Latest news with #hippocampus
Yahoo
11 hours ago
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This Diet May Reduce the Risk of Neuron Loss and Dementia, New Study Says
Reviewed by Dietitian Jessica Ball, M.S., RD Key Points This study links the MIND diet to less neuron loss in the hippocampus, which is key to memory and learning. Participants who followed the MIND diet closely had a 22% lower chance of hippocampal sclerosis. These findings build on evidence that food choices may influence brain aging and dementia risk. Everyone wants to protect their memories. The idea of forgetting familiar faces or treasured moments drives many people to look for ways to protect their brain health. That motivation has fueled growing interest in lifestyle habits—especially diet—that could help keep the mind sharp. One part of the brain researchers are particularly focused on is the hippocampus, a hub for learning and memory. When it sustains damage in the form of hippocampal sclerosis (a severe loss of neurons in this region) it's often linked to dementia. These cells don't grow back. A new study, published in JAMA Network Open, offers intriguing evidence that what you eat may influence the odds of developing this type of brain damage. It examined the MIND diet, an eating pattern built to support cognitive health, and found that people who followed it more closely were less likely to lose neurons in their hippocampus. It's a new piece in the larger puzzle of how diet may help preserve brain function with age. How Was This Study Conducted Researchers analyzed data from 809 participants in the long-running Rush Memory and Aging Project, all of whom had agreed to donate their brains for research after death. None had dementia when they joined the study, and they completed annual food questionnaires for up to 18 years. Using these detailed diet records, scientists calculated a MIND diet score for each person, with higher scores reflecting closer adherence to the diet. After death, brain tissue was examined for signs of hippocampal sclerosis, hippocampal sclerosis with limbic-predominant age-related TDP-43 encephalopathy (LATE-NC), and general hippocampal neuronal loss. The participants had an average age of 91 at death, and most were white. What Did the Study Find? Those with the highest MIND diet scores had about a 22% lower chance of having hippocampal sclerosis compared to those with the lowest scores. They were also less likely to have hippocampal sclerosis alongside limbic-predominant age-related TDP-43 encephalopathy (LATE-NC) and had less overall neuronal loss in the hippocampus. The link held even after accounting for age, sex, education, total calorie intake, genetic risk for Alzheimer's disease, Alzheimer's pathology and vascular disease in the brain. The study also found that hippocampal sclerosis explained about 21% of the connection between the MIND diet and lower odds of dementia at the time of death. Still, the authors note important limitations: the study was observational, so it cannot prove the diet prevented brain damage. Other factors not measured could play a role. And because the participants were almost entirely non-Hispanic white older adults, the findings may not apply to all populations. How Does This Apply to Real Life Even though this study can't prove that the MIND diet directly prevents neuron loss, it builds on earlier research showing the diet's link to slower cognitive decline and a lower risk of dementia. Taken together, the evidence paints a consistent picture: your daily food choices may play a meaningful role in how well your brain ages. The MIND diet isn't about perfection or rigid rules. It's about tipping the balance toward foods known to nourish the brain. That means: Eating leafy greens most days of the week Including berries a few times per week Choosing nuts, beans, whole grains and olive oil regularly Eating fish and poultry more often than red meat Limiting foods like butter, full-fat cheese, pastries, sweets, fried food and fast food If that sounds like a big leap from where you are now, start small. Picture your week of meals and identify one easy win: maybe swapping your usual side of fries for a green salad a couple of times, or tossing a handful of walnuts into your afternoon yogurt. Keep a carton of blueberries in the fridge—or a bag in the freezer—so you can grab a brain-friendly snack without thinking twice. If you cook with butter by habit, try drizzling olive oil over vegetables instead and notice how quickly the swap becomes second nature. If you're ready for a bigger overhaul, trying something like our weeklong Cognitive Health Meal Plan could be a great next step. We also love MIND diet recipes like our Chicken & Spinach Salad with Creamy Feta Dressing and Lemon-Garlic Chicken Casserole, since they include big flavor, plenty of veggies and some whole grains, too. And these changes aren't just good for your hippocampus. They may also improve heart health, lower inflammation and help you feel more energetic day to day—benefits you can notice long before any memory test. The beauty of the MIND diet is that you don't have to overhaul your entire plate at once; you just have to start leaning, meal by meal, in the right direction. The Bottom Line This is the first human study to show that following the MIND diet is linked with a lower likelihood of hippocampal sclerosis, a type of neuron loss tied to dementia. While it can't prove the diet directly prevents brain cell loss, it adds to a growing body of evidence that what you eat matters for brain health. Focusing on plant-rich meals, healthy fats, and limiting processed foods may be one step toward protecting your memory in the years ahead. Read the original article on EatingWell
