A new study from the University of California has shown that the cause of Alzheimer’s disease may be breakdowns in the tau protein, which affects the stability of the cellular architecture of neurons. With age, the body loses the ability to get rid of such proteins, and this leads to the destruction of brain cells.
Researchers note that 20% of people with amyloid plaques have no signs of dementia. This prompted them to think that this factor may not be decisive in the development of Alzheimer’s disease. Scientists have suggested that the fault is not beta-amyloid at all, but just tau protein. And they began to look for the smallest differences in protein structures in patients with amyloid plaques without signs of dementia and with them.
It turned out that since proteins are complex three-dimensional molecules, their properties may also depend on how they are located in space. One of the authors of the study, chemistry professor Ryan Julian compared this phenomenon to gloves: “If you try to put a glove for the right hand on the left, then you will not succeed. It’s the same in biology: molecules can work incorrectly if they are turned the wrong way.”
Normally, such broken proteins should be excreted from the body. This process is called autophagy. However, with age, it slows down, our body simply does not have time to clean out the broken proteins, they accumulate and form the same plaques and tangles.
At the same time, a recent study on mice showed that if autophagy is accelerated, the body again removes tau proteins from the body. And the symptoms of Alzheimer’s are receding. However, this method is still far from testing on humans.
Another solution is a direct effect on the tau protein. Here, the researchers went further and suggest using a peptide vaccine. The drug stimulates the production of antibodies that attack tau proteins. The drug has been successfully tested on rats. And they are already being tested on humans.
