阿兹海默病相关肽破坏线粒体 z-bo 2020-10-19 298

　　A research team led by Dr. Chris Meisinger of the Institute of Biochemistry and Molecular Biology at the University of Freiburg in Germany discovered the mechanism by which Alzheimer's disease destroys mitochondria. In recent years, researchers have learned that the energy supply of brain cells in Alzheimer's disease patients is disturbed, and speculated that this is the cause of the death of immature neurons during the disease.

　　However, people do not know the exact cause of nerve cell death, and many attempts and methods to find effective treatments have not achieved obvious results. But what is certain is that small protein fragments called "amyloid beta" play an important role in this process. Mitochondria are composed of 1,500 proteins. Most of these proteins need to be transferred to the mitochondria via signal transduction sequences-small protein extensions before they can work. When the protein enters the mitochondria, the signal sequence is cleared. Meisinger's research team used model organisms and brain samples from Alzheimer's disease patients and found that amyloid beta protein can inhibit mitochondrial function, clear these signal sequences, and accumulate immature proteins in mitochondria.

　　These immature proteins are unstable and cannot function normally in the energy metabolism system. Researchers have demonstrated the process by which amyloid beta reduces energy production and accumulates more harmful substances in modified yeast cells. In the brain, the above mechanisms can cause nerve cell death as well as brain atrophy and dementia.

　　Meisinger believes that elucidating the key components of Alzheimer's disease will help develop new treatments and diagnostics in the future. The researchers speculate that the mitochondrial changes observed in nerve cells can also be detected in the blood cells of Alzheimer's disease patients, and the Alzheimer's disease blood test is being developed to detect the accumulation of precursor proteins in mitochondria.