Yahoo
11-08-2025
- Health
- Yahoo
Newron Notes the Publication of New Preclinical Research Suggesting Evenamide Ameliorates Schizophrenia-Related Dysfunction
Ad hoc announcement pursuant to Art. 53 LR New findings published in Neuropsychopharmacology are the first to demonstrate that evenamide targets the key site of schizophrenia pathology in the hippocampus, and so could be an ideal therapeutic agent for treatment of the disorder Systemic, acute administration of evenamide in the neurodevelopment MAM model of schizophrenia improved positive, negative and cognitive symptoms of schizophrenia Time-course analysis indicates effects of a single dose of evenamide last long after elimination of drug, suggesting effect on neuronal plasticity Evenamide's glutamate modulation may improve overall outcomes in poorly responding or treatment resistant patients with schizophrenia on current antipsychotics, offering a novel strategy for managing the disorder MILAN & MORRISTOWN, N.J., August 11, 2025--(BUSINESS WIRE)--Newron Pharmaceuticals S.p.A. ("Newron") (SIX: NWRN, XETRA: NP5), a biopharmaceutical company focused on the development of novel therapies for diseases of the central and peripheral nervous system, notes the publication of new preclinical research in the peer-reviewed journal Neuropsychopharmacology on the unique mechanism and site of action of evenamide as a potential treatment for schizophrenia.1 The findings by researchers at the University of Pittsburgh, using the neurodevelopmental methylazoxymethanol acetate (MAM) animal model, indicated that evenamide, Newron's first-in-class glutamate modulator, could offer a novel therapeutic strategy capable of addressing positive, cognitive, and negative symptoms of schizophrenia. Schizophrenia is a neurodevelopmental disorder affecting approximately 1% of the world's population, and is characterized by positive, negative, and cognitive symptoms. However, current dopamine D2 antagonist-based antipsychotic drugs only address primarily positive symptoms. It is known that limbic hippocampus hyperexcitability is a key pathological state of schizophrenia and therefore represents an ideal therapeutic target. This newly published research shows how evenamide, a selective voltage-gated sodium channel blocker, uniquely targets hippocampal hyperexcitability and selectively inhibits hyperactive neurons. Additionally, time-course analysis indicates effects of a single dose of evenamide last long after its elimination, suggesting evenamide may have an effect on neuronal plasticity. Studies to date suggest evenamide is devoid of activity at any other central nervous system target, and it normalizes excessive synaptic glutamate induced by NMDA hypofunction. "The study examined the effect of acute evenamide treatment on the hyperdopaminergic state, hippocampal hyperexcitability, social deficits, and recognition memory in the methylazoxymethanol acetate (MAM) neurodevelopmental model," explained Daniela L. Uliana, first author of the study, from the Departments of Neuroscience, Psychiatry and Psychology of the University of Pittsburgh. "The MAM model consists of injecting MAM during gestational day 17 into pregnant rats at a time that approximates the human second trimester; a period of vulnerability in pregnancy during which prenatal disruptions can result in increased schizophrenia incidence in adults. The MAM-treated rats show multiple anatomical, behavioral, neurochemical, and physiological changes consistent with schizophrenia." "The study findings suggest that evenamide has high therapeutic potential for treating multiple symptom domains of schizophrenia," said Senior study author Dr. Anthony A. Grace of the University of Pittsburgh. "Evenamide is a unique NCE agent in acting at the site of the deficit in schizophrenia by reducing hippocampal hyperexcitability. This represents a significant advancement in treatment, as evenamide can downregulate the hyperdopaminergic state without producing D2 blockade-related side effects while also improving behavioral deficits that are not properly treated by D2 blocking antipsychotic agents." "The recognition memory improvement induced by evenamide in the study's MAM model may indicate that it may also enhance cognitive function in patients with schizophrenia and ultimately lead to a better functional outcome," continued Grace. "Current D2-based antipsychotic agents do not effectively address cognitive symptoms, which