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New research reveals the role of the brain in the fight against Alzheimer’s disease

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

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

It was one of the first studies to show that glycogen can actively influence health and brain diseases, according to the main author of Dr. Pankaj Kapahi, professor at the Buck Institute for Research on Aging in California.

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“The study started with fruit flies (Drosophilia) that have been genetically modified to imitate tauopathy, a condition where a protein called Tau accumulates in the brain, similar to what is happening in Alzheimer’s disease,” Kapahi told Fox News Digital.

The flies used in the study have proven to have brain damage and a shortened lifespan, according to the researcher.

Older couple at Doctor

The brain has a hidden “sugar code” which could lead to better treatments for neurological diseases such as Alzheimer’s disease, according to new research. (istock)

To ensure that the results could result in humans, the research team has also studied nerve cells made in the laboratory from human patient cells bearing tau mutations, as well as post-mortem brain samples of people who had alzheimer or related conditions, according to a press release.

Study results

In flies and human models, researchers have found increased levels of glycogen (stored glucose) in the brain, as well as signs that glycogen degradation has been altered, Kapahi told Fox News Digital.

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

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They also found that excess glycogen had contributed to the disease. The tau proteins of the models of scientists have interacted with glycogen, preventing it from decomposing and the nerves have lost their ability to remove cellular damage.

However, the researchers found that they could decrease damage to the flies of human fruits and nerves by stimulating an enzyme called glycogen phosphorylase (GLYP), which breaks down the glycogen.

“The next step in the process can be a potentially harmful cleaning of free radicals wandering our brain.”

The nerve cells have used glycogen to combat cellular damage, which suggests that the enzymes responsible for the decomposition of sugar could be promising targets for future therapies.

Researchers were also curious to know if a limited diet could improve the health of the brain of flies.

When they reduced the amount of protein in the diet of insects, flies lived longer and their brain health has improved.

TEP results

The study revealed that rupture of glycogen (stored glucose) in the brain could reduce the accumulation of toxic proteins linked to Alzheimer’s disease. (AP photo / Evan Vucci, file)

“We then discovered that improvement was linked to an increase in glycogen break,” said Kapahi.

This has led to the main observation of the study – that the rupture of glycogen in neurons can protect the brain from damage caused by the accumulation of tau.

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Scientists have also developed a drug using a special molecule called 8-BR-CAMP which has reproduced similar effects of food restriction, the press release noted.

The authors have said that they do not yet recommend protein diets – but said this research could open the way for food strategies or medication to help slow Alzheimer’s disease and related diseases.

Brain

The study revealed that rupture of glycogen in neurons can protect the brain from damage caused by TAU accumulation. (istock)

Dr. Michael Okun, Florida neurologist and medical advisor to the Parkinson Foundation, was not involved in the study but commented on the meaning of the results.

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“Instead of channeling sugar in energy combustion processes, the breakdown glycogen seemed to be transported in an antioxidants producing path,” said Okun, who is also the author of “The Parkinson’s Plan”, said Fox News Digital.

“The next step in the process may be to clean the potentially harmful free radicals wandering our brain,” he said.

Doctor with patient

Alzheimer’s disease, the most common form of dementia in the United States, affects more than seven million people in the United States (istock)

Okun also confirmed that food restrictions activate a protective brain and stimulate the degradation of brain sugar.

“It finally reduced damage to the Tau protein linked to Alzheimer’s,” he said.

Study limitations

The study – which was supported by the National Institutes of Health, as well as by the American Federation of Research on Aging and other sources – had certain limits, recognized the experts.

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The researchers did not specify whether the rupture of the cerebral glycogen could prevent the cells of the human brain from dying, noted Okun.

“We still do not know if targeting the degradation of glycogen will work in human patients – and above all, whether it is a safe approach.”

“We do not yet know why glycogen accumulates in the disease, nor if it is a cause or a result of the Tau pathology – although our data suggest that it can amplify the progression of the disease,” added Kapahi.

Research has also been carried out only on models of flies and human cells and has not yet been tested on living humans.

Amyloid beta

“We do not yet know why glycogen accumulates in the disease, nor if it is a cause or a result of the Tau pathology – although our data suggest that it can amplify the progression of the disease,” said the researcher. (istock)

“We still do not know if targeting the degradation of glycogen will work in human patients – and above all, whether it is a safe approach,” said Okun.

Alzheimer’s disease, the most common form 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 drugs can temporarily slow down progression and improve quality of life.

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