Release date: 2017-11-09 In recent years, major pharmaceutical companies have been horrible in the development of drugs for Alzheimer's disease, and many drugs that have invested billions of dollars have failed. A year ago, Lilly’s drug, solanezumab, which treats Alzheimer's disease, also failed unfortunately in a phase III clinical trial. It is reported that this drug is more than a billion dollars (1). However, compared to the difficult development of Alzheimer's disease drug research, scientists in the basic research on Alzheimer's disease can be described as triumphant, refreshing our perception again and again. This is not the case, the first two months of the singularity cake just wrote an article, saying that the "culprit" of Alzheimer's disease beta amyloid may have been an antibacterial fighter in the brain. Now, scientists have discovered that beta amyloid, produced by other tissues in the body, can also enter the brain and induce Alzheimer's disease. Recently, Professor Wang Yanjiang from the Department of Neurology, Daping Hospital, Chongqing Third Military Medical University, and Professor Song Weihong from the University of British Columbia in Canada, confirmed for the first time that beta amyloid in peripheral blood can also cross the blood-brain barrier and deposit in the brain. Plaque formation, resulting in a series of symptoms of Alzheimer's disease. This finding was published in the journal Molecular Psychiatry (2). Professor Wang Yanjiang Although the etiology of Alzheimer's disease is still unclear, the deposition of amyloid beta in the brain parenchyma and blood vessel walls has long been considered a hallmark of Alzheimer's disease (3). At the same time, it has long been believed that the amyloid beta protein deposited in the brain of Alzheimer's disease patients is produced by neurons in the brain. In recent years, a series of studies have found that beta amyloid is not only produced in the brain, but also many other tissue cells outside our brain can produce a large amount of amyloid beta (4), for example, platelets, skin fibroblasts, Skeletal muscles and more. However, it is unclear whether the beta amyloid produced by these peripheral tissues can break through the blood-brain barrier and deposit in the brain to promote the development of Alzheimer's disease. In order to understand these issues, the researchers started this experiment. First, they need to determine if beta amyloid in the blood can enter the brain. Fluorescently labeled human beta amyloid was injected intravenously into mice. The researchers found that after 2 hours, the presence of amyloid beta was detected in the mouse brain. This means that beta amyloid in peripheral tissues can enter the brain. However, after 4 hours, these beta amyloid proteins were cleared again. Since these beta amyloid proteins are cleared shortly after entering the mouse brain, can the beta amyloid produced by peripheral tissues deposit in the brain and induce Alzheimer's disease? The researchers believe that as the age increases, the blood-brain barrier of the mouse will gradually weaken, so the beta amyloid protein entering the brain may become more. At the same time, getting older is often accompanied by a decrease in the ability to clear amyloid beta. Eventually, beta amyloid produced by surrounding tissues is likely to deposit in the brain and induce Alzheimer's disease (5). To test this idea, the researchers used a heterobiosis mouse model to suture two litters of mice at 10 months to allow blood exchange and normal life. One of the mice carries a humanized amyloid beta gene that can express beta amyloid in large amounts. The other is just a normal wild mouse. Subsequent observations of wild mice revealed that the levels of beta amyloid in the blood of the two mice were the same after surgery. At the same time, by Western blot analysis, the researchers found that humanized amyloid beta was deposited in the brain tissue of wild mice 4 months after surgery. Moreover, by using humanized and murine amyloid-specific antibodies, the researchers also determined that the beta amyloid in the brain of wild mice is primarily a humanized amyloid beta protein. In addition, at 12 months after surgery, the researchers also observed that not only a large amount of beta amyloid protein was accumulated in the brain of wild mice, but also a series of symptoms of Alzheimer's disease. Including, high phosphorylation of tau protein, neurodegeneration, neuroinflammation and the like. More importantly, the researchers also observed severe damage to the hippocampus associated with memory and brain vascular lesions in the mouse brain. Heterogeneous symbiotic mice Similarly, the researchers also demonstrated that at this time, almost all of the amyloid beta protein in the brain of wild mice is derived from the amyloid beta protein produced in the blood of transgenic mice. All of these phenomena indicate that beta amyloid in other parts of the body can also be deposited in the brain through the blood barrier to the brain barrier, which induces Alzheimer's disease in mice. Overall, this experiment demonstrates for the first time that beta amyloid produced by peripheral tissues can cross the blood-brain barrier of mice and deposit in the brain to induce Alzheimer's disease. Because many tissues outside the human brain also produce beta amyloid, and as we age, our brain barriers become weaker and our brain's ability to clear Alzheimer's disease is reduced (6). This means that the amyloid-producing protein produced by peripheral tissues is likely to be deposited in the brain, and accelerates the progression of Alzheimer's disease in humans based on the beta-amyloid protein produced by the brain itself. Therefore, in the future, when we are treating Alzheimer's disease, we may need to remove the peripheral amyloid beta. Source: Singularity Network (micro signal geekheal_com) Fresh Half Shell Mussel Meat,Half Shell Mussel Meat,Frozen Cooked Mussel Meat,Frozen Mussel Shengsi Huali Aquatic Products Co.,Ltd , https://www.mytilus-edulis.com