Latest news with #JamesRowe
The Sun
3 days ago
- Entertainment
- The Sun
Dancing On Ice star Vanessa Bauer stuns in sizzling swimsuit snaps from Bali getaway with boyfriend
DANCING On Ice star Vanessa Bauer has stunned in a series of sizzling swimsuit snaps from her Bali getaway with her boyfriend. It was back in December when the skating pro revealed new boyfriend James Rowe, after a romantic trip to Lapland. 6 6 6 Both she and James, 33, took to Instagram to share loved-up posts from their winter wonderland holiday. Footballer James previously played for Reading FC and went on to play for Cheltenham town, followed by Aldershot Town. Now, the brunette beauty and her man have jetted off again, this time to Bali. Vanessa shared some stunning photos sat on the shore at night. She penned: 'liquid or frozen, happiest by the water 🌊🧊 (once I've eaten) 'thanks to a kind stranger @momohead_ for taking the covert last picture from a far, this was such a beautiful moment ♥️' The brunette beauty put on a sensational display in the series of photos, in a glistening orange bikini. Vanessa let her hair down in beachy waves and sported a makeup free look, while standing up for some of the photos. In another snap, she could be seen with her boyfriend James, as they posed in swimwear while enjoying an al-fresco feast. Dancing on Ice star quits series just hours before live show after devastating injury 'How absolutely beautiful,' one fan wrote, while another said: 'I aspire to be as happy as you whether it's on the ice or off you're just radiating it.' The star's romance with James comes after she split from boyfriend of nine months Dan Underwood in June of last year. And Vanessa previously hinted she could quit Dancing On Ice as she pursues an acting career. She told The Sun: "My acting pursuit is going really well. "I'm actually working on a movie right now as well, so I'm super excited for this to come out next year. "I love Dancing On Ice and I would love to continue doing it for as long as I can but at the same time, other opportunities are piling up and I'm super grateful for everything coming my way right now." The show was recently shelved by ITV with no plans for a new series. It comes after ratings dwindled for this year's series, which was won by Corrie's Sam Aston. 6 6
Daily Mail
3 days ago
- Entertainment
- Daily Mail
Vanessa Bauer sizzles in a skimpy metallic bikini during moonlit swim as she jets off on romantic trip to Bali with her new boyfriend James Rowe
Vanessa Bauer sizzled in a skimpy metallic bikini as she shared an album of loved-up holiday snaps from her romantic trip to Bali with her new boyfriend James Rowe. The professional figure skater, 28, took to Instagram on Tuesday to share a series of eye-popping snaps of herself showing off her incredible figure in the racy two-piece. She let her beachwear outfit do all the talking as she kept her accessories minimal while striking a series of sultry poses during her moonlit dip in the sea. Vanessa also shared a sweet picture of her cuddling up to her new boyfriend James while they enjoyed a meal together. The couple were later seen watching the sun rise as they sat next to one another on the beach. Alongside the post, she penned: 'liquid or frozen, happiest by the water (once I've eaten) thanks to a kind stranger @momohead_ for taking the covert last picture from a far, this was such a beautiful moment.' Vanessa went public with her James in December as she shared a series of loved-up Instagram snaps from their trip to Lapland. James is a football coach and FIFA-licensed football agent. He retired from professional football after playing for Reading FC, Cheltenham Town and Aldershot Town. Alongside the sweet carousel of snaps, Vanessa took the opportunity to reflect on her father's death in 2021, claiming she has now got to a place in her life where she feels 'the happiest I've ever been.' 'A pull between feeling the happiest I've ever been but the moment I fly home for Christmas a different reality kicks in,' she added. 'I believe that the pulls between my upbringing, our families' loss and the beautiful life I get to live now is not a burden but in a way it can be seen as a blessing. 'And I certainly am grateful for my family and the 25 years I got to know my dad.' She continued: 'Perspective has created the person I am now, to keep me grounded, driven, to know life in its many different ways and remain resilient.' 'Gratitude is an understatement and I'll retain the discipline to keep growing my luck.' 'Anything is possible and love and magic truly is everywhere (love heart emoji).' In June last year, Vanessa split from her boyfriend Dan Underwood after just nine months together after sources claimed they had drifted apart. While Vanessa wanted to focus on her career, she and Dan remained friends, and the pair continued to still follow each other on social media. A source told The Sun at the time: 'Vanessa and Dan are still on good terms and are friends, but their job takes them to different parts of the world and they have struggled with the distance.' 'They realised they better off as friends for now, but still have a lot of love and respect for each other. 'Vanessa is busy with her career and is focusing on herself and her acting right now. While Dan is busy travelling the world for work, so it's been difficult to maintain something long-term.' She and Dan previously made their romance official in September 2023, when they posed for snaps together at the premiere of The Creator.
