Prince Harry's striking claim that his mental health struggles were passed on through 'bad parenting'
But Prince Harry has done even more work on the issue since stepping down as a working royal and relocating to California.
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The Independent
an hour ago
- The Independent
This fuzzy animal friend may be the key to treating schizophrenia
Llamas – likely without red pajamas – may hold the key to treating schizophrenia. The serious brain disorder causes people to interpret reality abnormally, and affects approximately 3.7 million U.S. adults between the ages of 18 to 65 years old, according to the nonprofit RTI International. But the domesticated South American woolly animal might be be able to help. French researchers said this week that they had used llama antibodies, or proteins that help to protect the immune system, to design a tiny fragment of an antibody known as a 'nanobody' that will trigger a neurotransmitter in the brain involved in regulating neural activity. Neurotransmitters are chemical molecules that carry messages or signals from one nerve cell to the next target cell, according to the Cleveland Clinic. No llamas were harmed in the study and researchers can identify nanobodies in a petri dish. In the past, llama antibodies have also proven effective in fighting Covid and other 'SARS-like' viruses. When scientists at the Institute of Functional Genomics injected the molecule into the veins or the muscles, it was able to break the blood-brain barrier and effectively reach brain receptors. The barrier is a a tightly locked layer of cells that defend your brain from harmful substances. Studying the impact of the nanobodies in two tests using mice, the researchers found that they corrected cognitive deficits that were observed. There was an improvement of cognitive function with just one shot, and a prolonged effect over one week. Clinical studies are now required to show that their findings could be a new avenue of treatment for schizophrenia. "In humans obviously we don't know [yet], but in mice yes, it is sufficient to treat most deficits of schizophrenia," molecular biologist Jean-Philippe Pin told Newsweek.. He was a co-author of the research which was published in the journal Nature. Pin said that medications currently given to schizophrenia patients "treat the symptoms well, but less the cognitive deficits." The cause of the chronic condition remains unknown, but the World Health Organization says it is thought that an interaction between genes and a range of environmental factors may be the reason. The exact prevalence of schizophrenia is difficult to measure. Some have tied cases in Canada to cannabis use. Although schizophrenia can occur at any age, people are typically diagnosed between the ages of 16 and 30. Symptoms vary from person to person. There is no cure, but it can be treated through antipsychotic medications, talk therapy, and self-management strategies, the National Alliance on Mental Illness says. The study's authors hope to add this strategy to the list. 'This research confirms the potential of nanobodies as a new therapeutic strategy for acting on the brain, with their use eventually being broadened to include the treatment of other neurological illnesses,' the institute said in a statement.
The Guardian
2 hours ago
- The Guardian
Group confronted suspect who stabbed 11 at a Michigan Walmart, video shows
Several passersby helped apprehend a knife-wielding suspect who stabbed 11 people at a Walmart in Michigan, video has revealed. Footage circulating on social media showed several citizens in Traverse City confronting a 42-year old man outside the supermarket on Saturday during the attack. Among the people confronting the suspect included an armed citizen who could be seen pointing his gun at the man. 'Throw it away!' some of the passerby could be heard yelling, with others saying: 'Put it down!' and 'Get on the fucking ground.' One passerby could be seen pushing a shopping cart towards the suspect. Moments later, law enforcement could be seen arriving on scene and arresting the man. Speaking to Channel2Now, Walmart employee Tasha Nash said: 'It was a guy with a knife – people were screaming and running in all directions … I saw someone stabbed in the eye.' Another shopper, Kathryn Ann Clark, told the outlet and her friend's son and another shopper helped confront the suspect. 'It was definitely a stabbing,' Clark said, adding: 'There were no shots fired, just brave people stepping in.' Eleven victims were treated at the nearby Munson Medical Center. On Sunday, the hospital said that there were 'encouraging signs of recovery' among the victims. According to the hospital, seven people are in fair condition and four are in serious condition. There are no longer any patients from the attack who are in critical condition, the hospital added. In a statement released on Sunday, the hospital said: 'Our dedicated team of physicians, surgeons, nurses, clinicians, and support staff remain focused on providing a healing environment for all those affected by this tragic incident … Additionally, we are working on providing additional emotional support for our employees in light of this incident. We extend our continued support to the victims and their families during this very difficult time.' Michigan's governor, Gretchen Whitmer, said that she was aware of the attack, writing on X: 'Our thoughts are with the victims and the community reeling from this brutal act of violence. I am grateful to the first responders for their swift response to apprehend the suspect.'
The Independent
2 hours ago
- The Independent
Millions of people are suffering from brain fog. A new study will find out why
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.
