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Medical News Today
5 days ago
- Health
- Medical News Today
Alzheimer's: How does exercise protect the brain as people age?
A new study aims to explain exercise's protective effect on the brain from neurodegenerative diseases like Alzheimer's. Guille eFaingold/Stocksy Past studies show that certain lifestyle changes — such as getting more physical activity — may help lower a person's risk for Alzheimer's disease or slow its progression. A new study sheds light on how physical activity helps protect the brain from Alzheimer's disease on a cellular level. Scientists believe these findings may one day lead to new prevention and treatment strategies for Alzheimer's disease. While there is currently no cure for Alzheimer's disease, past studies show that certain lifestyle changes may help decrease a person's risk for the disease or slow down its progression. One of these main lifestyle changes is physical activity. A study published in April 2025 reported that increasing physical activity in middle age may help protect the brain from Alzheimer's disease. A study published in May 2025 says older adults who sit less may lower their risk for the condition. Now, a new study recently published in the journal Nature Neuroscience sheds light on how physical activity helps protect the brain from Alzheimer's disease on a cellular level. Scientists believe these findings may one day lead to new prevention and treatment strategies for Alzheimer's disease. 'Single-nuclei RNA sequencing (snRNA-seq) is a technique that allows (us to) analyze gene activity by examining the RNA inside on a cell by cell level, giving us precise information about the activation state of each and every single cell in the tissue examined,' Christiane D. Wrann, DVM, PhD, a neuroscientist and leader of the Program in Neuroprotection in Exercise at the Mass General Brigham Heart and Vascular Institute and the McCance Center for Brain Health at Massachusetts General Hospital, and senior author of this study, explained to Medical News Today . 'We used this sophisticated technology to examine how exercise reshapes [the] brain in an important region in the brain of mouse models for Alzheimer's disease,' Wrann added. Scientists focused on the hippocampus of the brain, which is responsible for making new memories and keeping old ones, as well as processing emotions and learning new information. Using a mouse model of Alzheimer's disease — that were later verified in human Alzheimer's disease brain tissue samples — researchers found that exercise changed activity in the hippocampus' immune cells called microglia , as well as a specific type of neurovascular-associated astrocyte (NVA) . NVAs are cells associated with the brain's blood vessels that help make sure the brain receives enough oxygen and is an important part of the blood-brain barrier . '[Our findings mean] that exercise can remodel these important cell types on the transcriptional/gene expression level, which likely increases their neuroprotective properties. 'It [is] one example, how on the molecular level exercise can improve brain cells in Alzheimer's disease, hopefully rendering them more functionally.' — Christiane D. Wrann, DVM, PhD Additionally, Wrann and her team pinpointed a metabolic gene called ATPIF1 as an important regulator to create new neurons in the brain. 'ATPIF1 is a mitochondrial protein that regulates cellular energy production AKA — a gene that regulates energy metabolism,' Wrann detailed. 'Research has shown that stimulating neurogenesis can protect against cognitive decline in aging or Alzheimer's disease. In our study, we show that ATPIF1 is an important regulator of neurogenesis.' 'Exercise is important for your brain health — please keep exercising to protect your brain,' she continued. 'Alzheimer's disease is incurable at the moment. There are smart and dedicated scientists working on finding innovative treatment options.' 'This work not only sheds light on how exercise benefits the brain but also uncovers potential cell-specific targets for future Alzheimer's therapies,' Nathan Tucker, PhD, a biostatistician at SUNY Upstate Medical University and co-senior of the study said in a press release. 'Our study offers a valuable resource for the scientific community investigating Alzheimer's prevention and treatment.' MNT also had the opportunity to speak with Gary Small, MD, chair of psychiatry at Hackensack University Medical Center in New Jersey, about this study. Small commented that this study's findings are consistent with the well-documented link between physical activity and brain health, including its role in reducing the risk of Alzheimer's and of slowing its progression in people who already suffer from the disease. 'While the basic conclusion that exercise is important to brain health is not new, these new findings showing the impact of physical activity on key brain cells such as microglia and neurovascular-associated astrocytes provide a more nuanced and deeper understanding why the brain responds to exercise,' he explained. 'Astrocytes and microglia play a crucial role in both initiating and regulating the inflammatory response. Thus, these results further elucidate the link between heightened brain inflammation and cognitive decline,' he said. 'Brain health has a strong influence on our quality of life. Cognitive decline affects not just the physical and behavioral health of the patient, but also has an impact on their caregivers and all who care about the person. The bottom line is that dementia and Alzheimer's disease are not inevitable parts of aging. We can take steps to reduce the risk through lifestyle habits. And even for those who develop the disease, making changes in diet, physical activity, and stress management can slow the progression and extend the time when a person can enjoy a fulfilling quality of life.' — Gary Small, MD 'The more we understand how cognitive decline occurs, and what can change the course of its development and progression, the more opportunities there are to find ways to treat it,' Small added.
