
COVID-19 pandemic may have aged your brain, even if you weren't infected, finds UK study
Using brain scans from nearly 1,000 healthy adults from before and after the pandemic, researchers found signs of faster brain ageing, especially in older adults, men, and those from disadvantaged backgrounds. Of these samples, those who were infected with COVID-19 also showed some decline in thinking speed and flexibility. But overall, the pandemic's stress alone did shift brain structure in all individuals whose scans were reviewed.
New Delhi: A new study from the University of Nottingham has found that just living through the COVID-19 pandemic may have aged people's brains faster, even if they never got infected with the virus itself. The peer-reviewed study was published on 22 July in the journal Nature Communications and is based on data from the UK Biobank Study.
It's a powerful reminder that our environment matters for our brain's growth. Read more here.
Also Read: A UK health study has collected a whopping 100,000 full-body scans, and Neanderthals had 'family recipes'
Spiders originally came from the sea?
Next, we might have evidence that spiders could have originally been sea creatures. At least that is what a new peer-reviewed study published in the journal Current Biology on 22 July suggests, after researchers closely examined a preserved fossil from half a billion years ago.
The fossil is called Mollisonia symmetrica, and it has a nervous system very similar to that of modern-day arachnids like spiders and scorpions. Until now, scientists thought these creatures only evolved once their ancestors moved onto land 400 million years ago and have remained the same ever since.
But this new study flips that theory on its head, quite literally. It cites evidence of the brain of the fossil Mollisonia, which shows a reversed organisation—a signature trait seen in today's arachnids. This arrangement may have given them faster reflexes, better control, and precision, which are all traits modern-day spiders use to hunt and weave webs.
The fossil places Mollisonia as a close relative of modern arachnids, meaning these creatures might have started evolving in the ocean long before they crept onto land. Read more here.
Scientists genome sequence 100-yr-old Spanish Flu virus
A 100-year-old lung sample from Switzerland helped scientists decode the deadliest flu in human history. A new peer-reviewed study by researchers from the Universities of Basel and Zurich published in BMC Biology Journal on 1 July sequenced the genome of the 1918 'Spanish flu' virus. They used preserved tissue from a young patient who died during the pandemic's first wave in Switzerland. The Spanish flu that spread across Europe and Asia in the 1910s is said to have killed between 20-100 million people.
By decoding the genome, scientists now have insights into how this flu had already adapted to humans early on. They found three key mutations in the genome—two which helped the virus evade the human immune system, and one which boosted its ability to infect human cells.
What makes this study stand out is also how they conducted the study.
In viral flus, the genetic information rests in the RNA, not the DNA. The RNA is very quick to degrade but these scientists developed a method to recover ancient viral RNA. This technique could open the door to learning more from historic outbreaks. Read more here.
Arctic winter is melting, and researchers have noticed it
A group of scientists led by Dr James Bradley from Queen Mary University, London, published a commentary in Nature Communications on 21 July talking about the 'shockingly warm' winter conditions in the Arctic. The team described how they had geared up for winter Arctic fieldwork in Svalbard, wearing layers of thermal clothing, only to find themselves drenched in rain, standing on bare grass, and working without even needing gloves in what is supposed to be the middle of winter in February 2025.
Svalbard is a Norwegian archipelago located where the Arctic Ocean converges with the Atlantic Ocean.
In the commentary, they raised alarms about melted snow pools, blooming vegetation, and rain replacing snow in the Arctic Circle during winters. Svalbard is heating up six to seven times faster than the global average, and the Arctic winter is no longer reliably frozen, said the team.
These conditions not only disrupted their research but also raised safety concerns, like how to retreat from polar bears without their snowmobiles working. The team warns that winter warming in the Arctic is not a fluke but rather the new norm. The message sent by the commentary is clear: climate policy needs to catch up, and fast. Read more here.
