Latest news with #GlyP
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
Daily Record
03-07-2025
- Health
- Daily Record
Scientists just found a sugar switch that 'protects your brain from Alzheimer's'
The lead author of a new study believes "our brain's hidden sugar code could unlock powerful tools for combating dementia" Brits with a sweet-tooth might actively try to curb temptation when they feel they have been raiding the cupboards or sweetie drawer too much. However, did you know sugar could actually hold a major brain benefit? Scientists have uncovered a surprising sugar-related mechanism inside brain cells that could transform how we fight Alzheimer's and other dementias. In Scotland, an estimated 90,000 people are living with dementia, and approximately 66 per cent of those have Alzheimer's disease, according to Alzheimer's Research UK. Now, a new study from scientists at the Buck Institute for Research on Aging has revealed a surprising player in the battle against Alzheimer's disease and other forms of dementia - brain sugar metabolism. Published in Nature Metabolism, the research uncovers how breaking down glycogen - a stored form of glucose - in neurons may protect the brain from toxic protein build-up and degeneration. Glycogen is typically thought of as a reserve energy source stored in the liver and muscles. While small amounts also exist in the brain, its role in neurons has long been dismissed. "This new study challenges that view, and it does so with striking implications," says Professor Pankaj Kapahi, PhD, senior scientist on the study. "Stored glycogen doesn't just sit there in the brain; it is involved in pathology." The researchers discovered that in both fly and human models of tauopathy (a group of neurodegenerative diseases including Alzheimer's), neurons accumulate excessive glycogen. More importantly, this build-up appears to contribute to disease progression. But tau, the protein that clumps into tangles in Alzheimer's patients, appears to physically bind to glycogen, trapping it and preventing its breakdown. When glycogen can't be broken down, the neurons lose an essential mechanism for managing oxidative stress, a key feature in aging and neurodegeneration. By restoring the activity of an enzyme called glycogen phosphorylase (GlyP), researchers found they could reduce tau-related damage in fruit flies and human stem cell-derived neurons. "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," said postdoc Sudipta Bar. Even more promising, the team demonstrated that restricting one's diet naturally enhanced GlyP activity and improved tau-related outcomes in flies. They further mimicked these effects and showed that the benefits of DR might be reproduced through drug-based activation of this sugar-clearing system. "This work could explain why GLP-1 drugs, now widely used for weight loss, show promise against dementia, potentially by mimicking dietary restriction," said Kapahi. "Work in this simple animal allowed us to move into human neurons in a much more targeted way." Kapahi says this study not only highlights glycogen metabolism as an unexpected hero in the brain but also opens up a new direction in the search for treatments against Alzheimer's and related diseases. "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," he added. Join the Daily Record WhatsApp community! Get the latest news sent straight to your messages by joining our WhatsApp community today. You'll receive daily updates on breaking news as well as the top headlines across Scotland. No one will be able to see who is signed up and no one can send messages except the Daily Record team. All you have to do is click here if you're on mobile, select 'Join Community' and you're in! If you're on a desktop, simply scan the QR code above with your phone and click 'Join Community'. We also treat our community members to special offers, promotions, and adverts from us and our partners. If you don't like our community, you can check out any time you like. To leave our community click on the name at the top of your screen and choose 'exit group'.
