Scientists have identified a hidden mechanism for triggering Alzheimer's disease
Researchers have proposed a new explanation for the mechanism of development of Alzheimer's disease. The disease can begin with the displacement of tau protein from the microtubules of neurons under the influence of amyloid beta. This was reported on June 18 in the journal Science Daily.
"Our work shows that beta-amyloid and tau protein compete for the same binding sites on microtubules, and that a-beta-amyloid can interfere with the proper functioning of tau protein," said Ryan Julian, a professor of chemistry at the University of California, Los Angeles, and the head of the study.
Tau protein normally stabilizes microtubules, the intracellular transport routes of neurons. The scientists drew attention to the structural similarity of the part of tau that attaches to microtubules with the amyloid beta molecule. Experiments with a fluorescent label have shown that both proteins bind to microtubules with the same strength.
According to the authors, it is precisely this competitive displacement of tau that triggers a cascade of damage: intracellular transport is disrupted, and tau begins to stick together and move into atypical areas of the neuron. The new model explains why numerous clinical trials of drugs aimed at removing amyloid plaques from outside cells have not had a significant effect: the key process unfolds inside neurons. According to the hypothesis, the accumulation of amyloid beta inside cells accelerates with age as the effectiveness of autophagy, the cellular "cleaning" system, decreases.
Researchers from the Swiss Higher Technical School of Zurich on June 9 discovered that the accumulation of an inactive form of the GRK2 protein may be a key factor in the development of Alzheimer's disease. The study showed that the GRK2 protein, which normally supports the functioning of nerve cells and the heart, begins to accumulate in the brains of people with dementia when it becomes inactive.
Переведено сервисом «Яндекс Переводчик»
