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Indian Express
5 days ago
- 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.
Irish Times
01-05-2025
- Health
- Irish Times
‘Great progress' in the race to turn brainwaves into fluent speech
Neuroscientists are striving to give a voice to people unable to speak in a fast-advancing quest to harness brainwaves to restore or enhance physical abilities. Researchers at universities across California, and companies such as New York-based Precision Neuroscience, are among those making headway towards generating naturalistic speech through a combination of brain implants and artificial intelligence. Investment and attention have long been focused on implants that enable severely disabled people to operate computer keyboards, control robotic arms or regain some use of their own paralysed limbs. But some labs are making strides by concentrating on technology that converts thought patterns into speech. 'We are making great progress – and making brain-to-synthetic voice as fluent as chat between two speaking people is a major goal,' says Edward Chang, a neurosurgeon at the University of California, San Francisco. 'The AI algorithms we are using are getting faster, and we are learning with every new participant in our studies.' READ MORE Chang and colleagues, including from the University of California, Berkeley, last month published a paper in Nature Neuroscience detailing their work with a quadriplegic woman – paralysed limbs and torso – who had not been able to speak for 18 years after suffering a stroke. She trained a deep-learning neural network by silently attempting to say sentences composed using 1,024 different words. The audio of her voice was created by streaming her neural data to a joint speech synthesis and text-decoding model. The technique reduced the lag between the patient's brain signals and the resultant audio from the eight seconds the group had achieved previously to one second. This is much closer to the 100-200 millisecond time gap in normal speech. The system's median decoding speed was 47.5 words per minute, or about a third the rate of normal conversation. Even if you could, you wouldn't want people to hear your inner speech — Nick Ramsey of University Medical Centre Utrecht. Many thousands of people a year could benefit from so-called voice prosthesis. Their cognitive functions remain more or less intact but they have suffered speech loss due to stroke, the neurodegenerative disorder ALS and other brain conditions. If successful, researchers hope the technique can be extended to help people who have difficulty vocalising because of conditions such as cerebral palsy or autism. The potential of voice neuroprosthesis is beginning to trigger interest among businesses. Precision Neuroscience claims to be capturing higher-resolution brain signals than academic researchers, since the electrodes of its implants are more densely packed. The company has worked with 38 patients and plans soon to collect data from more, providing a potential pathway to commercialisation. Precision received regulatory clearance on April 17th to leave its sensors implanted for up to 30 days at a time. That would enable its scientists to train their system with what could within a year be the 'largest repository of high-resolution neural data that exists on planet Earth', says chief executive Michael Mager. The next step would be to 'miniaturise the components and put them in hermetically sealed packages that are biocompatible so they can be planted in the body forever', says Mager. [ Brain tech breakthrough restores ALS patient's ability to speak Opens in new window ] Elon Musk's Neuralink, the best-known brain-computer interface (BCI) company, has focused on enabling people with paralysis to control computers rather than giving them a synthetic voice. An important obstacle to the development of brain-to-voice technology is the time patients take to learn how to use the system. A key unanswered question is how much the response patterns in the motor cortex – the part of the brain that controls voluntary actions, including speech – vary between people. If they remained very similar, machine-learning models trained on previous individuals could be used for new patients, says Nick Ramsey, a BCI researcher at University Medical Centre Utrecht. That would accelerate a process that today takes 'tens or hundreds of hours, generating enough data by showing a participant text and asking them to try to speak it'. Ultimately a voice neuroprosthesis should provide the full expressive range of the human voice Ramsey says all brain-to-voice research focuses on the motor cortex where neurons activate the muscles involved in speaking, with no evidence that speech could be generated from other brain areas or by decoding inner thoughts. 'Even if you could, you wouldn't want people to hear your inner speech,' he adds. 'There are a lot of things I don't say out loud because they wouldn't be to my benefit or they might hurt people.' The development of a synthetic voice as good as healthy speech could still be 'quite a ways away', says Sergey Stavisky, co-director of the neuroprosthetics lab at University of California, Davis. His lab has demonstrated it can decode what someone is trying to say with about 98 per cent accuracy, he says. But the voice output isn't instantaneous and it doesn't capture important speech qualities such as tone. It is unclear if the recording hardware – electrodes – being used can enable the synthesis to match a healthy human voice, he adds. Scientists need to develop a deeper understanding of how the brain encodes speech production and better algorithms to translate neural activity into vocal outputs, says Stavisky. 'Ultimately a voice neuroprosthesis should provide the full expressive range of the human voice, so that for example they can precisely control their pitch and timing and do things like sing.' – Copyright The Financial Times Limited 2025
Forbes
18-04-2025
- Health
- Forbes
