动物造模,帕金森氏症,痴呆症 z-bo 2020-09-10 399

　　In a study conducted on mice and zebrafish at the University of Cambridge, prescription drugs used to treat Cambridge hypertension showed the potential for Parkinson's disease, Huntington's disease and dementia. The common feature of these diseases (collectively called neurodegenerative diseases) is the accumulation of misfolded proteins. These proteins form "aggregates" that may cause irreversible damage to nerve cells in the brain, such as Huntington's protein in Huntington's disease and some dementias.

　　In healthy individuals, the body uses a mechanism to prevent the accumulation of this toxic substance. This mechanism is called autophagy or "self-eating" and involves cells like "peacocks" engulfing and breaking down substances. However, in neurodegenerative diseases, this mechanism is weakened and it is impossible to clear the protein accumulated in the brain. With the aging of the global population, more and more people are diagnosed with neurodegenerative diseases, and it is becoming more and more urgent to find effective drugs. However, there is currently no drug that can effectively induce autophagy in patients.

　　In addition to finding new drugs, scientists often seek to reuse existing drugs. Their advantage is that they have been proven safe for humans. If they can be proved to be effective for the target disease, the clinical use process will be faster. In a study published today in Nature Communications, scientists from the Institute of Dementia in the United Kingdom and the Cambridge Institute of Medicine at the University of Cambridge found that the hypertension drug ferredoxin may be a potential reuse candidate in mice. The epidemiological studies of the drug I have taken indicate that there may be a link between the drug and the reduced risk of Parkinson's disease, but now researchers suggest that it can induce autophagy in certain neurodegenerative diseases. Show that it is possible. The research team led by Professor David Rubinstein used genetically modified mice to express mutations that cause Huntington’s disease or certain Parkinson’s disease, while zebrafish mimic a type of dementia. The short life span and fast reproduction speed of mice make them a useful model for studying human diseases. Therefore, mice can study biological processes in many fields. Their biology and physiology share many important characteristics with humans, including similar nervous systems. Ferrodipine can effectively reduce the accumulation of mouse aggregates in mutant mice of Huntington's disease, Parkinson's disease and zebrafish dementia models. The treated animals also showed no signs of disease. Mouse studies usually use doses much higher than those known to be safe for humans. Professor Rubinstein and his colleagues have shown that mice with Parkinson's disease can produce beneficial effects at concentrations similar to those acceptable to humans. They did this by using a small pump under the mouse's skin to control the concentration.

　　"This is the first time we have noticed a study that shows that approved drugs can slow the accumulation of harmful proteins in the brains of mice, and the dose used can be found in the human body. You can simulate the concentration of the drug," Lu Professor Binstein said. "Therefore, we believe that the drug needs to be tested on patients because it can slow the progression of these potentially devastating diseases."

　　"But this is the first step. That's it. Humans produce the same effects as mice. We need to be cautious, but what I want to say is that we should be cautious and optimistic.