Alzheimers researchers say that heading to brain sugar could help protect against dementia

The brain has a hidden “sugar code that could lead to better treatments for neurological diseases such as Alzheimer’s, according to new research.

A study recently published in Nature Metabolism magazine found that decomposing glycogen (stored glucose) in the brain could reduce the accumulation of toxic proteins linked to common dementia.

This was one of the first studies to show that glycogen can actively influence health and brain disease, according to the main author, Dr. Pankaj Kapahi, 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 imitate tauopathy, a condition in which a protein called Tau accumulates in the brain, similar to what happens in Alzheimer’s disease,” Kapahi told News Digital.

It was found that the flies used in the study have brain damage and shortened lives, according to the researcher.

To ensure that the results could translate to humans, the research team also studied nerve cells made in the laboratory from cells of human patients who carry Tau mutations, as well as postmortem brain samples of people who had Alzheimer’s or related conditions, according to a press release.

Study findings

Both in the fly and humans, the researchers found higher levels of glycogen (stored glucose) in the brain, as well as the signs that glycogen decomposition was affected, Kapahi told News Digital.

This was a surprising discovery, since the researchers previously thought that glycogen was mainly stored in the muscles and liver.

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They also found that excess glycogen contributed to the disease. Tau proteins in the scientists’ models interacted with glycogen, blocking to break, and nerves lost their ability to avoid cell damage.

However, the researchers found that they could reduce damage to fruit flies and human nerves by increasing an enzyme called phosphorylase glycogen (Glyp), which decomposes glycogen.

“The next step in the process can be potentially mop the free radicals that roam our brains.”

Nervous cells used glycogen to fight cell damage, suggesting that the enzymes responsible for breaking sugar could be promising objectives for future therapies.

The researchers were also curious to know if a restricted diet could improve the health of the brain of flies.

When they reduced the amount of protein in the insect diet, flies really lived more and their brain health improved.

“Then we discovered that this improvement was linked to an increase in glycogen decomposition,” Kapahi said.

This led to the main finding of the study: that breaks down glycogen in neurons can protect the brain from the damage caused by the accumulation of Tau.

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Scientists also developed a medication with a special molecule called 8-Br-Camp that replied similar effects of dietary restriction, the press release said.

The authors clarified that they are still not recommending low protein diets, but said that this research could pave the way for dietary or drug -based strategies to help stop Alzheimer’s diseases and related diseases.

Dr. Michael Okun, a Florida neurologist and medical advisor to the Parkinson’s foundation, did not participate in the study, but commented on the importance of the findings.

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“Instead of channeling the sugar in energy burning processes, the broken glycogen seemed to be routed on an antioxidant production route,” said Okun, who is also the author of “Parkinson’s plan,” he told News Digital.

“The next step in the process can be potentially mop the free radicals that roam our brains,” he said.

Okun also confirmed that dietary restrictions activated a path of the protective brain and increased the decomposition of brain sugar.

“Ultimately, he reduced the damage of the Tau protein related to Alzheimer’s,” he said.

Study limitations

The study, which was supported by the National Health Institutes, as well as by the American Aging Research Federation and other sources, had some limitations, experts recognized.

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The researchers did not clarify whether the decomposition of cerebral glycogen could prevent human brain cells from dying, Okun said.

“We still do not know whether to go to the decomposition of glycogen will work in human patients, and most importantly, if it will be a safe approach.”

“We still do not know why glycogen accumulates in the disease, or if it is a cause or a result of Tau pathology, although our data suggests that it can amplify the progression of the disease,” Kapahi added.

The research was also carried out only in fly models and human cells and has not yet been tested in living humans.

“We still do not know whether to address glycogen decomposition will work in human patients, and most importantly, if it will be a safe approach,” Okun said.

Alzheimer’s disease, the most common way of dementia in the United States, affects more than seven million people in the United States, according to the Alzheimer’s association.

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Neurological disorder affects memory, thought and behavior.

There is no cure for the disease, but some medications can temporarily delay progression and improve the quality of life.