Scientists have reviewed the causes of Alzheimer's disease

Alzheimer's disease has been associated for decades with the accumulation of toxic proteins in the brain. However, today more and more research is forcing scientists to reconsider this theory. New data indicate that changes can begin much earlier — in the circulatory system and the protective barrier of the brain. What made the researchers change their view of one of the most common neurodegenerative diseases is in the Izvestia article.

Amyloid no longer looks like the main culprit.

Alzheimer's disease remains the most common cause of dementia. For many years, the so-called amyloid hypothesis has been the basis of research. According to her, the disease begins with the accumulation of beta-amyloid proteins in the brain, which form characteristic plaques. Later, they are joined by another pathological protein, tau, which forms neurofibrillary tangles. It was believed that these processes gradually destroy neurons and lead to deterioration of memory and other cognitive functions.

That is why most of the new drugs were aimed at removing amyloid plaques. However, the results were mixed. Despite a significant decrease in the amount of amyloid, the disease continued to progress, and the improvement in patients' condition remained limited.

Another question arose after amyloid plaques were found in some elderly people without signs of dementia. This made scientists think: perhaps the protein deposits themselves are not the root cause of the disease, but only a consequence of earlier processes. The work was published in the journal Medical Xpress.

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The trace of the disease increasingly leads to blood vessels

More and more studies indicate that the vascular system of the brain may play an important role in the development of the disease. Scientists pay special attention to the blood—brain barrier, a complex system that separates blood flow from brain tissue and controls the penetration of various substances.

If this barrier is damaged, its protective properties decrease. As a result, cells and molecules that normally shouldn't enter the brain tissue can enter. According to the authors of the article, it is a violation of the vascular system that can trigger inflammatory processes that contribute to the development of neurodegeneration.

This hypothesis is in good agreement with the long-known risk factors for Alzheimer's disease. High blood pressure, type 2 diabetes, obesity, smoking, high cholesterol and lack of physical activity simultaneously worsen the condition of blood vessels and increase the likelihood of developing dementia.

The authors recall that one of the largest reviews in recent years, published in The Lancet, showed that up to 45% of dementia cases are potentially associated with modifiable risk factors, a significant part of which relate specifically to vascular health.

What made scientists reconsider the old theory?

According to the researchers, the main problem with the amyloid hypothesis is not that it is wrong, but that it can only describe one of the stages of the disease. The authors offer a simple analogy: if rust appears on a car, it is useless to endlessly clean it off without eliminating the cause of corrosion. Similarly, removal of amyloid plaques will not necessarily stop the disease if the pathological process started much earlier.

Therefore, today the attention of scientists is gradually shifting towards the search for the earliest changes that occur even before the onset of symptoms and the formation of large amounts of amyloid deposits. Biomarkers are becoming one of the most promising areas, making it possible to detect disorders in the functioning of blood vessels and the blood-brain barrier long before the clinical manifestations of the disease.

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New clues found in blood

One of the arguments in favor of the new hypothesis was studies showing signs of a violation of the integrity of the blood-brain barrier. So, scientists have discovered that some blood cells are able to enter the central nervous system, a phenomenon that normally practically does not occur. According to the authors of the article, such changes correlate simultaneously with the deterioration of cognitive functions and the presence of amyloid plaques.

In addition, new vascular biomarkers are emerging that make it possible to assess the state of the blood-brain barrier in the early stages of the disease. The researchers hope that they will help to understand what changes occur in the brain decades before the first symptoms of dementia appear.

What does this change for future treatment?

The authors emphasize that we are not talking about abandoning the amyloid hypothesis. Rather, the new findings allow us to consider Alzheimer's disease as a much more complex disease that simultaneously involves neurons, the immune system, blood vessels, and the blood-brain barrier.

If this concept is confirmed, not only treatment can change, but also the approach to prevention. Instead of fighting exclusively with already formed amyloid plaques, scientists expect to learn how to detect the disease much earlier — at the stage of the first vascular disorders, when the pathological process can still be slowed down. So far, this model remains a scientific hypothesis, but today it is becoming one of the most actively developing areas of research into Alzheimer's disease.