Scientists have found a sugar key that protects your mind from Alzheimer’s disease

Glycogen is usually believed as a reserve energy source stored in the liver and muscles. Although there are also small quantities in the brain, especially in support cells called stellar cells, their role in neurons has been rejected long ago as minimal. “This new study is looking, and it does this with the amazing effects,” says Professor Banakaj Kapahi, Professor Capahi, the chief scientist in the study. “Stored glycogen not only sits there in the brain; it is involved in pathology.”

The research team, led by the post -PhD, discovered the doctorate, that in both the volatile and human models of Tau (a group of neurological degenerative diseases including Alzheimer’s), excessive neurons accumulate glycogen. More importantly, this accumulation appears to contribute to the development of the disease. Bar, the notorious protein that is conglomerate into your tangle in Alzheimer’s patients, appears to be physically associated with glycogen, carries and prevents it.

When glycogen cannot be divided, neurons lose an essential mechanism for oxidative stress management, which is a major advantage in aging and nervous reproduction. By restoring an enzyme activity called glypine phosphoryllas (Glyp)-which begins the process of collapsing glycogen-researchers found that they could reduce the damage associated with repentance in the flies of fruits and neurons derived from human stem cells.

Instead of using glycogen as fuel for energy production, these enzyme-backed neurons have re-sugar molecules in the Pentose phosphate path (PPP)-a critical path to the generation of NADPH (nicotinamide adenamine and phosphate) and glutathione, molecular that protects against oxardial stress. “By increasing the Glyp activity, the brain cells can better remove toxins from harmful interactive oxygen types, thus reducing damage and even extending the age of Taupathy flies,” said Barr.

The most promising thing, the team showed that the dietary restriction (DR)-a well-known intervention to extend the naturally known Glyp activity and improve the results associated with Tau in flies. They simulated these effects as well using a molecule called 8-BR-Camp, which indicates that DR benefits may be cloned through the drug-based activation of this sugar removal system. “This work can explain the reason for showing GLP-1 medications, which are now widely used for weight loss, a promise against dementia, and perhaps through the imitation of food restriction,” Kabahi said.

The researchers also confirmed the accumulation of the similar glycogen and the preventive effects of Glyp in the human neurons derived from patients with anterior front dementia (FTD), which enhances the possibility of translation treatments. Kapahi says that the study emphasizes the strength of the fly as a typical system in revealing how the metaphysical system defect affects nervous degeneration. “Working in this simple animal allowed us to move to human neurons in a more targeted way,” he said.

Kapahi also admits a very cooperative Back atmosphere as a major worker at work. His laboratory, with experience in airline aging and nervous refraction, benefited from the experience of proteins in the Schilling Laboratory and the Seyfric Laboratory (at Emory University) as well as the ELLERBY Laboratory that has experience in human IPScs and nervous drawing.

Capahi says that this study not only highlights the metabolism of glycogen as an unexpected hero in the brain, but also opens a new trend in searching for treatments against Alzheimer’s disease and related diseases. “By discovering how to manage neurons sugar, we may discover a new treatment strategy: targeting the internal chemistry of the cell to fight the decline associated with age,” he says. “As we continue to age as a society, such results expose hope to be the best understanding – and perhaps balance – the hidden sugar symbol in our brain can open strong tools to combat dementia.”

Coauthors: Among the collaborators in Back Kenneth A. Wilson, Tyler or Hilbec, Sydney Aldfar, Jordan in Burton, Samah Shah, Anja Holtz, Enrique M. Among the other collaborators are Eric B. Dammar, and Simah Sephar and Nicholas T. Sephrid, the Emori Center for Neurological Diseases, the University of Imori University, Atlanta, Georgia as well as Annath Chantarmanan, Department of Biochemistry, Faculty of Medicine at Emory University, Atlanta, Georgia

Thanks and appreciation: The work has been supported by Nih Grants R01ag038688, R21g054121, AG045835, R01ag071995, R01ag0193, T32ag000266-23, R01ag061879, P01ag06591 and 1S10 OD016281. Another support from Hevolution, the American Agency Research Federation, and the Larry L. Hilbred and Motivation^x Award from Alex and Bob Griswold