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Time of India
8 hours ago
- Health
- Time of India
TN discus thrower Krishna Jayasankar does a first on US soil
Krishna Jayasankar (l) with her coach Jordan Roach CHENNAI: After navigating a series of challenges over the past few years, Krishna Jayasankar has started to reap the rewards of her labour. The 22-year-old Tamil Nadu athlete became the first Indian woman thrower to qualify for the NCAA Outdoor Championships. She made the cut in discus throw, one of her pet events along with shot put . Following her move to the USA, Krishna was without a coach at the University of Nevada, where she is currently studying. Krishna first competed in the NCAA circuit in 2022 and had to take a break due to injuries before making a comeback last year. The return was not ideal, as she did not achieve the desired outcome. However, Krishna continued to push herself, and the results have began to show. She broke the indoor national record in shot put earlier this year and has recorded multiple personal bests in discus throw. What has made the year more special for Krishna is her qualification to the Outdoor Championships with a personal-best throw of 55.61m in discus throw. 'The reaction when I threw 55.61m was insane. This is my final year competing in the outdoors and I wanted to give it my all. I am happy to have achieved what I did. by Taboola by Taboola Sponsored Links Sponsored Links Promoted Links Promoted Links You May Like Dermatologista recomenda: simples truque elimina o fungo facilmente Acabe com o Fungo Undo I wanted to redeem myself after what I went through last year. It takes a village to help an athlete achieve the goals and I am grateful to the coaching staff. I have had a calf injury for the past 12 months, but I am able to manage it and perform,' Krishna told TOI from the USA. 'I told myself that one bad season will not define who I am, rather it will help me develop and learn from the mistakes. If not for the challenges that I faced, I would have breached the 60m mark earlier. I am on the right path and will look to progress at a good pace.' Jordan Roach has been training Krishna for the past few years. Having missed out on qualifying for the NCAA Championships in his college days, Roach wants to see his student achieve what he could not. 'Krishna did a lot of good work in the off-season and it is starting to show now. I knew she could do it and it was just a matter of time. What she has improved is her balance while throwing and she has the capacity to reach 60m in a few years. In the final, we expect to match the personal best and if possible, go another metre further,' Roach said. Multiple Olympic and World Championships medallist Carmelita Jeter, who is the head coach at the University of Nevada, said: 'I have seen so much growth from Krishna over the past year, and I believe that her failures are what changed her attitude.'
Mint
14 hours ago
- 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
a day ago
- 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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South Wales Guardian
a day ago
- Health
- South Wales Guardian
6 things you need to know about Alzheimer's – as drug trials bring new hope
Led by an expert from the University of Nevada in the US and published in the journal Alzheimer's & Dementia: Translational Research and Clinical Interventions, the review reveals that 182 clinical trials are underway in 2025, a rise of 11% from the previous year, assessing the impact 138 potential drugs. Notably, one-third of these drugs are repurposed medications originally developed for other conditions like diabetes, multiple sclerosis, and high cholesterol. A post shared by Alzheimer's Research UK (@alzheimersresearchuk) 1. Alzheimer's and dementia are not the same thing 'A lot of people get confused between Alzheimer's and dementia and aren't really sure what the difference is,' recognises Taylor. 'The way I describe it is that dementia is the group of symptoms – so things like memory loss, confusion, personality and behavioural changes – and Alzheimer's is one of the causes of those symptoms.' Research generally associates Alzheimer's disease with the accumulation of two proteins, amyloid and tau, says Taylor. 'These toxic proteins damage our brain cells, which are what is used to communicate messages throughout our body,' she explains. 'Overtime, as more brain cells die, it becomes harder for our brain overall to carry out its normal functions. So, depending on where in the brain the damage starts, that indicates what kind of symptoms someone will experience. 'That's why in Alzheimer's early symptoms are often memory loss and confusion because Alzheimer's tends to, but doesn't always, start in the memory centres of the brain.' 2. There are 14 potential risk factors 'A lot of the risk factors for dementia are linked to our heart health,' says Taylor. 'So, we know that what's good for your heart is good for your brain as well. 'Things like having a healthy diet, exercising regularly, limiting the amount of alcohol you drink, not smoking, keeping your blood pressure and cholesterol under control etc is really important to improve or maintain our brain health and reduce our risk of dementia. 'These risk factors, there are 14 in total, have been linked to 45% of dementia cases worldwide. So, if those risk factors were completely eliminated, then up to 45% would be prevented or delayed.'3. It isn't an inevitable part of ageing 'A lot of people think it's an inevitable part of ageing, but it's definitely not – we can do things to reduce our risk of dementia,' says Taylor. While Alzheimer's disease is more common in older adults, it can also affect younger people. 'People as young as 30 have developed Alzheimer's and obviously that is quite rare, but it really does show that it's not just a part of ageing,' says Taylor. 'It's a biological disease and if something goes wrong, then we can try and find a way to make it right – that's where research comes in.' 4. It isn't just about memory loss 'I think a lot of people just think of Alzheimer's as memory loss, but it can affect a lot of different aspects of someone's memory and thinking,' highlights Taylor. 'Someone might become very confused and might not be sure of the time or the date, they might misplace things a lot or put them in odd places, like putting a TV remote in the fridge.' Alzheimer's can also really affect language skills. 'People might have problems finding the right words or understanding the meaning of words or might struggle to follow conversations, and that might mean that they become quite withdrawn,' says Taylor. In addition, there's a lot of links between Alzheimer's and mood and behaviour changes. 