Latest news with #BuckInstitute
Yahoo
08-07-2025
- Health
- Yahoo
Surprise Discovery Could Rewrite What We Know About Alzheimer's
A new study just uncovered a surprising link between how brain cells manage sugar and the progression of Alzheimer's disease—and the implications could reshape future treatments. Researchers at the Buck Institute for Research on Aging have discovered that stored glucose, in the form of glycogen, may not be the passive energy reserve scientists once assumed. Instead, it may actively contribute to the buildup of tau proteins, a hallmark of Alzheimer's and other neurodegenerative diseases. Tauopathies like Alzheimer's are characterized by toxic tangles of tau inside neurons. But this study, published in Nature Metabolism, found that those tangles may form, at least in part, because of disruptions in how glycogen is processed in the brain. 'Stored glycogen doesn't just sit there in the brain,' said Buck Institute biologist Pankaj Kapahi. 'It is involved in pathology.' Using fruit fly models and postmortem brain cells from people with Alzheimer's, scientists found elevated levels of both tau and glycogen. The buildup appeared to be driven by a breakdown in how glycogen is metabolized, specifically through the enzyme glycogen phosphorylase (GlyP), which normally helps convert glycogen into usable fuel. When researchers increased GlyP activity in the flies, they saw significant benefits. Brain cells reduced oxidative stress, protected themselves better, and even lived longer. The team also tested whether a low-protein diet, already linked to improved brain health, might produce similar effects. It did. Fruit flies fed this restricted diet showed fewer signs of damage and extended lifespans, suggesting that dietary changes could naturally shift brain metabolism in a protective direction. Even more intriguing, the researchers developed a drug that mimicked the effect of dietary restriction. It worked. And they noted potential crossover with medications like Ozempic, which may also support brain health by targeting glycogen-related pathways. 'By discovering how neurons manage sugar,' said lead researcher Sudipta Bar, 'we may have unearthed a novel therapeutic strategy—one that targets the cell's inner chemistry to fight age-related decline.' If future studies replicate these results in humans, this could mark a turning point in our understanding and treatment of Alzheimer' Discovery Could Rewrite What We Know About Alzheimer's first appeared on Men's Journal on Jul 7, 2025
Yahoo
08-07-2025
- Health
- Yahoo
Surprise Discovery About Sugar in The Brain Could Help Fight Alzheimer's
Stores of glucose in the brain could play a much more significant role in the pathological degeneration of neurons than scientists realized, opening the way to new treatments for conditions like Alzheimer's disease. Alzheimer's is a tauopathy; a condition characterized by harmful build-ups of tau proteins inside neurons. It's not clear, however, if these build-ups are a cause or a consequence of the disease. A new study now adds important detail by revealing significant interactions between tau and glucose in its stored form of glycogen. Led by a team from the Buck Institute for Research on Aging in the US, the research sheds new light on the functions of glycogen in the brain. Before now, it's only been regarded as an energy backup for the liver and the muscles. "This new study challenges that view, and it does so with striking implications," says molecular biologist Pankaj Kapahi, from the Buck Institute. "Stored glycogen doesn't just sit there in the brain, it is involved in pathology." Related: Building on links previously found between glycogen and neurodegeneration, the researchers spotted evidence of excessive glycogen levels both in tauopathy models created in fruit flies (Drosophila melanogaster) and in the brain cells of people with Alzheimer's. Further analysis revealed a key mechanism at play: tau proteins interrupt the normal breakdown and use of glycogen in the brain, adding to the dangerous build-up of both tau and glycogen, as well as lowering protective neuron defense barriers. Crucial to this interaction is the activity of glycogen phosphorylase or GlyP, the main enzyme tasked with turning glycogen into a fuel the body can use. When the researchers boosted GlyP production in fruit flies, glycogen stores were utilized once more, helping to fight back against cell damage. "By increasing GlyP activity, the brain cells could better detoxify harmful reactive oxygen species, thereby reducing damage and even extending the lifespan of tauopathy model flies," says Buck Institute biologist Sudipta Bar. The team wondered if a restricted diet – already associated with better brain health – would help. When fruit flies affected by tauopathy were put on a low-protein diet, they lived longer and showed reduced brain damage, suggesting that the metabolic shift prompted by dieting can help boost GlyP. It's a notable set of findings, not least because it suggests a way that glycogen and tau aggregation could be tackled in the brain. The researchers also developed a drug based around the 8-Br-cAMP molecule to mimic the effects of dietary restriction, which had similar effects on flies in experiments. The work might even tie into research involving GLP-1 receptor agonists such as Ozempic, designed to manage diabetes and reduce weight, but also now showing promise for protecting against dementia. That might be because these drugs interact with one of glycogen's pathways, the researchers suggest. "By discovering how neurons manage sugar, we may have unearthed a novel therapeutic strategy: one that targets the cell's inner chemistry to fight age-related decline," says Kapahi. "As we continue to age as a society, findings like these offer hope that better understanding – and perhaps rebalancing – our brain's hidden sugar code could unlock powerful tools for combating dementia." The research has been published in Nature Metabolism. Air Pollution 'Strongly Associated' With DNA Mutations Tied to Lung Cancer FDA Issues Warning Over Dangerous 'Gas Station Heroin' Substance Mysterious Leprosy Pathogen Has Lurked in The Americas For 4,000 Years