The Guardian
13-06-2025
- Health
- The Guardian
‘Transformative': the UK lab working on a way to halt genetic type of dementia
Behind the gleaming glass facade of an office block in east London's docklands, Dr Martina Esposito Soccoio is pipetting ribonucleic acid into test tubes. Here, not far from Canary Wharf's multinational banks, a British university spinout is working on a breakthrough treatment for a form of dementia suffered by millions of people worldwide. There is no cure for dementia at present, but scientists at AviadoBio hope their clinical studies can stop the progression of a particular genetic type of frontotemporal dementia (FTD). 'It may be one of the first dementias to have a definitive treatment, a cure if you like, a really transformative treatment that allows people to live much longer and much more normal lives,' says Prof James Rowe, consultant neurologist at Cambridge's Addenbrooke's Hospital. FTD mainly affects the front and sides of the brain and unlike Alzheimer's disease, does not begin with memory loss, which tends to occur later. It is characterised by progressive loss of language and changes in personality and behaviour. Most cases are diagnosed in people aged 45 to 65, but it can affect people in their 20s and 30s. There are an estimated 20,000 to 40,000 people living with FTD in the UK, and between 1m and 2m in the world. Rowe says: 'It's a double-edged sword: the young onset, the high genetic burden and rapid illness are also features that perhaps make it more tractable to treat.' The Die Hard and Pulp Fiction actor Bruce Willis, who recently celebrated his 70th birthday, was diagnosed with FTD two years ago, with his family calling it a 'cruel disease'. They have not said whether he has a genetic form of FTD. The gene therapy developed by AviadoBio, which was spun out of Prof Christopher Shaw's research lab at King's College London in 2021, targets a type of FTD known as FTD-GRN. This is caused by mutations of a gene that lead to a deficiency of progranulin (GRN), a protein that is essential for maintaining healthy brain cells. AviadoBio, which employs 60 people, signed an exclusive licence agreement with the Japanese pharma firm Astellas last October to develop the therapy. It is now recruiting patients for its clinical trial in the UK, as well as the US, Poland, Spain, Sweden and the Netherlands. The first patient received the infusion in Warsaw in March 2024, out of six patients who have had the treatment so far, in Poland and the US. All patients will be followed for up to five years as part of the trial. AviadoBio expects to publish the first data next year. Three years ago, Jessica Crawford, from Beverley in Yorkshire, lost her mother to FTD, caused by mutations of another gene, C9orf72. In 2014, when her mother was 58, her behaviour changed; the family suspected depression. Previously very sociable, she stopped going out and started playing games like Candy Crush or watching TV shows 'over and over,' her daughter recounts. Her mother initially did not want to see a doctor, and was only diagnosed with FTD in February 2019. By this time she was so confused she once put raw chicken in a sandwich. 'Getting the diagnosis wasn't easy because FTD wasn't well known; my mum was aceing in the memory tests,' Crawford says. But her mother became increasingly confused and lost the ability to speak, and to communicate at all. Crawford became her full-time carer in 2020, until her mother deteriorated so much that she had to go to a care home in late 2021, and died the following year. Crawford, 33, found out that she herself carries the gene mutation, and with her husband decided to conceive through IVF with a pre-implantation genetic diagnosis. When their five embryos were screened, four had the gene mutation, and the fifth resulted in the birth of their son. The couple donated their other four embryos to science and she takes part in GENFI – a long-running UK-led global study of families with FTD across 40 sites. AviadoBio itself was born out of the research done at King's by Shaw, a neurologist who has focused on FTD and amyotrophic lateral sclerosis (ALS) for more than three decades, and Dr Youn Bok Lee and Dr Do Young Lee from the UK Dementia Research Institute's centre based at King's. ALS, the most common form of motor neurone disease, has also been linked to mutations of the GRN gene and leads to muscle weakness, paralysis and eventually death. Sign up to Business Today Get set for the working day – we'll point you to all the business news and analysis you need every morning after newsletter promotion Shaw acts as the company's chief scientific and clinical adviser, and while the Lees are no longer involved in the firm's research, all three remain shareholders. David Cooper, AviadoBio's chief medical officer, says: 'It was something that hit me when I first joined the company, you look at the MRI scans of patients with a GRN mutation, the frontal and temporal parts of their brain are just melting away … So we really need earlier treatment, an, earlier diagnosis and a more organised healthcare approach to deal with it.' AviadoBio's lead product, known as AVB-101, is infused directly into the brain by a neurosurgeon using a cannula as thin as a strand of angel hair pasta, during a 90-minute procedure guided by MRI. It delivers a functional copy of the progranulin gene to restore appropriate levels of the protein to affected areas of the brain. It is a once-only treatment, and no immunosuppressant drugs are needed subsequently. 