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The brain has a hidden “sugar code” that could lead to better treatments for neurological diseases like Alzheimer’s, according to new research.
A study recently published in the journal Nature Metabolism found that breaking down glycogen (stored glucose) in the brain could reduce the buildup of toxic proteins linked to the common dementia.
This was one of the first studies to show that glycogen may actively influence brain health and disease, according to lead author Dr. Pankaj Kapahi, a professor at the Buck Institute for Research on Aging in California.
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“The study began with fruit flies (Drosophila) that were genetically modified to mimic tauopathy, a condition where a protein called tau builds up in the brain, similar to what happens in Alzheimer’s disease,” Kapahi told Fox News Digital.
The flies used in the study were found to have brain damage and shortened lifespans, according to the researcher.
To ensure that the results could translate to humans, the research team also studied nerve cells made in the lab from human patient cells carrying tau mutations, as well as postmortem brain samples from people who had Alzheimer’s or related conditions, according to a press release.
Study findings
In both the fly and human models, the researchers found increased levels of glycogen (stored glucose) in the brain, as well as signs that glycogen breakdown was impaired, Kapahi told Fox News Digital.
This was a surprising discovery, as researchers previously thought glycogen was mainly stored in the muscles and liver.
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They also found that the excess glycogen contributed to disease. The tau proteins in the scientists’ models interacted with glycogen, blocking it from breaking down, and the nerves lost their ability to ward off cell damage.
However, the researchers found they could decrease damage to the fruit flies and human nerves by boosting an enzyme called glycogen phosphorylase (GlyP), which breaks down glycogen.
“The next step in the process may be mopping up potentially damaging free radicals roaming our brains.”
The nerve cells used the glycogen to fight against cell damage, suggesting that the enzymes responsible for breaking down sugar could be promising targets for future therapies.
The researchers were also curious whether a restricted diet could improve the flies’ brain health.
When they reduced the amount of protein in the insects’ diet, the flies indeed lived longer and their brain health improved.
“We then discovered this improvement was linked to an increase in the breakdown of glycogen,” Kapahi said.
This led to the study’s main finding — that breaking down glycogen in neurons can protect the brain from damage caused by tau buildup.
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The scientists also developed a drug using a special molecule called 8-Br-cAMP that replicated similar effects of dietary restriction, the press release noted.
The authors clarified that they are not recommending low-protein diets just yet — but said this research could pave the way for dietary or drug-based strategies to help slow Alzheimer’s and related diseases.
Dr. Michael Okun, a Florida neurologist and medical advisor to the Parkinson’s Foundation, was not involved in the study but commented on the significance of the findings.
“Instead of funneling sugar into energy-burning processes, the broken-down glycogen seemed to be routed into an antioxidant-producing pathway,” Okun, who is also author of “The Parkinson’s Plan,” told Fox News Digital.
“The next step in the process may be mopping up potentially damaging free radicals roaming our brains,” he said.
Okun also confirmed that dietary restrictions activated a protective brain pathway and boosted the breakdown of brain sugar.
“It ultimately reduced damage from the Alzheimer’s-related tau protein,” he said.
Study limitations
The study — which was supported by the National Institutes of Health, as well as the American Federation of Aging Research and other sources — did have some limitations, the experts acknowledged.
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The researchers did not clarify whether breaking down brain glycogen could stop human brain cells from dying, Okun noted.
“We still don’t know if targeting glycogen breakdown will work in human patients — and most importantly, whether it will be a safe approach.”
“We don’t yet know why glycogen builds up in disease, or whether it’s a cause or a result of tau pathology — though our data suggest it may amplify disease progression,” Kapahi added.
The research was also conducted only on fly and human cell models and has not yet been tested on living humans.
“We still don’t know if targeting glycogen breakdown will work in human patients — and most importantly, whether it will be a safe approach,” Okun said.
Alzheimer’s disease, the most common form of dementia in the U.S., affects more than seven million people in the U.S., according to the Alzheimer’s Association.
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The neurological disorder affects memory, thinking and behavior.
There is no cure for the disease, but some medications can temporarily slow progression and improve quality of life.
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