Yahoo
08-07-2025
- Health
- Yahoo
Surprise Discovery About Sugar in The Brain Could Help Fight Alzheimer's
Stores of glucose in the brain could play a much more significant role in the pathological degeneration of neurons than scientists realized, opening the way to new treatments for conditions like Alzheimer's disease. Alzheimer's is a tauopathy; a condition characterized by harmful build-ups of tau proteins inside neurons. It's not clear, however, if these build-ups are a cause or a consequence of the disease. A new study now adds important detail by revealing significant interactions between tau and glucose in its stored form of glycogen. Led by a team from the Buck Institute for Research on Aging in the US, the research sheds new light on the functions of glycogen in the brain. Before now, it's only been regarded as an energy backup for the liver and the muscles. "This new study challenges that view, and it does so with striking implications," says molecular biologist Pankaj Kapahi, from the Buck Institute. "Stored glycogen doesn't just sit there in the brain, it is involved in pathology." Related: Building on links previously found between glycogen and neurodegeneration, the researchers spotted evidence of excessive glycogen levels both in tauopathy models created in fruit flies (Drosophila melanogaster) and in the brain cells of people with Alzheimer's. Further analysis revealed a key mechanism at play: tau proteins interrupt the normal breakdown and use of glycogen in the brain, adding to the dangerous build-up of both tau and glycogen, as well as lowering protective neuron defense barriers. Crucial to this interaction is the activity of glycogen phosphorylase or GlyP, the main enzyme tasked with turning glycogen into a fuel the body can use. When the researchers boosted GlyP production in fruit flies, glycogen stores were utilized once more, helping to fight back against cell damage. "By increasing GlyP activity, the brain cells could better detoxify harmful reactive oxygen species, thereby reducing damage and even extending the lifespan of tauopathy model flies," says Buck Institute biologist Sudipta Bar. The team wondered if a restricted diet – already associated with better brain health – would help. When fruit flies affected by tauopathy were put on a low-protein diet, they lived longer and showed reduced brain damage, suggesting that the metabolic shift prompted by dieting can help boost GlyP. It's a notable set of findings, not least because it suggests a way that glycogen and tau aggregation could be tackled in the brain. The researchers also developed a drug based around the 8-Br-cAMP molecule to mimic the effects of dietary restriction, which had similar effects on flies in experiments. The work might even tie into research involving GLP-1 receptor agonists such as Ozempic, designed to manage diabetes and reduce weight, but also now showing promise for protecting against dementia. That might be because these drugs interact with one of glycogen's pathways, the researchers suggest. "By discovering how neurons manage sugar, we may have unearthed a novel therapeutic strategy: one that targets the cell's inner chemistry to fight age-related decline," says Kapahi. "As we continue to age as a society, findings like these offer hope that better understanding – and perhaps rebalancing – our brain's hidden sugar code could unlock powerful tools for combating dementia." The research has been published in Nature Metabolism. Air Pollution 'Strongly Associated' With DNA Mutations Tied to Lung Cancer FDA Issues Warning Over Dangerous 'Gas Station Heroin' Substance Mysterious Leprosy Pathogen Has Lurked in The Americas For 4,000 Years
Yahoo
06-07-2025
- Health
- Yahoo
Surprise Discovery About Sugar in The Brain Could Help Fight Alzheimer's
Stores of glucose in the brain could play a much more significant role in the pathological degeneration of neurons than scientists realized, opening the way to new treatments for conditions like Alzheimer's disease. Alzheimer's is a tauopathy; a condition characterized by harmful build-ups of tau proteins inside neurons. It's not clear, however, if these build-ups are a cause or a consequence of the disease. A new study now adds important detail by revealing significant interactions between tau and glucose in its stored form of glycogen. Led by a team from the Buck Institute for Research on Aging in the US, the research sheds new light on the functions of glycogen in the brain. Before now, it's only been regarded as an energy backup for the liver and the muscles. "This new study challenges that view, and it does so with striking implications," says molecular biologist Pankaj Kapahi, from the Buck Institute. "Stored glycogen doesn't just sit there in the brain, it is involved in pathology." Related: Building on links previously found between glycogen and neurodegeneration, the researchers spotted evidence of excessive glycogen levels both in tauopathy models created in fruit flies (Drosophila melanogaster) and in the brain cells of people with Alzheimer's. Further analysis revealed a key mechanism at play: tau proteins interrupt the normal breakdown and use of glycogen in the brain, adding to the dangerous build-up of both tau and glycogen, as well as lowering protective neuron defense barriers. Crucial to this interaction is the activity of glycogen phosphorylase or GlyP, the main enzyme tasked with turning glycogen into a fuel the body can use. When the researchers boosted GlyP production in fruit flies, glycogen stores were utilized once more, helping to fight back against cell damage. "By increasing GlyP