLP-1 medicines used for type 2 diabetes and weight loss, including Ozempic and Wegovy, may be linked to improved mental health outcomes, according to a large new analysis of Swedish health data. Researchers tracked changes in psychiatric care and work absence during periods when patients were using these drugs.

    The study, led by scientists from the University of Eastern Finland, Karolinska Institutet and Griffith University, examined national register data spanning 2009 to 2022. Nearly 100 000 people were included, with more than 20 000 having used a GLP-1 receptor agonist at some point during follow-up.

    What the study found

    Across the dataset, GLP-1 use was associated with fewer psychiatric hospital visits and fewer days of sickness absence related to mental health conditions. The strongest associations were reported for semaglutide, the active ingredient in Ozempic and Wegovy.

    During periods of semaglutide use, psychiatric hospital care and sickness absence were reported as 42% lower than during periods off treatment. The analysis also linked semaglutide exposure with a 44% lower risk of depression and a 38% lower risk of anxiety disorders.

    Signals beyond mood and anxiety

    The researchers also reported a lower rate of hospital care and work absence tied to substance use disorders during semaglutide treatment periods, with a reduction of 47%. They additionally found an association between GLP-1 receptor agonist use and reduced suicidal behavior, though the study design cannot determine causality.

    One author, Professor Mark Taylor of Griffith University, said the direction of the results aligned with earlier register-based research suggesting GLP-1 use may be associated with a reduced risk of alcohol use disorder. Because alcohol problems can worsen mood symptoms, the team said this could be one pathway behind the observed patterns.

    Why it may happen, and what it means

    Experts caution that registry studies can show links but cannot prove the drugs directly prevent depression or anxiety, since unmeasured factors could influence who starts or stays on treatment. Researchers said potential explanations range from improved blood sugar control and weight loss to reduced alcohol use and better quality of life.

    They also pointed to possible direct effects on the brain, including changes in reward-related pathways, as a hypothesis that needs targeted clinical research. The findings were published in The Lancet Psychiatry, adding weight to an ongoing debate as regulators and clinicians continue to watch for both potential benefits and risks affecting mental health.

  • Penn State-linked study suggests perceived control can cut daily stress by driving faster problem-solving

    Penn State-linked study suggests perceived control can cut daily stress by driving faster problem-solving

    New research involving scientists affiliated with Penn State suggests that feeling more in control of everyday problems can make people more likely to resolve them, easing day-to-day stress. The findings add to evidence that small psychological shifts can influence how people respond to routine hassles.

    The study, published in Communications Psychology, analyzed daily reports from more than 1 700 adults participating in the National Study of Daily Experiences, a project linked to the broader MIDUS health survey. Participants logged stressors over eight consecutive days and noted whether each issue was resolved by day’s end.

    Control and stress resolution link

    Researchers found that on days when individuals reported greater perceived control over a stressor, they were substantially more likely to take action that led to resolution. Examples included addressing an interpersonal conflict, handling a home problem, or responding to work overload.

    The analysis indicated that perceived control varies from day to day rather than functioning as a fixed personality trait. That matters because it suggests control can potentially be strengthened through context, planning, or support, rather than being something people either have or lack.

    Why age may amplify effects

    The link between perceived control and resolving stressors appeared to strengthen with age across the two survey waves taken roughly a decade apart. Researchers reported that later in the study period, higher-than-usual perceived control was associated with an even greater likelihood of resolving the day’s stressor.

    Scientists cautioned that perceived control does not remove stressors, but it may help people respond in ways that prevent problems from lingering. The authors say the next step is to examine whether faster resolution could also reduce the health impact of chronic stress over longer periods.

  • A simple blood test could spot depression risk early by tracking immune cell aging

    A simple blood test could spot depression risk early by tracking immune cell aging

    Researchers are testing whether a routine blood sample could help flag depression earlier, using measures of biological aging in specific immune cells. The work adds to a growing push for objective biomarkers that could complement symptom-based mental health screening.

    The study, published in The Journals of Gerontology: Series A, examined epigenetic changes that act like molecular timestamps on DNA. These so-called epigenetic clocks estimate biological age, which can advance faster than chronological age under stress, illness, or other factors.