'The patients who have FTD are born with almost half of the progranulin levels that you and I might have,' says chief executive Lisa Deschamps. 'Our goal in the study is to supplement the GRN gene and restore as much progranulin in these individuals as possible to normal levels to reduce the neurodegeneration effect. Other medications in development at AviadoBio include two gene therapies, from Philadelphia-based Passage Bio and Eli Lilly-owned Prevail Therapeutics, but they do not target the thalamus, the 'relay station' in the brain. Passage Bio's therapies are delivered directly to the cerebrospinal fluid in a single treatment. Denmark's Vesper Bio has developed an oral capsule, designed to act on the GRN gene, that is being trialled at University College London Hospital. AviadoBio, whose investors include Johnson & Johnson's innovation arm and the UK not-for-profit LifeArc Ventures, is part of a growing life science cluster in Canary Wharf. At its labs, scientists – assisted by robotics – research how to target a particular gene. 'The UK has real strengths in this area,' says Rowe, pointing to the international GENFI study, run since 2011 by Prof Jonathan Rohrer, a neurologist from UCL Queen Square Institute of Neurology who also sits on AviadoBio's scientific advisory board. 'It's a real win for the UK.'
Mint
04-06-2025
- Business
- Mint
The Alzheimer's drug pipeline is healthier than you might think
Of all the medical challenges that scientists have faced, Alzheimer's disease, the most common form of dementia, has been one of the trickiest. Between 1995 and 2021 private money spent on Alzheimer's research totalled $42.5bn, but more than 140 trials failed to deliver a single drug capable of slowing the disease. Yet the tide may be turning. There are two working drugs, offering modest benefits, on the market. A new review paper suggests more could soon follow. There are 182 clinical trials for Alzheimer's treatments under way in 2025—an 11% increase on the previous year—testing 138 different drugs, of which 12 are set to complete their final 'phase 3' trials this year. Moreover this pipeline includes medicines aimed at a diverse range of targets in the brain, reflecting an increasingly sophisticated understanding of the molecular processes behind Alzheimer's and dementia more broadly. For decades, the theory that has dominated Alzheimer's research, and drug pipelines, is known as the amyloid hypothesis. It argues that the primary cause of the disease is the accumulation of plaques of beta-amyloid proteins in the brain. These would lead to a cascade of negative effects including neuronal dysfunction, brain-cell death and neuroinflammation. The amyloid hypothesis was supported by genetic evidence, which showed mutations in key genes within families to be linked to early onset of the disease. The success of the two drugs already treating Alzheimer's—lecanemab and donanemab, which arrived on the market in 2023 and 2024, respectively—proves that a connection exists. Both help to clear amyloid from the brain, and offer modest help to a subset of patients for whom the drug is thought to be safe and useful. They slow the progression of the disease by about one-third, according to clinical trials, meaning patients can retain their quality of life for longer. The excitement generated by these drugs was tinged, however, with a feeling that they were not much to show for decades of effort. The singular focus on amyloid was probably misplaced. James Rowe, a professor of cognitive neurology at the University of Cambridge, says that although amyloid accumulation is a critical 'early trigger' for the disease, by the time patients arrive at his clinic there are other neural processes accelerating the illness. These include the accumulation of a misshapen version of a protein called tau; increased metabolic stress on brain cells; neuroinflammation; and degeneration of the brain's blood supply. A more nuanced understanding of Alzheimer's is at last being reflected in drug development. That is the conclusion of Jeffrey Cummings at the University of Nevada, Las Vegas, and colleagues in a review published on June 3rd in the journal Translational Research & Clinical Interventions. Academic experts, and investors, agree. Dame Kate Bingham is the managing partner of SV Health Investors, a venture-capital firm based in London that in 2015 started the first fund dedicated to discovering new treatments for dementia in 2015. At the time the drug pipeline for Alzheimer's was mainly focused on tackling amyloid. She says the growing diversity of potential targets today gives her increased optimism. Fully one-third of the new drugs are repurposed, which means they are already approved for use in other conditions and are being redeployed to Alzheimer's. The appeal of this approach is that the drugs already have known safety and toxicity profiles, and can be approved quickly and developed cheaply. One of the more well-known is semaglutide, a diabetes and weight-loss drug whose anti-inflammatory and metabolic benefits have led to its being tested as a treatment for mild cognitive impairment. The drug piromelatine, meanwhile, works on melatonin and serotonin receptors in the brain, which help regulate sleep. As healthy sleep is thought to increase the rate at which amyloid and other waste proteins are cleared, improving it may slow the progression of Alzheimer's. Then there is AR1001 (also known as mirodenafil), which was originally developed for erectile dysfunction and is being tested for its neuroprotective properties. The drug increases levels of a