activity, the brain cells could better detoxify harmful reactive oxygen species, thereby reducing damage and even extending the lifespan of tauopathy model flies," says Buck Institute biologist Sudipta Bar. The team wondered if a restricted diet – already associated with better brain health – would help. When fruit flies affected by tauopathy were put on a low-protein diet, they lived longer and showed reduced brain damage, suggesting that the metabolic shift prompted by dieting can help boost GlyP. It's a notable set of findings, not least because it suggests a way that glycogen and tau aggregation could be tackled in the brain. The researchers also developed a drug based around the 8-Br-cAMP molecule to mimic the effects of dietary restriction, which had similar effects on flies in experiments. The work might even tie into research involving GLP-1 receptor agonists such as Ozempic, designed to manage diabetes and reduce weight loss, but also now showing promise for protecting against dementia. That might be because these drugs interact with one of glycogen's pathways, the researchers suggest. "By discovering how neurons manage sugar, we may have unearthed a novel therapeutic strategy: one that targets the cell's inner chemistry to fight age-related decline," says Kapahi. "As we continue to age as a society, findings like these offer hope that better understanding – and perhaps rebalancing – our brain's hidden sugar code could unlock powerful tools for combating dementia." The research has been published in Nature Metabolism. Air Pollution 'Strongly Associated' With DNA Mutations Tied to Lung Cancer FDA Issues Warning Over Dangerous 'Gas Station Heroin' Substance Mysterious Leprosy Pathogen Has Lurked in The Americas For 4,000 Years
Daily Mail
30-06-2025
- Health
- Daily Mail
Researchers pinpoint diet followed by millions that may ward off dementia
Cutting back on carbohydrates could potentially stave off Alzheimer's, researchers suggested today. Calling the strategy a 'powerful tool for combatting dementia', they showed reducing the amount of blood sugar in the brain via diet could slash the number of harmful proteins that trigger dementia symptoms. Carbohydrates are converted to a type of sugar called glycogen, which is a form of energy that's used by the brain to function. While a small amount is needed, the California-based researchers discovered that an excess can bind to a toxic protein in the brain called tau, stopping it from breaking down. Significant clumps of this protein, as well as another—amyloid—can form plaques and tangles—and this is thought to be behind the symptoms of Alzheimer's, the leading cause of dementia. The latest experiments found high levels of enzymes that break down glycogen in the brain could help destroy the build-up of tau. And eating fewer carbohydrates, the researchers, said was an effective way to increase the presence of this enzyme. Professor Pankaj Kapahi, an expert in metabolism and brain ageing at the Buck Institute for Research on Ageing in California and study co-author, said the team may have uncovered a new 'therapeutic strategy' to tackle dementia early-on. He added: 'As we continue to age as a society, findings like these offer hope that better understanding our brain's hidden sugar code could unlock powerful tools for combating dementia.' In the new study on fruit flies, the scientists found when glycogen can't be broken down, brain cells lose an essential mechanism for managing oxidative stress that ultimately kills them. But, by restoring the activity of an enzyme called glycogen phosphorylase (GlyP)—which triggers glycogen breakdown—they could reduce this damage. Writing in the journal Nature Metabolism, they said that by restricting certain foods that are converted to glycogen such as carbohydrates, GlyP activity is 'enhanced' and sugar levels in the brain reduced. Professor Pankaj Kapahi also said: 'This work could explain why GLP-1 drugs, now widely used for weight loss, show promise against dementia, potentially by mimicking dietary restriction.' Slimming injections, known medically as GLP-1 drugs, have ushered in a new era in the war on obesity. The treatment spurs weight loss by mimicking the actions of a hormone released in the gut after eating—GLP-1. As well as telling the pancreas to make more insulin, the GLP-1 hormone feeds back to the brain and makes us feel full—stopping patients from over-eating. The team hopes that by raising awareness of risk factors—which change as we age—people can take steps to reduce their chances of getting the disease. It comes as a landmark study last July suggested almost half of all Alzheimer's cases could be prevented by tackling 14 lifestyle factors from childhood. World-leading experts found two new risk factors—high cholesterol and suffering vision loss—were, combined, behind almost one in ten dementia cases globally. They join 12 existing factors, ranging from genetics to smoking status, that experts have identified as increasing the risk a person would suffer dementia. Experts claimed the study, published in the prestigious journal The Lancet, provided more hope than 'ever before' that the memory-robbing disorder that blights the lives of millions can be tackled. Recent analysis by the Alzheimer's Society estimates the overall annual cost of the dementia to the UK is £42billion a year, with families bearing the brunt. An ageing population means these costs—which include lost earnings of unpaid carers—are set to soar to £90billion in the next 15 years. Alzheimer's Disease is the most common form of dementia and affects 982,000 people in the UK. Memory problems, thinking and reasoning difficulties and language problems are common early symptoms of the condition, which then worsen over time. Alzheimer's Research UK analysis found 74,261 people died from dementia in 2022 compared with 69,178 a year earlier, making it the country's biggest killer.
