Alzheimer's Vaccine
Scientists from the USA have created a gene therapy that suppresses Alzheimer's disease
Geneticists from Texas has created and tested a gene therapy that forces the immune system to fight the accumulation of protein "garbage" in brain cells during the development of Alzheimer's disease. The results of the first experiments on mice were presented in the journal Alzheimer's Research and Therapy.
"Our study is a natural result of ten years of experiments and observations that have repeatedly shown that this vaccine is safe for animal health and that it really helps the body fight the cause of Alzheimer's disease. I believe that we are close to the start of clinical trials on volunteers," he said Roger Rosenberg from the University of Texas at Dallas (USA).
At the top: a section of the hippocampus of a mouse that received a DNA vaccine, at the bottom - mice from the control group. Amyloid plaques are highlighted in red, clusters of tau protein are highlighted in green. Figure from the press release of UT Southwestern DNA vaccine reduces both toxic proteins linked to Alzheimer's – VM.
A spark of consciousness
It is believed that Alzheimer's disease is caused by the accumulation of a pathogenic substance inside neurons, the beta-amyloid protein. It is formed from the "scraps" of the APP protein, which is involved in the processes of repairing damaged neurons and forming connections between them. Violations in the processing of molecules of this protein lead to the appearance of beta-amyloid plaques and the destruction of nerve cells.
In the last two years, biologists have made significant progress in understanding what causes this disease and what it is. For example, scientists have recently found out that Alzheimer's disease can be transmitted from one patient to another, and also found that beta-amyloid plaques can be an important part of the innate immune system.
These discoveries, as Rosenberg notes, have long made scientists think about whether it is possible to prevent the development of Alzheimer's disease by "disabling" certain genes in the neurons themselves or by increasing the activity of other DNA sites in immune cells responsible for processing protein debris.
The first attempts to carry out such a procedure on volunteers ended disastrously – every tenth patient developed encephalitis, as the immune system began to attack not only beta-amyloid plaques, but also healthy neurons. This forced biologists to switch to other methods of fighting the disease, including synthetic antibodies, which later turned out to be extremely ineffective.
Rosenberg and his team did not abandon this idea. Over the past ten years, they have continued to change the "stuffing" of such a vaccine, trying to find a variant that would not cause inflammation and at the same time effectively combat the accumulation of protein "garbage".
Simulator for immunity
As a rule, all past variants of such gene therapy were based on fragments of beta-amyloid and other proteins that cause Alzheimer's disease. Texas molecular biologists used a radically different approach – they created a retrovirus that forces skin cells to produce copies of beta-amyloid "building blocks", the so-called alpha-beta-42 protein, combine its molecules into triples and throw them into the bloodstream.
When a sufficiently large number of them accumulate, immune cells notice these chains and begin to attack them, producing antibodies capable of attaching to beta-amyloid "blanks" and marking them for destruction by macrophages and "killer" cells.
Such an approach, as shown by experiments on mice predisposed to the development of the "human" version of Alzheimer's disease, simultaneously does not cause encephalitis and reduces the concentration of beta-amyloid in neurons by about 40%. This delays the onset of senile dementia by several months, which is equivalent to ten years of life for a person.
In addition, vaccination led to another useful but unexpected consequence. The immune system began to destroy not only the APP protein clippings, but also to fight against accumulations of tau protein, another possible "culprit" for the development of Alzheimer's disease Its concentration in the neurons of mice decreased by almost 1.5 times.
Such an approach, as Rosenberg admits, can only help those people in whose brain large accumulations of beta-amyloid have not yet appeared – the vaccine prevents their appearance, but does not force the immune system to destroy already formed protein plaques. Scientists hope that further experiments will help them solve this problem.
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