India Today
11-06-2025
- Health
- India Today
Why some students can memorize anything : Science has the answer
It's the day before the history exam. Inside Class 8B, the tension is thick. One corner of the room is buzzing , Neha flips her notebook at lightning speed, mumbling under her breath, repeating dates of battles and names of Mughal emperors. Next to her, Aarav stares at his book, overwhelmed. "How do you do this?" he asks, watching Neha recite a paragraph she's read just all know a Neha that student who can mug up entire chapters effortlessly. But what makes some students such fast memorizers while others struggle to remember a few lines? Scientists say the answer lies deep inside the SCIENCE OF MUGGING UP: WHAT'S HAPPENING IN THE BRAIN Rote learning is memorizing by repeating something over and over without truly understanding it. It taps into specific mental processes, and the truth is, some people's brains are naturally better wired for it than others. MEMORY CAPACITY AND THE HIPPOCAMPUS Deep inside our brain is a small, seahorse-shaped structure called the hippocampus that stores memories. Studies show that when this part of the brain works efficiently, people are much better at holding onto information, especially when they learn through study from the University of California, Davis found that greater activation of the hippocampus during learning tasks leads to stronger long-term memory consolidation. This means that some students, by virtue of neural efficiency, can encode and retrieve information to this, Dr. Anshul Gupta, Senior Consultant, Dept. of Neurosurgery at Sir Ganga Ram Hospital, explains: "Rote learning is actually not a gift, it is an adaptation of a weak mind to survive. There is no specific centre in the brain called a 'mugging up' centre. While the hippocampus, amygdala, and Papez circuit are well-known centres for memory, learning, and understanding, a person who is not that intelligent or doesn't have robust learning centres often relies on the most basic part of this system to make short-term memories. Through sheer repetition, this basic function is stretched until the brain retains it just long enough to finish a task - and then forgets it thereafter." His view underscores a critical distinction: rote learning is a coping mechanism, not a higher cognitive MAY BE PLAYING A ROLE TOOSome students are biologically better equipped to retain facts.A 2006 study in Nature Neuroscience found that a variant of the BDNF (Brain-Derived Neurotrophic Factor) gene enhances synaptic plasticity - the brain's ability to form and strengthen new connections. This is crucial for learning and gene, COMT, influences dopamine regulation in the prefrontal cortex and is linked to differences in working memory capacity - a key ingredient in successful rote STYLES MATTERNot all students are designed for rote memory and that's in the Journal of Educational Psychology shows that students absorb more information when it's delivered in alignment with their preferred learning style - be it visual, auditory, reading/writing, or kinaesthetic. So a student who struggles to memorize text might thrive using mind maps or through STRESS, AND NUTRITION: THE HIDDEN INFLUENCERSIt's not just about innate ability. Environmental and lifestyle factors also play a big role in memory formation and recall. A Harvard Medical School study highlights how sleep significantly enhances memory consolidation, especially after new learning. Conversely, chronic stress elevates cortisol levels, which can interfere with the hippocampus and impair matters too - Vitamin B12, Omega-3 fatty acids, and iron are essential for brain function. Deficiencies in these can reduce cognitive performance and memory CAN YOU TRAIN YOURSELF TO BE A 'MUGGER'? To an extent, yes. While not everyone can memorize at lightning speed, cognitive strategies can help improve memory:Spaced repetition (reviewing material at increasing intervals)Mnemonics and visualization techniquesChunking information into manageable piecesWriting notes by hand, which enhances recall more than typingWith practice, these tools can make memory tasks significantly BRAINS, DIFFERENT LANESIn India's academic landscape, where exams often prioritise recall, rote learners may have an advantage. But not being good at mugging up doesn't mean you're a poor learner - it may simply mean your brain learns differently. Some students are logical thinkers. Others thrive with visuals or interaction. These learning differences are not only valid but scientifically supported, shaped by genes, brain structures, and education evolves toward critical thinking and experiential learning, rote memory may no longer be the benchmark of academic excellence. But until then, understanding your brain may be your best study Watch
Indian Express
03-06-2025
- Health
- Indian Express
Inemuri: Does this Japanese method of napping help boost productivity?
