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Now, scientists at the RIKEN Brain Research Center in Japan have discovered a protein called CAPON, which is associated with Alzheimer's disease (AD), which may promote a link between amyloid plaques and Tau pathological manifestations, which interact to cause brain cell death and dementia. The findings were published in nature-newsletter.
Alzheimer's disease is a complex disease known as amyloid protein-β and nerve fiber entanglement, also known as the "Tau pathological manifestation" of brain tissue.
the CAPON protein gene is at risk for other mental illnesses because Alzheimer's can induce other mental illnesses, and the team speculates that the CAPON protein may be linked to these symptoms. In fact, when they studied an experimental mouse with Alzheimer's disease, they found that capon protein had accumulated in their sea mass. In addition, their study showed that the more CAPON protein accumulates, the more pathological manifestations β amyloid protein-protein.
using the new App/MAPT dual gene implantation process, they bred mice to form another type of Alzheimer's disease, when researchers implanted the CAPON protein gene into the mouse brain, resulting in the over-expression of the CAPON protein. These experimental mice showed significant neurodegenerative diseases, Tau pathology, and sea mass atrophy.
, study author and author of the study, Shoko Hashimoto of the RIKEN Brain Research Center, said: "This means that the accumulation of CAPON protein increases the pathological manifestations of Alzheimer's disease. Although cell death caused by the CAPON protein can occur in many different ways, we can determine that the protein is a promoter between neuroinstitive and Tau pathological manifestations. This is the first mouse experiment using the App/MAPT dual gene implant, which is designed to have a human-like MAPT gene and an App gene that contains disease-caused mutations. The
team concluded that the lack of CAPON protein could have the opposite effect. In this test, the researchers eliminated the CAPON protein from another type of Alzheimer's disease, which significantly increased Tau pathological performance.
found that insufficient CAPON protein led to lower pathological performance of Tau, producing fewer amyloid proteins - β, fewer neurodegenerative diseases, and less brain atrophy. Therefore, reducing the CAPON protein index in mice with Alzheimer's disease will effectively reduce the physiological symptoms of Alzheimer's disease. (Source: Liu Yanyang, China Science Journal)
relevant paper information: