Study reveals new therapeutic target for Alzheimer’s
Researchers at Tokyo Metropolitan University have identified a crucial link between glucose metabolism in glia cells – fundamental components of the nervous system – and the degeneration processes caused by Alzheimer’s. Using fruit fly retinas as an experimental model, the scientists demonstrated that stimulating glucose metabolism in these cells, even in the presence of tau protein accumulation (characteristic of the disease), can reduce inflammation and preserve the retina’s photoreceptors. The discovery paves the way for the development of new therapeutic approaches against neurodegenerative diseases.
Alzheimer’s is currently the leading cause of dementia in the elderly worldwide and continues to have a profound impact on the quality of life of millions of people. Although it is already known that the disease is related to the accumulation of tau protein inside nerve cells, the exact mechanisms behind neuronal degeneration are still a great enigma to science.
It was with this challenge in mind that the team led by Professor Kanae Ando decided to investigate the role of glial cells in this process. Unlike neurons, these cell types act as vital support for the central nervous system – they feed, protect and even remove abnormal proteins. It was already known that the inflammation caused by glia is among the main characteristics of Alzheimer’s, as well as the sharp drop in cerebral glucose metabolism. What wasn’t clear until then was how these changes were linked to the accumulation of tau protein.
In experiments with Drosophila melanogaster, a fly widely used in biomedical research, scientists observed that the accumulation of tau protein in the retina led to neural degeneration, swelling in adjacent regions and the formation of abnormal structures. Curiously, these anomalies seemed to be associated with the hyperactivity of glia cells.
To understand the connection with glucose metabolism, the researchers used genetic engineering to increase the expression of a glucose transporter protein (GLUT) in glia cells. The result was surprising: even without reducing the presence of the tau protein, there was a significant decrease in inflammation and neuronal degeneration. This suggests that the accumulation of tau directly compromises the energy metabolism of these cells, affecting their ability to protect nervous tissue.
Based on these findings, the researchers propose that glucose metabolism in glial cells may represent a new and promising target for the treatment of neurodegenerative conditions. Since diseases such as Parkinson’s also involve inflammatory processes in the brain, the implications of this discovery go far beyond Alzheimer’s. New therapies based on this principle could revolutionize the fight against various neurological disorders, offering hope to millions of patients around the world.
The study was published in the journal Disease Models & Mechanisms.