limits their overall efficacy and produces a significant functional burden on patients. Therefore, evenamide would offer advantages over existing antipsychotic drugs by targeting positive symptoms, cognitive deficits and social isolation." "This study provides important learnings, which explain the results of our earlier Phase II and Phase III trials in patients with chronic schizophrenia. The prolonged effect in the MAM model explains the continuing improvement in symptoms even one year after starting treatment with evenamide in TRS patients in our phase 2 trial. In the Phase 3 trial in patients who were not responding to their current 2nd-generation antipsychotic drugs, including clozapine, the addition of evenamide led to significant improvements on the primary efficacy measure (PANSS total) as well as a clinically and statistically significant increases in responder rates," said Ravi Anand, Newron's CMO. "The preclinical and clinical results suggest high likelihood of success for our ongoing pivotal Phase III program and to potentially offering a completely new treatment paradigm to patients with schizophrenia." About schizophrenia Approximately 25 million people worldwide are affected by schizophrenia. Despite more than 60 different types of atypical and typical antipsychotics used to treat schizophrenia globally, a considerable number of patients remain severely ill or resistant to treatment. Overall, 30-50% of patients do not respond to the available medications and are defined as treatment resistant. In addition to the patients with treatment-resistant schizophrenia (TRS), another 20-30% are described as "poor responders to antipsychotic medication", even if not meeting the criteria for TRS. New findings indicate that patients with TRS have abnormalities in the glutamatergic system, but not in dopaminergic transmission, so there is a significant unmet medical need for treatments with a glutamatergic mechanism of action, efficacious both in TRS patients and in those who are poor responders to the current treatments. About evenamide Evenamide is the first new chemical entity that has demonstrated significant benefits in this difficult-to-treat patient population, as seen in the potentially pivotal Phase III study 008A trial, as an add-on treatment to second generation antipsychotics including clozapine, in 291 poorly responding patients with chronic schizophrenia. The primary endpoint, the Positive and Negative Syndrome Scale (PANSS)2, and the key secondary endpoint, the Clinical Global Impressions Scale – Severity (CGI-S), were met and showed statistical significance compared to placebo. Importantly, evenamide treatment was associated with statistically significant increases in the proportion of patients who experienced "clinically meaningful benefit" on the outcome variables. Evenamide was extremely well tolerated, without any of the usual side effects of available antipsychotics. About Newron Pharmaceuticals Newron (SIX: NWRN, XETRA: NP5) is a biopharmaceutical company focused on developing novel therapies for patients with diseases of the central and peripheral nervous system. Headquartered in Bresso, near Milan, Italy, Newron is advancing its lead compound, evenamide, a first-in-class glutamate modulator, which has the potential to be the first add-on therapy for treatment-resistant schizophrenia (TRS) and for poorly responding patients with schizophrenia. Evenamide is currently in Phase III development and clinical trial results to date demonstrate the benefits of this drug candidate in the TRS patient population, with significant improvements across key efficacy measures increasing over time, as well as a favourable safety profile, which is uncommon for available antipsychotic medications. Newron has signed development and commercialization agreements for evenamide with EA Pharma (a subsidiary of Eisai) for Japan and other Asian territories, as well as Myung In Pharm for South Korea. Newron has a proven track record in bringing CNS therapies to market. Its Parkinson's disease treatment, Xadago® (safinamide), is approved in over 20 markets, including the USA, UK, EU, Switzerland, and Japan, and commercialized in partnerships with Zambon and Meiji Seika. For more information, please visit: Important Notices This document contains forward-looking statements, including (without limitation) about (1) Newron's ability to develop and expand its business, successfully complete development of its current product candidates, the timing of commencement of various clinical trials and receipt of data and current and future collaborations for the development and commercialization of its product candidates, (2) the market for drugs to treat CNS diseases and pain conditions, (3) Newron's financial resources, and (4) assumptions underlying any such statements. In some cases, these statements and assumptions can be identified by the fact that they use words such as "will", "anticipate", "estimate", "expect", "project", "intend", "plan", "believe", "target", and other words and terms of similar meaning. All statements, other than