    Why depression has been hard to test

    Depression is typically diagnosed through clinical interviews and questionnaires, not lab confirmation, partly because the condition can look very different across patients. Some people primarily experience somatic symptoms such as sleep and appetite changes, while others struggle most with mood and cognition, including hopelessness and loss of pleasure.

    That variability can complicate detection, especially when physical symptoms overlap with other chronic conditions. Clinicians may order bloodwork to rule out medical causes, but there is still no widely accepted biological test that can confirm depression on its own.

    Monocytes emerge as a key signal

    The research analyzed data from 440 women, including 261 living with HIV and 179 without HIV, drawing on the long-running Women’s Interagency HIV Study. Depression symptoms were assessed using the Center for Epidemiologic Studies Depression Scale, a 20-item tool that captures both somatic and non-somatic features.

    Blood samples were used to calculate epigenetic aging in two ways: a broad measure across multiple cell types and a monocyte-focused clock. Monocytes are white blood cells involved in immune responses and inflammation, processes increasingly studied for their links to mental health.

    The monocyte-specific aging measure tracked most strongly with non-somatic depression symptoms such as anhedonia, hopelessness, and a sense of failure, in women with and without HIV. By contrast, the broader multi-tissue aging measure did not show the same relationship, suggesting the signal may be cell-type specific.

    What this could change in care

    The authors caution that the findings are not yet ready for clinical use and do not mean a single blood draw can diagnose depression today. Larger studies, replication in different populations, and clearer thresholds would be needed before a test could be validated for real-world screening.

    Still, the results point to a possible path toward earlier, more precise detection, particularly for people whose physical symptoms might be attributed to other illnesses. If confirmed, immune-cell epigenetic measures could also support more personalized care by helping researchers distinguish depression subtypes and refine treatment matching.

  • How reward bias can make lies feel true, especially from friends

    How reward bias can make lies feel true, especially from friends

    New neuroscience research is adding detail to a familiar problem: people often struggle to spot dishonesty, particularly when the message sounds beneficial. The findings suggest that the promise of a gain can subtly weaken how carefully we evaluate whether information is true.

    The study, led by Yingjie Liu of North China University of Science and Technology, tested how people judge messages depending on who delivers them. Researchers focused on whether trust shifts when information comes from a friend versus a less familiar person.

    Inside the brain during deception

    Using brain imaging with 66 healthy adults, the team examined neural activity while participants exchanged information through computer screens. Messages were framed around outcomes described as gains or losses, allowing scientists to track how reward and risk contexts shape belief.

    Across the experiment, participants were more likely to accept false information in gain situations. Brain regions linked to reward processing, risk assessment and interpreting others’ intentions showed patterns consistent with relaxed scrutiny when a positive outcome seemed possible.

    Why friends can be persuasive

    Friendship added another layer: when a friend delivered the potentially misleading message, the pair showed synchronized brain activity. That alignment shifted with context, strengthening in reward-related areas during gains and in risk-related areas during losses.

    Researchers reported that these shared neural patterns helped predict when someone was most likely to be misled by a friend. The results point to a mechanism in which social closeness and reward expectations combine to make certain claims feel credible even when they should prompt doubt.

    While the work does not mean people always trust friends blindly, it highlights a consistent vulnerability. In everyday decisions, offers that appear mutually beneficial may deserve extra verification, precisely because the brain can treat them as safer than they are.

  • Creatine research shifts beyond the gym: What studies suggest about brain health, mood and aging

    Creatine research shifts beyond the gym: What studies suggest about brain health, mood and aging

    Creatine has long been associated with strength and sprint performance, but a growing body of research is examining what it may do beyond muscle gains. Scientists are increasingly focused on its role in cellular energy, including in the brain, where energy demand is high.

    The compound is made in the body from amino acids and stored mainly in skeletal muscle, with smaller amounts in organs such as the brain and heart. In cells it supports the rapid recycling of ATP, the core energy molecule, which helps explain why supplementation can aid short, high-intensity efforts.

