Brain Sugar Metabolism May Protect Against Alzheimer’s: A New Study
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Brain Sugar Metabolism May Protect Against Alzheimer’s: A New Study
A new study from the Buck Institute for Research on Aging, published on June 30th, 2025, suggests that the way in which neurons store and break down glycogen (a form of sugar) could play a key role in preventing Alzheimer’s disease.
The findings show that boosting the breakdown of glycogen in neurons can reduce the buildup of tau, a protein linked to the development of Alzheimer’s disease. This revolutionary discovery may help us further support brain health thanks to lifestyle strategies such as nutrition and eating habits.
Full study here: Neuronal glycogen breakdown mitigates tauopathy via pentose-phosphate-pathway-mediated oxidative stress reduction
What the Study Found
Scientists from Buck Institute found that neurons store small amounts of glycogen, which is something that has been considered as insignificant in the past.
- In the development of Alzheimer’s disease, tau proteins stick to glycogen, which prevents our cells from breaking it down properly. This process results in the buildup of excess glycogen inside neurons, making them more vulnerable to oxidative stress – which is a major contributor to premature aging and neurodegeneration.
- Researchers found that increasing the activity of an enzyme called glycogen phosphorylase (GlyP) helps clear the sugar build-up inside neurons. In both fly and human models, boosting GlyP levels reduced tau tangles and improved the health of the brain cells.
These findings highlight new ways to detoxify the brain, potentially allowing people to enjoy more mental clarity even in later stages of their life.
How the Research Was Conducted
The research team used fly models with tautopathy, a group of conditions that mimics the buildup of toxic proteins as seen in Alzheimer’s disease.
Flies with boosted GlyP enzyme production had less buildup of tau, healthier neurons, and even managed to live longer than the flies that weren’t engineered to produce more GlyP.
The researchers then confirmed the results in human-derived neurons, suggesting that the same mechanism could be relevant in people.
Why The Findings Matter Now
This new study reveals a part of brain cell metabolism that has been previously overlooked. Its findings could offer hope for both treatment and prevention of Alzheimer’s disease and neurodegeneration.
Even more, the researchers also found that dietary restriction may naturally increase GlyP levels in flies, which hints that lifestyle interventions (such as intermittent fasting or calorie restriction) could bring similar results in humans.
In addition, the scientists showed a compound known as 8-Br-cAMP to mimic the benefits of dietary restriction by activating the same pathways. The team noted that some weight loss drugs may also stimulate similar processes in neurons.
“This work could explain why GLP-1 drugs, now widely used for weight loss, show promise against dementia, potentially by mimicking dietary restriction,” said Professor Pankaj Kapahi, PhD, senior scientist on the study.
Why This Study Brings Hope to Patients
According to the World Health Organization, more than 57 million people struggled with some form of dementia in 2021, of which 60-70% were Alzheimer’s cases. With the growing aging population in the West and limited treatments targeting the root causes of neurodegeneration, this study highlights an under-explored metabolic pathway.
As the society continues to age, science-backed strategies for promoting lifespan and healthspan become increasingly more important. Future research around brain health and preventing neurodegenerative issues can pave the way for new anti-aging diets, more effective medications, and finally understanding all the root causes behind dementia.
As new research continues to uncover how metabolic processes shape brain aging, supporting those pathways through targeted nutrition becomes more important than ever. That’s exactly where Restore Life comes in.
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What to Expect in the Future
In the future, neuronal glycogen management may be further leveraged in order to reduce the buildup of toxic proteins in the brain. Further exploring how lifestyle interventions like fasting and calorie restriction boost glycogen breakdown in humans could be the next breakthrough.
If confirmed, this could possibly influence future dietary recommendations for brain health and drug development for preventing and managing Alzheimer’s disease.
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