historical facts, contained herein regarding Newron's strategy, goals, plans, future financial position, projected revenues and costs and prospects are forward-looking statements. By their very nature, such statements and assumptions involve inherent risks and uncertainties, both general and specific, and risks exist that predictions, forecasts, projections and other outcomes described, assumed or implied therein will not be achieved. Future events and actual results could differ materially from those set out in, contemplated by or underlying the forward-looking statements due to a number of important factors. These factors include (without limitation) (1) uncertainties in the discovery, development or marketing of products, including without limitation difficulties in enrolling clinical trials, negative results of clinical trials or research projects or unexpected side effects, (2) delay or inability in obtaining regulatory approvals or bringing products to market, (3) future market acceptance of products, (4) loss of or inability to obtain adequate protection for intellectual property rights, (5) inability to raise additional funds, (6) success of existing and entry into future collaborations and licensing agreements, (7) litigation, (8) loss of key executive or other employees, (9) adverse publicity and news coverage, and (10) competition, regulatory, legislative and judicial developments or changes in market and/or overall economic conditions. Newron may not actually achieve the plans, intentions or expectations disclosed in forward-looking statements and assumptions underlying any such statements may prove wrong. Investors should therefore not place undue reliance on them. There can be no assurance that actual results of Newron's research programs, development activities, commercialization plans, collaborations and operations will not differ materially from the expectations set out in such forward-looking statements or underlying assumptions. Newron does not undertake any obligation to publicly update or revise forward-looking statements except as may be required by applicable regulations of the SIX Swiss Exchange or the Dusseldorf Stock Exchange where the shares of Newron are listed. This document does not contain or constitute an offer or invitation to purchase or subscribe for any securities of Newron and no part of it shall form the basis of or be relied upon in connection with any contract or commitment whatsoever. 1 Uliana DL, Walsh RA, Fabris D and Grace AA. Evenamide reverses schizophrenia-related dysfunction in a neurodevelopmental animal model, Neuropsychopharmacology (2025); 2 Positive and Negative Syndrome Scale (PANSS) is widely used in clinical trials of schizophrenia and is considered the "gold standard" for assessment of antipsychotic treatment efficacy (Innvo Clin Neurosci, 2017: View source version on Contacts For more information, please contact: Newron Stefan Weber – CEO; +39 02 6103 46 26, pr@ UK/Europe Simon Conway / Ciara Martin / Natalie Garland-Collins, FTI Consulting; +44 20 3727 1000, SCnewron@ Switzerland Valentin Handschin, IRF; +41 43 244 81 54, handschin@ Germany/Europe Anne Hennecke / Maximilian Schur, MC Services; +49 211 52925227, newron@ USA Paul Sagan, LaVoieHealthScience; +1 617 865 0041, psagan@ Error in retrieving data Sign in to access your portfolio Error in retrieving data Error in retrieving data Error in retrieving data Error in retrieving data
Yahoo
07-07-2025
- Health
- Yahoo
Brain's Memory Center Never Stops Making Neurons, Study Confirms
Though it's now clear humans continue to grow new brain cells throughout their entire lives, debate persists over whether this applies to specific areas involved with memory. Previous studies have made the case for and against the existence of neurogenesis in hippocampus beyond childhood. A new study now offers some of the clearest evidence yet that this crucial memory-forming region does form fresh neurons well into adulthood. The study is the work of researchers from the Karolinska Institute and the Chalmers University of Technology in Sweden, and looks specifically at the dentate gyrus section of the hippocampus, the part of the brain that acts as a key control center for emotions, learning, and storing episodic memories. Related: "This gives us an important piece of the puzzle in understanding how the human brain works and changes during life," says molecular biologist Jonas Frisén. Confirmation that humans can form new neurons in the hippocampus through life (as several other animals can) would inform a whole host of other scientific investigations, from how adults learn new skills to what happens to the brain as it deteriorates in old age. The team used RNA analysis to identify functions of brain cells in samples collected from people up to age 78, finding that some neurons were geared to function as neural progenitor cells (NPCs), which generate new nerve cells. The researchers also found similarities between human NPCs and those in mice, pigs, and monkeys. Through a process of machine learning, the researchers could also group cells according