Alzheimer’s disease and other forms of dementia are rising fast in South Asia, with millions of older adults at risk. A new study published in Nature Metabolism shines fresh light on a hidden part of this problem: how brain cells process sugar.

Researchers at the Buck Institute for Research on Ageing found that neurons—specialized brain cells responsible for transmitting information—can accumulate too much glycogen. Glycogen is a stored form of glucose, the body’s main energy source. Normally, it is kept in the liver and muscles, with smaller amounts in the brain’s support cells called astrocytes. But this study indicates that even neurones store glycogen, and when they can’t break it down, it becomes harmful.

“This new study challenges that view, and it does so with striking implications,” said Professor Pankaj Kapahi, senior scientist on the study. “Stored glycogen doesn’t just sit there in the brain; it is involved in pathology.”

In models of tauopathy—a family of diseases that includes Alzheimer’s and frontotemporal dementia—scientists found neurones with excess glycogen. Tau is a protein that, in Alzheimer’s, clumps into tangles and damages brain cells. This study suggests that tau also binds glycogen, stopping it from being broken down.

When glycogen piles up, neurones lose a crucial ability to fight oxidative stress. Oxidative stress happens when reactive oxygen species (ROS)—unstable molecules—damage cells. Normally, breaking down glycogen helps direct sugar into the pentose phosphate pathway (PPP). This chemical route generates NADPH and glutathione, two molecules essential for protecting cells from ROS.

By enhancing the enzyme glycogen phosphorylase (GlyP)—which breaks down glycogen—scientists successfully redirected sugar metabolism in neurones. “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 Dr Sudipta Bar, lead author of the study.

This isn’t just about flies. The team replicated these protective effects in human neurones derived from patients with frontotemporal dementia. This is important for South Asia, where dementia diagnoses often come late, and affordable treatments are scarce.

Even more promising, the study found that dietary restriction (DR)—eating fewer calories without malnutrition—naturally boosted GlyP activity in flies, reducing tau-related damage. Researchers also used a chemical called 8-Br-cAMP to mimic this effect, suggesting that drugs might someday offer the benefits of dietary restriction without major lifestyle changes.

Professor Kapahi explained, “This work could explain why GLP-1 drugs, now widely used for weight loss, show promise against dementia, potentially by mimicking dietary restriction.”

These findings could reshape how dementia is approached in South Asia, where health systems face challenges in providing specialist care. Affordable strategies such as carefully planned diets or repurposed drugs could help reduce the burden.

The study highlights that Alzheimer’s is not only about genetics or age but also about how cells manage their energy. Understanding and correcting these internal processes may offer new hope for millions.

As South Asia’s elderly population grows rapidly, the need for better, cheaper, and more accessible ways to fight dementia becomes urgent. This research suggests that rethinking something as simple as sugar metabolism in the brain could lead to groundbreaking solutions.