In Japan, the concept of 'Inemuri' has gained attention as a unique practice of napping that may sound unusual to many. The term directly translates to 'sleeping while present' and refers to the act of napping in public or during work hours. Often seen in offices, on trains, or in other public spaces, the Inemuri nap is considered a cultural norm rather than a sign of laziness. This practice has sparked curiosity around whether it offers a solution for those who find themselves sleep-deprived. With many people struggling to get adequate rest, the idea of napping strategically to boost productivity and mental clarity is gaining popularity. But can Inemuri truly help improve energy levels, or is it just a fleeting solution for a bigger sleep problem? Dr Jagadish Hiremath, public health intellectual, tells 'Inemuri naps can offer short-term relief for sleep-deprived individuals by allowing brief moments of rest during active participation in daily routines, such as meetings or public commuting. Unlike traditional naps taken in a private setting, Inemuri emphasises adaptability — individuals remain mentally prepared to re-engage with their surroundings quickly.' Dr Hiremath adds that inemuri usually involves light, non-REM sleep stages, which can improve alertness and cognitive function without inducing sleep inertia (the grogginess experienced after waking from deep sleep). 'A study published in Nature Neuroscience shows that even short periods of light sleep can enhance memory consolidation and focus,' he says. While regular naps aim for deeper restorative benefits, Dr Hiremath notes, Inemuri prioritises practicality, making it less effective for long-term recovery from significant sleep debt. The effectiveness of Inemuri naps largely depends on their duration and timing. 'Research suggests that naps lasting 10–20 minutes are ideal for improving alertness and reducing fatigue without disrupting nighttime sleep. Short naps help rejuvenate the body and mind, providing a quick boost of energy without the risk of feeling groggy afterward,' states Dr Hiremath. However, longer naps, ranging from 30 to 90 minutes, risk entering deeper sleep stages, which can lead to sleep inertia. Dr Hiremath states, 'Sleep inertia refers to the groggy, disoriented feeling some people experience after waking from a deep sleep. This can hinder the benefits of napping and make it harder to regain full alertness.' Inemuri's cultural practice allows for varying nap lengths, from just a few minutes to longer periods, depending on the individual's environment and schedule. The practice is quite flexible, allowing people to adjust the duration to suit their needs. However, it is most effective when aligned with the body's natural circadian rhythm, particularly during mid-afternoon energy slumps. Some drawbacks according to Dr Hiremath are: DISCLAIMER: This article is based on information from the public domain and/or the experts we spoke to. Always consult your health practitioner before starting any routine.
The Hindu
24-05-2025
- Health
- The Hindu
Does neurodegeneration start when blood vessels are damaged?