to their development, from their initial 'blank slate' stem cell characterization to being an immature neuron in the process of dividing. The results address questions raised by earlier studies (including one from some of the same researchers), which determined that new neurons were present in the human brain without being able to confirm exactly how they'd got there. "We have now been able to identify these cells of origin, which confirms that there is an ongoing formation of neurons in the hippocampus of the adult brain," says Frisén. By studying such a wide range of ages, the researchers confirmed neurogenesis keeps happening in the hippocampus throughout our adult lives – albeit at a slower rate, generally speaking, as we get older. It's also important to note that the analysis revealed different rates of neurogenesis in different people. That might point to differences in brain plasticity that affect learning, personality, and disease risk, but that's something that future studies will need to look at. One hypothesis is that certain brain conditions might be affected by how quickly fresh new neurons can be produced – some of the subjects in this study had a history of psychiatric or neurological diseases – but again this wasn't something that the researchers looked at directly, so follow-up studies will be needed. "Our research may also have implications for the development of regenerative treatments that stimulate neurogenesis in neurodegenerative and psychiatric disorders," says Frisén. The research has been published in Science. Pomegranates Could Limit Risks From Controversial Sports Supplement OCD's Origins Might Not Lie in The Brain Like We Thought The News Cycle Is a Stress Monster. But There's a Healthy Way to Stay Informed.
Yahoo
04-07-2025
- Health
- Yahoo
Human brains keep growing neurons even in old age, study finds for first time
For decades, scientists believed the human brain stopped producing new neurons after childhood. This long-held view painted the adult brain as a fixed organ, incapable of generating fresh cells in the very region responsible for memory and learning. But a landmark new study turns that dogma on its head, offering the clearest evidence yet that adult humans continue to form new neurons well into the old age. A team of researchers from Karolinska Institutet in Sweden has identified and tracked the formation of new neurons in the hippocampus, a region critical for memory, learning, and emotional regulation. In 2013, a team of researchers led by Professor Jonas Frisén made headlines with a study showing that new neurons can form in the hippocampus of adult humans. They used carbon-14 dating in DNA extracted from brain tissue to pinpoint when individual cells were created, providing rare evidence of adult neurogenesis. But while the study proved that new neurons could exist, it did not answer where these neurons come from. Until now, scientists lacked direct proof that the neural progenitor cells were present and actively dividing in the adult human brain. 'We have now been able to identify these cells of origin, which confirms that there is an ongoing formation of neurons in the hippocampus of the adult brain,' said Frisén. In the new study, the team analyzed post-mortem brain tissue from individuals ranging in age from infancy to 78 years to discover that neural progenitor cells—precursors to fully developed neurons—not only exist in the adult brain but are also actively dividing. The study used advanced techniques like single-nucleus RNA sequencing to map gene activity in individual brain cell nuclei. Combined with flow cytometry and machine learning, the approach allowed researchers to identify various stages of neuronal development, ranging from stem-like cells to immature, still-dividing neurons. To visualize where these new neurons were forming, the scientists employed RNAscope and Xenium, two powerful spatial transcriptomics tools. These confirmed that the cell formation was happening in the dentate gyrus, a part of the hippocampus linked to learning, cognitive flexibility, and the encoding of new memories. The findings reveal that adult human neural progenitor cells closely resemble those seen in mice, pigs, and monkeys, though some gene activity patterns differ between species. What's especially intriguing is the variability between individuals. While some adults had abundant neural progenitor cells, others had very few, raising new questions about what factors might influence adult neurogenesis. 'This gives us an important piece of the puzzle in understanding how the human brain works and changes during life,' Frisén explained. 'Our research may also have implications for the development of regenerative treatments that stimulate neurogenesis in neurodegenerative and psychiatric disorders.' The findings could also pave the way for new regenerative therapies for neurodegenerative and psychiatric conditions, potentially helping to restore or enhance brain function by stimulating neuron formation in targeted ways. The groundbreaking study has been published in the journal Science.
