神经元变性,质分子缺失 z-bo 2020-12-14 295

　　Recently, in a research report published in the international journal PNAS, researchers from the University of Alabama and others found through research that the reduction of a natural lipid level is directly related to the aging of the brain. This lipid molecule is A fat-like molecule that exists in the organism and plays an important role in many biochemical reactions in the body. Researchers have found that this fat-like molecule can trigger the death of dopamine-producing neurons. When dopamine-producing neurons die or function When the disorder occurs, it will cause the body to have symptoms related to Parkinson's disease. Researcher Professor Guy Caldwell said that in this study, we revealed the molecular mechanism of a type of fatty lipid molecule that triggers neuronal deformation; in the article, the researcher mainly studied a phosphatidylethanolamine lipid molecule called PE. The authors revealed how low levels of PE can increase the level of alpha-synuclein, which is directly related to Parkinson's disease. At the same time, the researchers also found that ethanolamine (ETA) can also increase the level of PE.

　　In order to function normally, the protein in the cell must be folded correctly. Once it is misfolded, it will cause disease, and the accumulation of misfolded protein in the cell will cause neuron abnormality and even death. In previous studies, researchers found that excessive alpha-synuclein may be an intracellular obstacle, inhibiting the transport of proteins, dopamine and other substances to the required parts. Such transport disruption can lead to serious mechanical obstacles. Using yeast and Caenorhabditis elegans as laboratory models, the researchers found that increasing the level of ETA can reverse the above-mentioned nutrient transport problem, and the supplementation of ETA also indirectly revealed that if the content of PE can be restored, it will cause nerves. Yuan maintains a healthy state and thus survives longer.

　　 Finally, the researcher Caldwell said that perhaps one day we will develop an additive that can inhibit the decline in PE levels, or develop a new type of drug to activate the function of enzymes that reverse ETA to PE.