Our brain depends on a finely tuned network of neurons, signals, and protective barriers to function seamlessly. This intricate setup underpins every thought, memory, and movement we make. But as we age, or under certain conditions, this system can break down. Neurodegenerative diseases like Alzheimer's, Parkinson's, and amyotrophic lateral sclerosis (ALS) slowly damage neurons and over time these conditions lead to severe memory loss, confusion, and loss of independence. Despite decades of research, the precise mechanisms driving these diseases have remained elusive. Shifting away from the traditional neuron-centric view of brain diseases, two studies published recently in Science Advances and Nature Neuroscience, offer a compelling new piece to this puzzle. The teams' research reveals a startling possibility: what if the trouble begins long before neurons die? The studies suggest that damage to the blood-brain barrier (BBB) may in fact be the first domino to fall in neurodegenerative diseases. First line of defence The BBB is one of the brain's most critical protections. It is made up of tightly packed endothelial cells that line blood vessels in the brain. Their job is to gatekeep: letting in vital nutrients while keeping out toxins, pathogens, and harmful immune cells. 'Endothelial cells are the first cells exposed to what we eat, what infections we carry, or even the medications we take,' Ashok Cheemala, lead author of the Science Advances study, said. 'If these cells become inflamed or damaged, the barrier becomes leaky. When that happens, harmful substances can slip into the brain and trigger inflammation.' This inflammation, in turn, can lead to neuron death, which causes memory loss and cognitive decline — the hallmarks of diseases like Alzheimer's and frontotemporal dementia (FTD). Helpful and harmful The TDP-43 protein regulates RNA and ensures proper gene expression inside cells in a process called splicing. Under healthy conditions, it is located in the nucleus of cells. But in people with neurodegenerative diseases, it goes rogue. 'If it accumulates in the cytoplasm, it starts to form toxic aggregates that can spread from one cell to another,' Cheemala said. While these aggregates have primarily been studied in neurons, researchers have been wondering whether endothelial cells that make up the BBB are also affected. King's College London neurologist Jemeen Sreedharan said, 'TDP-43 is found in virtually every cell in the body, not just in the brain. It's been detected in the skin, liver, kidneys, even reproductive organs. So its presence in endothelial cells isn't surprising. What's interesting is the idea that its dysfunction in these cells could kickstart the disease process.' Leaky in the barrier To investigate, the team used genetically modified mice carrying a disease-causing mutation in the Tardbp gene that encodes TDP-43. 'Even a single point mutation in TDP-43 in endothelial cells was enough to cause BBB leakage, brain inflammation, and behavioural changes in mice,' Cheemala said. As they aged, these mice showed increased leakage of molecules from the bloodstream into the brain, evidence of a compromised barrier. The researchers found that key proteins holding the BBB together, like claudin-5 and VE-cadherin, were lost, allowing molecules from the bloodstream to leak into brain tissue. These mice also displayed memory problems. The team also injected fluorescent dyes and tracked their penetration into the brain, analysing changes in the structure and protein composition of the BBB to verify their findings. 'This mutation is present from early development, even before birth,' Sreedharan said. 'These mice don't develop obvious brain disease but they do have vascular abnormalities. That points to blood vessel dysfunction as a possible early driver of neurodegeneration.' The human connection The team also analysed over 130,000 individual brain-cell nuclei from postmortem human brain samples from 92 donors aged 20-98, including both healthy individuals and those with certain neurodegenerative conditions. They profiled the RNA and nuclear proteins at the single-nucleus level and examined molecular changes in various brain cells. 'We specifically looked at TDP-43 levels in the nuclei of endothelial cells. In patient samples, the nuclear TDP-43 was dramatically reduced compared to healthy controls,' Cheemala said. The findings mirrored those of the mouse model. Loss of TDP-43 caused β-catenin to disintegrate, ramping up inflammatory signalling. The team also identified a specific group of damaged capillary cells that had low TDP-43 and high inflammation, suggesting they'd shifted from maintenance to damage mode. Still, the human data came with caveats. 'Post-mortem studies are limited by variability in tissue quality and timing,' Sreedharan said. 'But combining those with controlled mouse models makes the case much stronger.' 'It'll be important to see if this endothelial phenotype is specific to neurodegenerative diseases or a more general response to brain injury. Studying non-genetic conditions like multiple sclerosis or traumatic brain injury could help clarify this,' he added. Early detection opportunity The findings open a window for early diagnosis and prevention. 'It's compelling to think a disease we've long considered neuron-specific may actually start in the vasculature,' Sreedharan said. The team is now working on potential blood-based biomarkers, especially proteins that are regulated by TDP-43 and may be secreted into the bloodstream when endothelial cells are affected. 'One candidate is HDGLF2, a protein that changes when TDP-43 function is lost. If we can detect that in blood, we may be able to identify the number of years an at-risk individual has before their symptoms appear, Cheemala said. The researchers are also exploring whether exosomes — tiny particles released by cells, which may carry distinct protein signatures from damaged blood vessels — could serve as early indicators of disease. This could lead to non-invasive tests for diagnosing neurodegenerative diseases in their silent stages, long before symptoms appear and while interventions may still be effective. Manjeera Gowravaram has a PhD in RNA biochemistry and works as a freelance science writer.