Are ‘The Munchies' Real? Cannabis, Science, Food & Flavor, Explained
What are the munchies—and why does weed increase appetite in such a specific, intense way? This ... More explainer breaks down the biology, cravings, and cultural meaning behind the foods we reach for when we're high. Yes, it's more than a meme. The 'munchies' effect—those sudden, often intense cravings for salty, sweet, or high-fat snacks after cannabis use—isn't just anecdotal. It's biological. According to a 2009 study in Nature Neuroscience, cannabis compounds activate the brain's endocannabinoid system, which heightens our senses of smell and taste. That sensory boost makes food more appealing and can override the body's natural signals of fullness. THC also promotes the release of the hunger hormone ghrelin, which further stimulates appetite and encourages food-seeking behavior. In short, weed doesn't just make you hungry—it makes food feel more vivid, more rewarding, and harder to resist. But it's not just about flavor. A 2019 study in the Journal of Psychopharmacology found that cannabis also increases dopamine activity in the striatum, the part of the brain that controls reward-seeking behavior. So the munchies aren't just a reaction—they're a reward loop. A full-body yes to whatever feels good, fast, and easy. That said, the effect isn't one-size-fits-all. Chronic cannabis use can alter how the reward system responds over time, and not all users experience the same intensity of dopamine-driven food desire. That might explain why cannabis-friendly food holidays like 4/20 have become unofficial showcases for fast-food indulgence. From extra-cheesy nachos to triple-patty burgers, the food isn't just functional—it's engineered to satisfy every level. The appeal is emotional as much as it is physical. A craving, yes—but also a comfort. Fast food and weed go hand in hand—but it's not random. When you get the munchies, you're looking ... More for comfort, ease, and something that hits all your flavor buttons fast. But the munchies don't happen in a vacuum. What we reach for when that craving hits is shaped by something else entirely: culture. And in 2025, that culture is increasingly fast, familiar, and available through an app. A recent Tastewise survey found that 75% of Americans eat fast food at least once a week. Among Gen Z and Millennials, nearly half say they're eating more fast food than they were just a year ago. Their top reasons? Cravings, comfort, and convenience. That trifecta is also the blueprint for a munchies meal. Salty. Satisfying. No prep required. So when 4/20 rolls around, it's not just a stoner holiday anymore. It's a high-demand food moment—one where brands can lean into what consumers are already doing when they're tired, overstimulated, or emotionally frayed: reaching for something hot, fast, and reliable. The munchies aren't just slang. From global health surveys to neuroscience labs, researchers are ... More treating cannabis-induced appetite as a serious behavior worth tracking. What used to be whispered about is now tracked in government databases. In the latest WHO Global School-based Student Health Survey, cannabis use is listed right alongside fast food, soda, and physical activity as a behavioral health metric. That might not seem groundbreaking on its face. But it points to a broader shift in how cannabis is framed—not as moral failure, but as measurable behavior. Not as deviance but as data. That shift matters. When public health frameworks start treating cannabis use the same way they treat food frequency or screen time, brands are quick to follow. Not with warnings—but with promotions. With late-night bundles. With stoner-safe snacks that feel more like self-care than vice. Who gets the munchies? Not just teens or stereotypes. With cannabis use up across Millennials and ... More Gen X, this appetite shift is changing the way we snack, crave, and connect to food. That normalization shows up in the numbers, too. According to Gallup, 16% of U.S. adults said they smoke marijuana in 2022—up from just 7% in 2013. That's a doubling in less than a decade, thanks to legalization, cultural softening, and a generational shift in what cannabis means. It's not just a niche anymore. It's mainstream. And fast food brands are watching. For Millennials and Gen Z—many of whom came of age alongside dispensary menus and infused gummies—4/20 doesn't feel transgressive. It feels like a craving calendar. And the brands lining up to feed it? They know it's not just about the weed. It's about what comes after. The bite. The hit. The relief. Cannabis cravings don't always lead to junk food—and they aren't always unhealthy. As brands race to ... More meet 4/20 appetites, they're missing how deeply personal the munchies can be. Cannabis users aren't fringe anymore—and brands know it. In recent years, everyone from Taco Bell to Jack in the Box to Fatburger has rolled out food and drink promotions that nod to the 4/20 crowd without saying the quiet part out loud. The strategy is familiar: bigger, bolder, cheesier. Add more sauces. Name it something slightly chaotic. Drop it after 10 p.m. And yes—it's working. According to a recent GlobalData survey, early findings show a potential rise in the consumption of savory snacks, chocolate, and confectionery, especially in North America. Unlike the energy drink space, where Gen Z dominates, these snack spikes are driven largely by older Millennials and Gen X. In other words, the munchies market isn't just younger—it's broader. And it's reshaping what indulgence looks like across demographics. The relationship between cannabis, appetite, and health isn't as linear as it looks. While cannabis clearly heightens cravings, studies suggest it isn't necessarily linked to obesity—and may even correlate with lower diabetes risk. That tension between indulgence and impact complicates the old narratives. The munchies aren't just about eating more. They might be about eating differently—or seeking out satisfaction on entirely different terms.
