阿兹海默病 z-bo 2020-09-16 364

　　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 destroyed, and speculated that this is the cause of the death of immature neurons in the course of the disease. However, people know very little about the exact cause of nerve cell death, and many attempts and approaches to find effective treatments have not achieved significant results. But what is certain is that a small protein fragment called "amyloid-beta" plays a key role in this process.

　　Mitochondria are composed of 1,500 different proteins. Most of these proteins need to be transferred to the mitochondria with the help of signal sequences-small protein extensions before they can function. Once the protein is inside 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 inhibits the function of mitochondria to clear these signal sequences, leading to the accumulation of immature proteins in mitochondria. These immature proteins are unstable and cannot function normally in the energy metabolism system. Researchers have shown that amyloid beta protein reduces energy production and accumulates more harmful substances in modified yeast cells. In the brain, the above mechanisms may lead to the death of nerve cells, further leading to brain atrophy and dementia.

　　Meisinger believes that the elucidation of key components in Alzheimer's disease will promote the development of new treatments and diagnostics in the future. The researchers concluded that the mitochondrial changes observed in nerve cells can also be detected in the blood cells of Alzheimer's disease patients, and are developing an Alzheimer's disease blood test to detect the accumulation of precursor proteins in mitochondria .