'People can become low in mood. other people may become more agitated or aggressive, and that's a really heartbreaking thing for someone to go through,' says Taylor. A post shared by Alzheimer's Research UK (@alzheimersresearchuk) 'People often ring us and say why would I bother going to the doctor if there's no cure yet – but I think the benefits of getting a diagnosis is that support and understanding that you get from knowing what's going on, and the ability to plan ahead,' says Taylor. 'Getting a diagnosis means you can put things in place like the lasting power of attorney and sort out your will and finances while you have time. 'Getting an early diagnosis also means getting those treatments while they're likely to work best, and a diagnosis also provides more opportunities to take part in research, so the future generations don't have to go through the same thing.' 6. Remember to be patient with loved ones who have Alzheimer's 'Someone might change quite a lot when they have Alzheimer's, but it doesn't mean that they deep down aren't the same person,' emphasises Taylor. 'Someone's behaviour might change quite drastically throughout the course of the disease but it's not coming from a bad place. 'So, patience and understanding is really key when dealing with anyone with any form of dementia. Treasure the time that you have with them.'For more information about dementia, dementia research or taking part in research, visit Alzheimer's Research UK's website or contact its Dementia Research Infoline on 0300 111 5111 or email infoline@
Glasgow Times
2 days ago
- Business
- Glasgow Times
‘Hope on the horizon' as drugs assessed for Alzheimer's prevention
Some 138 treatments are being assessed in clinical trials. A third of drugs currently being trialled are 'repurposed' medications that are already being used to tackle other diseases, including diabetes, multiple sclerosis and cholesterol, according to the new review. One such trial is assessing whether semaglutide, the main ingredient for the weight loss and diabetes drug Ozempic and weight loss drug Wegovy, can slow the progression of dementia. And four late-stage trials are looking at preventing disease. Experts said that drugs targeting amyloid protein build up in the brain, such as lecanemab and donanemab, are 'only one part of the overall strategy' as they expressed excitement over the variety of new drugs, which are being tested among patients. The new review of Alzheimer's disease in clinical trials in 2025 found 182 clinical trials assessing the impact of 138 drugs. The number of trials represents an 11% increase on the previous year, according to the review, which was led by an expert from the University of Nevada in the US and has been published in the journal Alzheimer's and Dementia: Translational Research and Clinical Interventions. Commenting on the paper, Dr Sheona Scales, director of research at Alzheimer's Research UK, said: 'This year has really given us real cause for optimism.' She said that as well as more drugs coming through the pipeline, the treatment targets are 'more diverse' and 'looking at all stages of the disease'. She added: 'What this paper is showing us is that the pipeline of drug development is growing, it's diversifying and accelerating.' 'This latest report shows us that there is hope on the horizon for people with Alzheimer's, building on lecanemab and donanemab.' Dr Emma Mead, chief scientific officer of the Oxford Drug Discovery Institute, added: 'Today we are at a tipping point in dementia research as we understand more and more about the diseases that drive dementia. 'This gives us opportunities to slow and ultimately stop this devastating condition and today's announcement demonstrates that researchers are able to translate these understandings towards potential new treatments.' James Rowe, professor of cognitive neurology at the University of Cambridge and consultant neurologist, said: 'What strikes me is not just the number of new drugs, which is increasing year on year, but their range of targets (and) the range in which they work, giving us multiple shots on goal.' On the drugs which are being investigated for the prevention of disease, Prof Rowe said: 'One of the most exciting things of this report is the number of large-scale late-stage trials on prevention. 'And the aspiration to prevent, not just treat, is starting to be seen in the figures we see in these charts today.' He added: 'One way this can work is you take a treatment that you show to be working in people with symptoms with the illness, and then you simply bring it forward by some years. 'The ones that are in trial at the moment are really… bringing forward an effective treatment to earlier stage.' For instance, people with a genetic risk of Alzheimer's could receive some drugs earlier to see if they protect against the disease. On the repurposing of current drugs, Dr Mead said that it can usually take 10 to 15 years for new drugs to be tested and approved for use. 'Being able to repurpose drugs licensed for other health conditions could help to accelerate progress and help to open up other avenues to prevent or treat dementia causing diseases,' she said. 'A really promising example of this is the drug semaglutide, which is currently being trialled in people with mild cognitive impairment.' Meanwhile, academics said lecanemab and donanemab, which can be used for treating mild cognitive impairment in Alzheimer's patients, are an 'important first step' in the battle against the disease. The treatments were initially approved for UK use by regulators but then deemed not cost-effective for NHS use. The National Institute for Health and Care Excellence (Nice) is taking more evidence on donanemab and lecanemab and is expected to announce its decision in the summer. Dr Scales added: 'Lecanemab and donanemab have represented a huge leap forward in our understanding and ability to be able to treat Alzheimer's disease. 'What they've done is they've proved that we're able to modify the course of Alzheimer's disease, and what that has done is opened up the door to future treatments that we hope are more effective, easier to deliver and and able to deliver for our patients.' She said studies are showing 'even more complexities' around Alzheimer's and that in the future, people may be treated with a combination of drugs, depending on when they are diagnosed and the type of dementia they have. Dr Richard Oakley, associate director of research at Alzheimer's Society, said: 'This paper shows that 2025 is shaping up to be a landmark year for Alzheimer's disease drug development. 'With more trials under way than ever before and more drugs entering the pipeline, there is hope on the horizon for the nearly one million people living with dementia in the UK.'