molecule in the brain called cGMP which, in turn, activates pathways that support the survival of nerve cells and improve connections between brain cells. Drugs in this category are known to improve blood flow, so the drug might also have an impact on the brain's vascular health. Another repurposed drug is nabilone, which interacts with the cannabinoid receptors in the body. (The most well known molecule of this kind is tetrahydrocannabinol, the active compound in cannabis). It was originally developed to treat nausea and vomiting in those undergoing cancer chemotherapy. It is now being tested as a potential treatment for agitation and behavioural problems in those with Alzheimer's. Guanfacine, a drug that improves attention and executive function in those with ADHD, is also being tested to see if it can offer similar benefits. Repurposed drugs do not necessarily have a higher chance of success in late-stage trials than those with a novel mechanism. Dame Kate argues that innovative approaches that use new molecular targets, rather than repurposing, will have the greatest impact on the disease. One area of innovation centres around drugs that can tackle inflammation in the brain. Particular attention is being paid to brain cells called microglia, which play a central role in the brain's immune response and, most probably, its fight against Alzheimer's. Microglia have been described as acting as the brain's fire service, police and binmen, because they respond to emergencies, maintain order and clear up debris. A number of drugs are trying to target the protein TREM2 on the surface of microglia in the hope of boosting their activity. Combinations of drugs are also being tested. For example, it is hoped that a pairing of dasatinib, a cancer drug, and quercetin, a molecule derived from plants, will clear ageing and dysfunctional cells. Drug combinations that target different pathways and components of an illness have made big inroads into other complex and intractable diseases such as cancer and HIV. Some of the errors of the past have been corrected. Dr Rowe says that early attempts to design amyloid-clearing drugs did not remove enough amyloid, or did so too slowly. The patient selection in trials was also poor, with many patients included who—it later turned out—did not have Alzheimer's at all. Today's trials still have blind spots, warns Antonella Santuccione-Chadha, the founder of the Women's Brain Foundation, a non-profit that studies how sex affects brain and mental health. Many still fail to differentiate patients by sex, she says. Yet women are twice as likely to develop Alzheimer's, a difference that cannot be explained solely by their longer lifespans, and the disease seems to progress differently in their brains. At any given stage of the disease, tau proteins spread farther in women than in men, says Dr Chadha. It would help the trials—and patients—if more people were tested for Alzheimer's earlier on, so that they could be enrolled to try the new drugs. A single register of those with the disease would also be useful, making it easier for patients to find trials, and for drug companies to find patients. Much, therefore, remains to be done. But for those suffering from a horrible and as yet insurmountable disease that steals so many minds, there is also some much needed hope.
Hindustan Times
04-06-2025
- Business
- Hindustan Times
The Alzheimer's drug pipeline is healthier than you might think
OF ALL THE medical challenges that scientists have faced, Alzheimer's disease, the most common form of dementia, has been one of the trickiest. Between 1995 and 2021 private money spent on Alzheimer's research totalled $42.5bn, but more than 140 trials failed to deliver a single drug capable of slowing the disease. Yet the tide may be turning. There are two working drugs, offering modest benefits, on the market. A new review paper suggests more could soon follow. There are 182 clinical trials for Alzheimer's treatments under way in 2025—an 11% increase on the previous year—testing 138 different drugs, of which 12 are set to complete their final 'phase 3' trials this year. Moreover this pipeline includes medicines aimed at a diverse range of targets in the brain, reflecting an increasingly sophisticated understanding of the molecular processes behind Alzheimer's and dementia more broadly. For decades, the theory that has dominated Alzheimer's research, and drug pipelines, is known as the amyloid hypothesis. It argues that the primary cause of the disease is the accumulation of plaques of beta-amyloid proteins in the brain. These would lead to a cascade of negative effects including neuronal dysfunction, brain-cell death and neuroinflammation. The amyloid hypothesis was supported by genetic evidence, which showed mutations in key genes within families to be linked to early onset of the disease. The success of the two drugs already treating Alzheimer's—lecanemab and donanemab, which arrived on the market in 2023 and 2024, respectively—proves that a connection exists. Both help to clear amyloid from the brain, and offer modest help to a subset of patients for whom the drug is thought to be safe and useful. They slow the progression of the disease by about one-third, according to clinical trials, meaning patients can retain their quality of life for longer. The excitement generated by these drugs was tinged, however, with a feeling that they were not much to show for decades of effort. The singular focus on amyloid was probably misplaced. James Rowe, a professor of cognitive neurology at the University