Yahoo
04-07-2025
- Health
- Yahoo
Can adults make new brain cells? New study may finally settle one of neuroscience's greatest debates
When you buy through links on our articles, Future and its syndication partners may earn a commission. Researchers say they have found clear evidence that the human brain can keep making new neurons well into adulthood, potentially settling decades of controversy. This new neuron growth, or "neurogenesis," takes place in the hippocampus, a critical part of the brain involved in learning, memory and emotions. "In short, our work puts to rest the long-standing debate about whether adult human brains can grow new neurons," co-lead study author Marta Paterlini, a researcher at the Karolinska Institute in Stockholm, told Live Science in an email. Other experts agree that the work makes a strong case for adult neurogenesis. While a single study does not constitute absolute proof, "this is strong evidence in support of the idea" that stem cells and precursors to new neurons exist and are proliferating in the adult human brain, said Dr. Rajiv Ratan, CEO of the Burke Neurological Institute at Weill Cornell Medicine, who was not involved in the study. "This is a perfect example of great science teeing up the ball for the clinical neuroscience community," he told Live Science. Related: Babies' brain activity changes dramatically before and after birth, groundbreaking study finds The researchers combined advanced techniques, including single-nucleus RNA sequencing and machine learning, to sort and examine brain tissue samples from international biobanks, they reported in a paper published July 3 in the journal Science. RNA, a cousin of DNA, reflects genes that are "switched on" inside cells, while machine learning is a type of artificial intelligence often used to crunch huge datasets. Since the 1960s, researchers have known that mice, rats and some nonhuman primates make new brain cells in the dentate gyrus, part of the hippocampus, throughout life. But getting quality brain tissue samples from adult humans is extremely challenging. "Human tissue comes from autopsies or surgeries, so how it's handled — how long before it's fixed in preservative, which chemicals are used, how thin the slices are — can hide those newborn cells," Paterlini said. Employing new technologies enabled the team to overcome this challenge. They analyzed more than 400,000 individual nuclei of hippocampus cells from 24 people, and in addition, looked at 10 other brains using other techniques. The brains came from people ages 0 to 78, including six children and four teens. Using two cutting-edge imaging methods, the team mapped where new cells sat in the tissue. They saw groups of dividing precursor cells sitting right next to the fully formed neurons, in the same spots where animal studies have shown that adult stem cells reside. "We didn't just see these dividing precursor cells in babies and young kids — we also found them in teenagers and adults," Paterlini said. "These include stem cells that can renew themselves and give rise to other brain cells." The newer technologies enabled the researchers to detect the new brain cells at various stages of development and conduct research that wouldn't have been possible a few years ago, Ratan added. The team also used fluorescent tags to mark the proliferating cells. This enabled them to build a machine learning algorithm that identified the cells that they knew would turn into neurogenic stem cells, based on past rodent studies. This was a "clever approach" for tackling the challenges of studying brain-cell formation in adolescents and adults, Ratan said. As expected, the brains of children produced more new brain cells than the brains of adolescents or adults did. Meanwhile, nine out of 14 adult brains analyzed with one technique showed signs of neurogenesis, while 10 out of 10 adult brains analyzed with a second technique bore new cells. Regarding the few brains with no new cells, Paterlini said it's too soon to draw conclusions about the disparity between adult brains with evidence of new cells and those without. RELATED STORIES —How much of your brain do you need to survive? —You're born with most of your neurons — but the brain makes some mysterious new ones in adulthood —Brain aging accelerates dramatically around age 44 — could ketone supplements help? Next, the researchers could explore whether the adults who produced new brain cells did so in response to a neurological disease, such as Alzheimer's, or whether adult neurogenesis is a sign of good brain health, said Dr. W. Taylor Kimberly, chief of neurocritical care at Massachusetts General Brigham, who was not involved in the study. "They were able to find these needles in a haystack," Kimberly told Live Science. "Once you detect them and learn about them and understand their regulation," scientists can research how to track the precursor cells through time and see how their presence relates to disease, he said. He envisioned comparing patients who have dementia to "super agers" who are cognitively resilient in old age. If the link between neurogenesis and disease can be uncovered, perhaps that could open the door to treatments. "Although the precise therapeutic strategies in humans are still under active research," Paterlini said, "the very fact that our adult brains can sprout new neurons transforms how we think about lifelong learning, recovery from injury and the untapped potential of neural plasticity."
