阿尔兹海默症 z-bo 2020-10-08 370

　　Researchers at Massachusetts General Hospital (MGH) found that the spread of the Alzheimer's disease-related protein tau into the brain is caused by the aging of the brain itself, not by the length of time the neurons express the protein.

　　The lead author of the paper, Massachusetts General Hospital, neurodegenerative disease Alzheimer’s, said: "The fact that sporadic Alzheimer’s disease and other neurodegenerative diseases are related to aging is clear, but the reasons are not yet clear. Clear." said Dr. Bradley Hyman, director of the Center for Disease Research. "Existing animal models, such as mice with mutations at birth, will accumulate tangles, including tau, as they age. Therefore, it may be the age of the animal that causes this, or the brain has increased tau. Nothing. Distinguish lifetime exposure. Pathological effects. "In order to overcome this limitation, Heimann's research team has been able to induce pathological or normal expression of human tau protein. We have developed a gene vector. The vector also uses fluorescent labels on neurons that directly express tau protein to distinguish them from neurons that spread tau protein to neighboring cells. This may reflect the pathology of Alzheimer's disease tau protein in the brain. expansion. The researchers first confirmed that the introduction of the vector into the visceral cortex (EC) is the first mouse brain structure associated with Alzheimer's disease in tau pathology, which can induce human tau expression and transmission.

　　Researchers then used the vector. Induces ECs to express misfolded pathological or non-mutant tau, but the spread of tau between adjacent cells does not require the presence of misfolded proteins, but it will be mistakenly found to spread faster in the presence of folded tau proteins. The range will be greater. The researchers compared the effect of tau-induced pathological morphology on the brains of young mice and mice. The researchers found that in the area adjacent to the EC, the pathological protein of old mice was about twice that of young mice. It spreads at a speed of 15%, and found that older mice will accumulate more misfolded tau. However, when the vector is introduced into striatal neurons, it has a different effect of inducing tau protein expression, and striatal neurons are rarely affected in Alzheimer's disease.

　　Wegman said: "Age is the highest non-genetic risk factor for Alzheimer's disease, but so far, it has not been tested whether age alone makes the brain susceptible to pathological changes and the spread of tau protein. Other issues that need to be studied are those Make the aging brain a better platform for the spread of tau protein and identify the vulnerability of certain areas of the brain."

　　Heyman, a professor of neurology at Harvard Medical School, added: “I want to learn more about how the physiological mechanisms of brain aging promote the development of Alzheimer’s disease. This will help improve the prevention and treatment of many divine allergic diseases. "