of Cambridge, says that although amyloid accumulation is a critical 'early trigger' for the disease, by the time patients arrive at his clinic there are other neural processes accelerating the illness. These include the accumulation of a misshapen version of a protein called tau; increased metabolic stress on brain cells; neuroinflammation; and degeneration of the brain's blood supply. A more nuanced understanding of Alzheimer's is at last being reflected in drug development. That is the conclusion of Jeffrey Cummings at the University of Nevada, Las Vegas, and colleagues in a review published on June 3rd in the journal Translational Research & Clinical Interventions. Academic experts, and investors, agree. Dame Kate Bingham is the managing partner of SV Health Investors, a venture-capital firm based in London that in 2015 started the first fund dedicated to discovering new treatments for dementia in 2015. At the time the drug pipeline for Alzheimer's was mainly focused on tackling amyloid. She says the growing diversity of potential targets today gives her increased optimism. Fully one-third of the new drugs are repurposed, which means they are already approved for use in other conditions and are being redeployed to Alzheimer's. The appeal of this approach is that the drugs already have known safety and toxicity profiles, and can be approved quickly and developed cheaply. One of the more well-known is semaglutide, a diabetes and weight-loss drug whose anti-inflammatory and metabolic benefits have led to its being tested as a treatment for mild cognitive impairment. The drug piromelatine, meanwhile, works on melatonin and serotonin receptors in the brain, which help regulate sleep. As healthy sleep is thought to increase the rate at which amyloid and other waste proteins are cleared, improving it may slow the progression of Alzheimer's. Then there is AR1001 (also known as mirodenafil), which was originally developed for erectile dysfunction and is being tested for its neuroprotective properties. The drug increases levels of a molecule in the brain called cGMP which, in turn, activates pathways that support the survival of nerve cells and improve connections between brain cells. Drugs in this category are known to improve blood flow, so the drug might also have an impact on the brain's vascular health. Another repurposed drug is nabilone, which interacts with the cannabinoid receptors in the body. (The most well known molecule of this kind is tetrahydrocannabinol, the active compound in cannabis). It was originally developed to treat nausea and vomiting in those undergoing cancer chemotherapy. It is now being tested as a potential treatment for agitation and behavioural problems in those with Alzheimer's. Guanfacine, a drug that improves attention and executive function in those with ADHD, is also being tested to see if it can offer similar benefits. Repurposed drugs do not necessarily have a higher chance of success in late-stage trials than those with a novel mechanism. Dame Kate argues that innovative approaches that use new molecular targets, rather than repurposing, will have the greatest impact on the disease. One area of innovation centres around drugs that can tackle inflammation in the brain. Particular attention is being paid to brain cells called microglia, which play a central role in the brain's immune response and, most probably, its fight against Alzheimer's. Microglia have been described as acting as the brain's fire service, police and binmen, because they respond to emergencies, maintain order and clear up debris. A number of drugs are trying to target the protein TREM2 on the surface of microglia in the hope of boosting their activity. Combinations of drugs are also being tested. For example, it is hoped that a pairing of dasatinib, a cancer drug, and quercetin, a molecule derived from plants, will clear ageing and dysfunctional cells. Drug combinations that target different pathways and components of an illness have made big inroads into other complex and intractable diseases such as cancer and HIV. Some of the errors of the past have been corrected. Dr Rowe says that early attempts to design amyloid-clearing drugs did not remove enough amyloid, or did so too slowly. The patient selection in trials was also poor, with many patients included who—it later turned out—did not have Alzheimer's at all. Today's trials still have blind spots, warns Antonella Santuccione-Chadha, the founder of the Women's Brain Foundation, a non-profit that studies how sex affects brain and mental health. Many still fail to differentiate patients by sex, she says. Yet women are twice as likely to develop Alzheimer's, a difference that cannot be explained solely by their longer lifespans, and the disease seems to progress differently in their brains. At any given stage of the disease, tau proteins spread farther in women than in men, says Dr Chadha. It would help the trials—and patients—if more people were tested for Alzheimer's earlier on, so that they could be enrolled to try the new drugs. A single register of those with the disease would also be useful, making it easier for patients to find trials, and for drug companies to find patients. Much, therefore, remains to be done. But for those suffering from a horrible and as yet insurmountable disease that steals so many minds, there is also some much needed hope. Curious about the world? To enjoy our mind-expanding science coverage, sign up to Simply Science, our weekly subscriber-only newsletter. 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