Scientists have found a way to stop the development of Alzheimer's and Parkinson's diseases
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- Scientists have found a way to stop the development of Alzheimer's and Parkinson's diseases
Scientists from Baylor College of Medicine in the USA have identified a new approach to the treatment of Alzheimer's and Parkinson's diseases based on the use of tubulin protein to prevent the formation of toxic aggregates in the brain. This was reported on June 21 by Science Daily (SD) magazine.
Experts have found that tubulin, which serves as a building block for microtubules inside neurons, is able to prevent tau proteins and alpha-synuclein from forming dangerous clusters. Instead of sticking together and damaging cells, under the influence of tubulin, these proteins return to their normal functions of maintaining cell structure.
Lathan Lucas, the first author of the study and a researcher in the field of biochemistry and molecular pharmacology in the laboratory of Dr. Allan Ferreon
Tau proteins and alpha-synuclein are well known for their role in neurodegenerative diseases such as Alzheimer's and Parkinson's disease. In these conditions, these proteins may not fold properly, stick together, and form harmful aggregates that damage neurons and contribute to memory loss, movement problems, and other symptoms.
According to the scientist, tau and alpha-synuclein are important for the health of neurons, as they help to stabilize microtubules— the internal "transport pathways" of cells. Their transformation processes take place inside the droplets of protein condensates. Previously, scientists tried to completely prevent the formation of such droplets in order to stop the disease, but this could disrupt healthy brain activity.
During the experiments, the researchers found that with low levels of tubulin, which is often observed in patients with Alzheimer's disease, microtubules become smaller, which allows proteins to form toxic groups. However, the presence of a sufficient amount of tubulin redirects their activity in a productive direction.
Allan Ferreon, co-author of the study and Associate Professor of Biochemistry and Molecular Pharmacology
Our results significantly change the role of tubulin in neurodegeneration, turning it from a passive participant in the process into an active defender against toxic protein aggregation," said Ferreon. "Increasing the tubulin pool rather than blocking droplet formation can restrain toxic aggregation while preserving the beneficial functions of Tau protein and alpha-synuclein, suggesting a potential selective therapeutic strategy.
The authors believe that increasing tubulin reserves in cells may become a new selective therapeutic strategy. According to the study, this will help to curb the development of pathologies, while preserving the natural functions of proteins necessary for the normal functioning of the brain.
On June 18, Science Daily reported the discovery of a hidden mechanism for triggering Alzheimer's disease. According to scientists, the disease can begin with the displacement of tau protein from the microtubules of neurons under the influence of beta-amyloid. The researchers emphasized that it is precisely the oncompetitive displacement of tau that triggers the cascade of damage: intracellular transport is disrupted, and tau begins to stick together and move into atypical areas of the neuron.
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