    Why creatine matters in the brain

    Because brain tissue depends on steady energy supply, researchers are studying whether creatine can support cognition under stress, sleep loss or aging. Some studies have reported improvements in tasks linked to memory and processing speed, especially in people likely to start with lower creatine stores.

    Interest is also expanding into mental health and neurological disease, including depression and Parkinson’s disease, where energy metabolism and inflammation may play a role. Evidence remains mixed and condition-specific, and experts stress that early signals do not yet translate into routine medical use.

    What dosing research typically uses

    The most studied form is creatine monohydrate, commonly taken either as a short loading phase of about 20 g daily for 5 to 7 days or as a steady daily dose around 3 to 5 g. Research suggests both approaches can raise muscle stores, with loading working faster and lower daily dosing reaching saturation over several weeks.

    Absorption and retention vary between individuals, partly because tissues have a storage ceiling and excess is converted to creatinine and excreted. Some evidence indicates taking creatine with carbohydrates can increase uptake, though the real-world impact differs by person and diet.

    Safety, limits and who should ask first

    Large reviews and position statements have generally found creatine to be safe for healthy adults when used as studied, and it is not a steroid or hormone. The most common issues are practical rather than dangerous, such as water retention or stomach upset at higher single doses.

    Clinicians still advise caution for people with kidney disease or those advised to limit protein-related metabolites, since creatinine levels can rise with supplementation and complicate lab interpretation. Researchers emphasize that creatine is not a cure-all and works best as a targeted aid alongside training, nutrition and medical guidance when needed.

  • Deep Sleep and Growth Hormone: UC Berkeley Study Maps Brain Circuit That Links Nighttime Repair to Wakefulness

    Deep Sleep and Growth Hormone: UC Berkeley Study Maps Brain Circuit That Links Nighttime Repair to Wakefulness

    Deep non-REM sleep has long been tied to the body’s biggest overnight growth hormone surge, a rhythm linked to tissue repair, muscle maintenance and metabolic health. A new study from researchers at the University of California, Berkeley offers a clearer explanation of how the brain coordinates that hormone release during sleep.

    In work published in Cell, the team traced a neural circuit in the hypothalamus that helps control when growth hormone is released and how that signal is kept in balance. The findings come as sleep disruption is increasingly associated in research with higher risks for weight gain, insulin resistance and cardiovascular disease.

    A circuit with two hormone controls

    The study focuses on two hypothalamic signals that act as opposing levers: growth hormone releasing hormone, which promotes growth hormone output, and somatostatin, which suppresses it. By mapping how these systems behave across sleep stages, researchers aimed to explain why fragmented or reduced deep sleep can blunt growth hormone release.

    Using mice, the researchers recorded neural activity and manipulated specific neurons to observe how these signals shift across REM and non-REM sleep. They reported that the two hormones follow distinct patterns depending on the sleep stage, producing different growth hormone dynamics over the night.

    How growth hormone feeds back

    The team also describes a feedback loop connecting growth hormone signaling to the locus coeruleus, a brainstem hub involved in alertness and attention. As growth hormone levels build, the circuit can influence arousal, suggesting the hormone is not only an output of sleep but also a contributor to sleep-wake regulation.

    Because the locus coeruleus is implicated in a range of neurological and psychiatric conditions, the authors say the circuit-level map could help guide future work on sleep disorders and diseases where arousal systems are disrupted. However, the research was conducted in mice, and any clinical applications would require further validation in humans.

    Why the findings matter

    Growth hormone is best known for its role in childhood and adolescent growth, but it also supports adult physiology by influencing body composition and how the body handles sugar and fat. That is why chronically poor sleep, particularly reduced deep sleep, has been linked in broader research to metabolic problems over time.

    The researchers argue that identifying the wiring behind growth hormone regulation may eventually inform therapies that target specific nodes in the sleep-hormone system. For now, the study adds detailed biological context to a familiar health message: sleep quality can shape key hormonal processes, not just next-day energy.

    The work was supported by the Howard Hughes Medical Institute and the Pivotal Life Sciences Chancellor’s Chair fund, and included collaborators from UC Berkeley and Stanford University. The authors emphasize that the new circuit map is a foundation for future studies on how sleep architecture and hormones interact in health and disease.