Scientists continue to unravel complex brain changes associated with the emergence and progression of Alzheimer's disease. It is likely that brain damage begins about ten years before memory and other cognitive problems become apparent. In this preclinical stage of Alzheimer's disease it seems that it proceeds asymptomatic, but toxic changes, however, occur.
Abnormal deposition of proteins form amyloid plaques (protein-polysaccharide complex) and tau-clubs (accumulation of protein) throughout the brain. Healthy neurons cease to function, they lose contact with other neurons and die. Symptoms of memory impairment, motivation, perception, speech, loss of interest progress.
Protein plaques have long been associated with Alzheimer's disease. And now, researchers from the University of Alberta, Burmonds University, USA, having conducted a new study on laboratory animals, proved the correctness of the theory that the protein-polysaccharide complex can slow down blood supply to the brain and damage its functionality.
"We are becoming more and more aware that brain blood brain damage increases the risk of Alzheimer's disease," said Dr. Eric Roberson, associate professor of neurology at the University Press Release. It is early to talk about the completeness of the study of the effects of amyloids, but researchers have the ability to scan and receive high-tech images that allow visualization of how protein clumps affect blood flow.
As Robertson explained, neuronal brain cells require additional glucose uptake to provide active activity. Neurons "demand" its receipt from other cells - astrocytes, which have a supply of nutrients and provide the movement of substances to the membrane of the neuron.
The "endfeet" of astrocytes is attached to the blood vessels and "give a command" when it is necessary to increase blood supply. Robertson's group wondered, "If the accumulation of amyloid plaque around the vessels can" strangle ", worsen the functionality of the endfeet, will neural signals be received about the increase in blood circulation?".
By scanning the brain of rats, researchers were able to determine: a truly vascular amyloid displaced endfeet of astrocytes and interfered with the normal regulation of blood vessels. In places where amyloid was not present, scientists saw a very clear and steady reaction "legs," and in other cases where the receipt of the request was complicated, the "answer" did not function. Thus, when vascular amyloid builds up around blood vessels, it "binds" the legs of astrocytes, creates a rigid exoskeleton (skeleton) that prevents the feeding of the blood regulation signal. The brain begins to fail.
This research is still at the beginning of the path, and experts still have no assurance that animal studies can be reproduced for humans. But it is important that gradually, step by step, scientists are selected to secrecy of the disease. Everyone, even a small success gives hope that its causes will be revealed, methods of treating this devastating disease will be found, or at least it will be possible to slow down.
The risk of Alzheimer's disease with age is increasing, and the US population is aging. It is estimated that more than 5 million Americans are ill with it. And as the cause of the death of elderly people, it ranks third after cardiovascular and oncological diseases.
Reference: In the world, according to WHO, there are up to 35,600,000 people. With Alzheimer's Disease. According to forecasts, by 2050 their number will triple.
November, 24, 2015 (HealthDayNews).