Also Read: A fiery side-effect of melting glaciers & paging Dr Droid for gallbladder surgery
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Indian Express
44 minutes ago
- Indian Express
Study led by IISER Pune decodes mechanisms that help plants regrow injured parts with original shape
Gardeners are often seen pruning shrubs or tree branches to maintain plant health and promote fresh growth. Soon, however, the pruned branches regrow with stunning resemblance to their original form. An international group of scientists, led by biologists at the Indian Institute of Science Education and Research, Pune (IISER), has now zeroed in on the key mechanisms in plants that help restore damaged parts to their original shape. Unlike animal cells, plant cells are far more rigid and depend more on growth rates and anisotropy (how a material's physical characteristics change depending on its direction) during cell regeneration. Roots are important facilitators that support nutrient intake. Their naturally tapered shape and conical tip aid better soil penetration. When they get damaged due to natural or external causes, it is observed that the lost cell types and layers get restored and the root regrows to the original tapered shape. In the latest paper published on July 25 in the journal Current Biology, mathematicians and physicists from IISER, Pune and Thiruvananthapuram, Netherlands' Wageningen University, and UK-based John Innes Centre, have attempted to track the mechanisms that may be responsible for restoring the root's tapered shape. In the study, the researchers describe a distinct geometric pattern as per which plant roots regrow after being damaged. This understanding, they said, could help establish fundamental cellular processes, like cell shape and cell regeneration in plants and, in particular, plants vital for food cultivation and securing food security. Instinctive responses of injured roots The group studied the regeneration of the Arabidopsis thaliana root after it was surgically chipped off. They observed notable behaviour in the root regrowth from the 12th hour since being chipped. Instinctively, the injured root's first response was to generate new cells at the wound site. And their goal was to remain oriented in the right direction and help restore the shape and function of the root and maintain its original function. 'The usual cuboidal root cells got morphed into rhomboid shapes. These altered cells then divided diagonally, producing triangular prism-like cells. The diagonal divisions redirected the growth of neighbouring cells along a slanted path — collectively recreating the lost tapered tip,' Kalika Prasad, biologist at IISER-Pune and co-author of the paper, told The Indian Express. After about 18-19 hours post-cutting, the previously flat root end had grown and bulged. By 24 hours, it had become more prominent, indicating the onset of some trigger mechanisms. Corresponding to about 12 hours post the injury, the researchers said, a mechanical tension was noted developing during the growth stage of the injured root. And this tension, they said, guided and controlled the new cells to align and develop in a certain geometric manner. The root tip has multiple cell layers. While cells in the outermost layer grow slower, the cells present in the innermost layer grow rapidly. 'This differential growth then leads to build up in mechanical tension within the cells and, as a response, their shape or geometry starts aligning. In the end, we found the regrown root to have restored perfectly with respect to cell types and the shape. It functioned optimally like an uninjured root,' Prasad said. Similar post-injury cell regeneration behaviour was demonstrated by a mustard plant called Brassica, which the team tested.


The Hindu
an hour ago
- The Hindu
Why India's hepatitis crisis needs urgent attention
World Hepatitis Day, observed on July 28, is a global call to action to eliminate viral hepatitis, the second deadliest infectious disease after COVID-19. This year's theme, 'Hepatitis: Let's Break It Down', urges the dismantling of financial, social, and systemic barriers that delay timely diagnosis, treatment, and prevention of this silent killer. Understanding hepatitis Hepatitis refers to inflammation of the liver, primarily caused by five viruses: A, B, C, D, and E. Hepatitis A and E are transmitted through contaminated food or water and usually result in acute illness. Hepatitis B, C, and D, however, are more insidious and are transmitted through blood, unsafe medical procedures, unprotected sex, or from mother to child. If left untreated, these can lead to chronic liver disease, cirrhosis, or liver cancer. According to the World Health Organization's 2024 Global Hepatitis Report, India bears the world's second-highest burden, with 2.98 crore Hepatitis B and 55 lakh Hepatitis C cases. Alarmingly, nearly 90% of those infected are unaware of their condition and often present only when irreversible liver damage has set in. Despite the availability of vaccines for Hepatitis A and B, and curative treatments for Hepatitis C, hepatitis still claims one life every 30 seconds. Challenges that need addressing In line with the WHO's target to eliminate viral hepatitis as a public health threat by 2030, India must address pressing challenges such as high diagnostic costs, limited screening, and persistent stigma. Strengthening the healthcare response through routine screening, community-level education, and policies that ensure affordable access to diagnostics and treatment is essential. Across the country, public health institutions, medical colleges, and civil society partners are intensifying efforts through awareness campaigns, screening programs, and policy advocacy to improve access to diagnosis and treatment. Recent initiatives have included national summits bringing together experts and stakeholders to develop comprehensive elimination strategies. On this World Hepatitis Day, let's break the silence, end the stigma, and build a hepatitis-free world. Join the movement. Get tested, get treated, and protect your family. (Dr. Vivek Shanmugam is a liver transplant surgeon & managing trustee, Chennai Liver Foundation . Info@
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Business Standard
2 hours ago
- Business Standard
Long-Covid, viruses: New research looks for links to chronic fatigue
