Blood vessels and Alzheimer's disease
If we talk about European medicine, such a connection was first described in a book by the English physician and anatomist Thomas Willis, published almost three and a half centuries ago, in 1672.
Now this pathology has a common name – vascular dementia. It can develop as a result of gradual narrowing of the arteries supplying blood to the brain, and due to acute disorders of cerebral circulation, for example, cerebral infarcts. World medical statistics recognize vascular brain lesions as the second most common cause of age-related dementia after Alzheimer's disease. However, in Russia, China and some other countries vascular dementia is even in the first place.
The causes of vascular dementia have long been established. With vascular damage, certain areas of the brain stop receiving the amount of oxygen they need for normal operation (it is worth recalling that the brain is a very energy–consuming organ). Oxygen starvation causes the death of nerve cells, which turns into one or another manifestation of dementia.
Nerve cells, as you know, die in Alzheimer's disease, only for a completely different reason. This disease leads to the accumulation of abnormal peptides in brain tissues, short protein fragments belonging to the beta-amyloid family. They are deposited on the surface of the neurons of the hippocampus, the most important part of the brain that contains the main centers for processing and fixing memories. Such deposits not only directly disrupt the normal functioning of neurons, but also trigger other pathological processes, the so-called amyloid cascade.
As a result, tangles of tangled strands of insoluble tau protein appear inside the neurons, which destroy them from the inside. These lesions gradually cover the hippocampus, and then spread to the cortex of the cerebral hemispheres. As a result, patients lose their memory and intellectual abilities, stop moving and talking, and eventually die from diseases of internal organs, most often from pneumonia.
Thus, in Alzheimer's disease, nerve cells die not due to oxygen deficiency, but due to exposure to toxic substances - first beta–amyloids, and then tau proteins. The key and still unresolved question is which failures in the work of our body give rise to the primary accumulation of beta-amylides. A great many hypotheses have been proposed to solve it, none of which has yet become generally accepted.
Now researchers from the Feinberg School of Medicine at Northwestern University, together with colleagues from Germany and Belgium, have unveiled another model that casts light on the occurrence of beta-amyloid deposits. Interestingly, it has something in common with the generally accepted explanation of vascular dementia. The main culprit is also brain starvation, only of a different kind. We are no longer talking about a lack of oxygen, but about a progressive shortage of grape sugar, glucose, which the brain receives along with blood.
Professor of cellular and molecular biology Robert Vassar and his co-authors argue that glucose starvation of the brain can provoke biochemical reactions, which ultimately result in the appearance of amyloid plaques. Their findings are presented in an article that appeared in the journal on December 26 Neuron.
According to this work, grape sugar deficiency by itself does not affect the birth of beta-amyloids in any way. However, it triggers a cascade of molecular transformations that lead to just such a result. Prolonged reduction of the glucose diet of the brain changes the molecules of the protein elf2-alpha, which is produced by nerve cells. These molecules undergo phosphorylation, in other words, they attach phosphoric acid residues. Phosphorylated protein elf2-alpha increases the synthesis of the enzyme BACE1, which is also called beta-secretase. This enzyme cuts APP protein molecules into parts, which serve as raw materials for the manufacture of beta-amyloids. Thus, pathological events develop along a chain that begins with glucose starvation and ends with the appearance of neurotoxic amyloid plaques.
A new model of Alzheimer's disease puts its origin in direct connection with the sclerosis of blood vessels feeding the brain. When the lumen of these arteries is closed by fatty deposits, the brain begins to receive less blood and, consequently, less glucose. It turns out that arteriosclerosis is not only responsible for vascular dementia, but also provokes Alzheimer's disease. If this is the case, then both diseases require the same protective measures.
Methods of preventing sclerosis are well known – it is physical activity, lowering cholesterol levels and normalization of blood pressure. If the disease has already begun, but has not yet caused serious necrotic changes in the brain, vasodilators help. According to Professor Vassar, such a strategy simultaneously reduces the risk of both vascular dementia and Alzheimer's disease.
Portal "Eternal youth" www.vechnayamolodost.ru29.12.2008