AFP
16-05-2025
- Health
- AFP
Rubedo Life Sciences' Drug Discovery Platform, ALEMBIC™, Helps Identify Senescent or 'Zombie' Neurons in New Study Linking Neuropathic Pain and Aging Published in Peer-Reviewed Scientific Journal Natu
Rubedo Life Sciences, Inc. (Rubedo), an AI-driven, clinical-stage biotech focused on discovering and rapidly developing selective cellular rejuvenation medicines targeting aging cells, today announced that using open source codes integrated in the company's broader propriety drug discovery platform, ALEMBIC™, helped to identify senescent neurons in a new study that found senescent neurons drive chronic pain with injury and age.1 Senescent cells, often called 'zombie' cells, arise as the results of cellular stress and damage. These senescent cells do not die but undergo cellular changes, including secreting pro-inflammatory factors, thereby potentially contributing to inflammatory responses within the body.1 The study, led by Stanford University scientists, Vivianne Tawfik, MD, PhD, and Lauren Donovan, PhD, and co-authored by Rubedo team members, including Chief Scientific Officer Marco Quarta, PhD, and Chief Technology Officer Alex Laslavic, was published in the May 14th edition of Nature Neuroscience, a prestigious, peer-reviewed scientific journal, and will be featured on the cover of the May issue. This press release features multimedia. View the full release here: Image created by Clara Leibenguth for Stanford University; featured on cover of May 2025 issue of Nature Neuroscience. Dr. Quarta said, 'We know that senescent cells, which increase as people age, drive chronic degenerative diseases and conditions. In this study, we were able to show for the first time that neurons can become senescent, fueling neuropathic pain in both mouse models and human dorsal root ganglia tissue. The bioinformatic validation provided as part of our broader ALEMBIC™ platform with SenTeCh™ chemistry technology helped to uncover this link between aging and neuropathic pain, and further corroborates our experimental observations that treatments targeting these senescent cells could offer meaningful benefits for people experiencing age-related conditions.'1 About the Study In the study, researchers found that injury to peripheral axons of dorsal root ganglion (DRG) neurons results in sensory dysfunction, such as pain. This occurs at higher rates in aged individuals. Furthermore, cellular senescence is common to both aging and injury, and contributes to this sensory dysfunction. Elimination of senescent cells results in pain improvement, indicating a potential target for new pain therapeutics.1 'Chronic pain continues to be an area with high unmet need, especially among older adults. In this study, aging markedly increased the burden of senescent or 'zombie' neurons, which in turn worsened neuropathic pain severity. These insights demonstrate that selective targeting of senescent-like neurons may lead to novel strategies for the management of chronic pain,'1 said Vivianne, L. Tawfik, MD, PhD, Associate Professor, Department of Anesthesiology, Perioperative and Pain Medicine at Stanford University School of Medicine, and the senior author of the study. 'We appreciate the valuable support and expertise from the Rubedo team during this research.' About Rubedo Life Sciences Rubedo Life Sciences is a clinical-stage biotech developing a broad portfolio of innovative selective cellular rejuvenation medicines targeting aging cells that drive chronic age-related diseases. Our proprietary AI-driven ALEMBIC™ drug discovery platform is developing novel first-in-class small molecules to selectively target pathologic and senescent cells, which play a key role in the progression of pulmonary, dermatological, oncological, neurodegenerative, fibrotic, and other chronic disorders. Our lead drug candidate – RLS-1496, a potential first-in-class disease-altering GPX4 modulator – is set to begin Phase I clinical trials in Spring of 2025, marking the first ever GPX4 modulator to enter a human clinical trial. The Rubedo leadership team is composed of industry leaders and early pioneers in chemistry, AI technology, longevity science, and life sciences, with expertise in drug development and commercialization from both large pharmaceutical and leading biotechnology companies. The company is headquartered in Sunnyvale, CA, USA, and has offices in Milan, Italy. For additional information, visit References 1. Donovan, L.J., Brewer, C.L., Bond, S.F. et al. Aging and injury drive neuronal senescence in the dorsal root ganglia. Nat Neurosci (2025). 2. Data on file, Rubedo Life Sciences, Sunnyvale, CA 94085. View source version on Investor Contact: Rubedo Chief Business Officer Ali Siam alisiam@ 781-974-9559 Media Contact: Peter Collins 908-499-1200 © Business Wire, Inc. Disclaimer : This press release is not a document produced by AFP. AFP shall not bear responsibility for its content. In case you have any questions about this press release, please refer to the contact person/entity mentioned in the text of the press release.