Millions of people who recover from infections like Covid-19, influenza and glandular fever are affected by long-lasting symptoms. These include chronic fatigue, brain fog, exercise intolerance, dizziness, muscle or joint pain and gut problems. And many of these symptoms worsen after exercise, a phenomenon known as post-exertional malaise. Medically the symptoms are known as myalgic encephalomyelitis or chronic fatigue syndrome (ME/CFS). The World Health Organization classifies this as a post viral fatigue syndrome, and it is recognised by both the WHO and the United States Centers for Disease Control and Prevention as a brain disorder. Experiencing illness long after contracting an infection is not new, as patients have reported these symptoms for decades. But Covid-19 has amplified the problem worldwide. Nearly half of people with ongoing post-Covid symptoms – a condition known as long-Covid– now meet the criteria for ME/CFS. Since the start of the pandemic in 2020, it is estimated that more than 400 million people have developed long-Covid. To date, no widely accepted and testable mechanism has fully explained the biological processes underlying long-Covid and ME/CFS. Our work offers a new perspective that may help close this gap. Our research group studies blood and the cardiovascular system in inflammatory diseases, as well as post-viral conditions. We focus on coagulation, inflammation and endothelial cells. Endothelial cells make up the inner layer of blood vessels and serve many important functions, like regulating blood clotting, blood vessel dilation and constriction, and inflammation. Our latest review aims to explain how ME/CFS and long-Covid start and progress, and how symptoms show up in the body and its systems. By pinpointing and explaining the underlying disease mechanisms, we can pave the way for better clinical tools to diagnose and treat people living with ME/CFS and long-Covid. What is endothelial senescence? In our review, our international team proposes that certain viruses drive endothelial cells into a half-alive, 'zombie-like' state called cellular senescence. Senescent endothelial cells stop dividing, but continue to release molecules that awaken and confuse the immune system. This prompts the blood to form clots and, at the same time, prevent clot breakdown, which could lead to the constriction of blood vessels and limited blood flow. By placing 'zombie' blood-vessel cells at the centre of these post-viral diseases, our hypothesis weaves together microclots, oxygen debt (the extra oxygen your body needs after strenuous exercise to restore balance), brain-fog, dizziness, gut leakiness (a digestive condition where the intestinal lining allows toxins into the bloodstream) and immune dysfunction into a single, testable narrative. From acute viral infection to 'zombie' vessels Viruses like SARS-CoV-2, Epstein–Barr virus, HHV-6, influenza A, and enteroviruses (a group of viruses that cause a number of infectious illnesses which are usually mild) can all infect endothelial cells. They enable a direct attack on the cells that line the inside of blood vessels. Some of these viruses have been shown to trigger endothelial senescence. Multiple studies show that SARS-CoV-2 (the virus which causes Covid-19 disease) has the ability to induce senescence in a variety of cell types, including endothelial cells. Viral proteins from SARS-CoV-2, for example, sabotage DNA-repair pathways and push the host cell towards a senescent state, while senescent cells in turn become even more susceptible to viral entry. This reciprocity helps explain why different pathogens can result in the same chronic illness. Influenza A, too, has shown the ability to drive endothelial cells into a senescent, zombie-like state. What we think is happening We propose that when blood-vessel cells turn into 'zombies', they pump out substances that make blood thicker and prone to forming tiny clots. These clots slow down circulation, so less oxygen reaches muscles and organs. This is one reason people feel drained. During exercise, the problem worsens. Instead of the vessels relaxing to allow adequate bloodflow, they tighten further. This means that muscles are starved of oxygen and patients experience a crash the day after exercise. In the brain, the same faulty cells let blood flow drop and leak, bringing on brain fog and dizziness. In the gut, they weaken the lining, allowing bits of bacteria to slip into the bloodstream and trigger more inflammation. Because blood vessels reach every corner of the body, even scattered patches of these 'zombie' cells found in the blood vessels can create the mix of symptoms seen in long-Covid and ME/CFS. Immune exhaustion locks in the damage Some parts of the immune system kill senescent cells. They are natural-killer cells, macrophages and complement proteins, which are immune molecules capable of tagging and killing pathogens. But long-Covid and ME/CFS frequently have impaired natural-killer cell function, sluggish macrophages and complement dysfunction. Senescent endothelial cells may also send out a chemical signal to repel immune attack. So the 'zombie cells' actively evade the immune system. This creates a self-sustaining loop of vascular and immune dysfunction, where senescent endothelial cells persist. In a healthy person with an optimally functioning immune system, these senescent endothelial cells will normally be cleared. But there is significant immune dysfunction in ME/CFS and long-Covid, and this may enable the 'zombie cells' to survive and the disease to progress. Where the research goes next There is a registered clinical trial in the US that is investigating senescence in long-Covid. Our consortium is testing new ways to spot signs of ageing in the cells that line our blood vessels. First, we expose healthy endothelial cells in the lab to blood from patients to see whether it pushes the cells into a senescent, or 'zombie,' state. At the same time, we are trialling non-invasive imaging and fluorescent probes that could one day reveal these ageing cells inside the body. In selected cases, tissue biopsies may later confirm what the scans show. Together, these approaches aim to pinpoint how substances circulating in the blood drive cellular ageing and how that, in turn, fuels disease. Our aim is simple: find these ageing endothelial cells in real patients. Pinpointing them will inform the next round of clinical trials and open the door to therapies that target senescent cells directly, offering a route to healthier blood vessels and, ultimately, lighter disease loads.