The loss of lipid molecules is directly related to neuronal degeneration

  Recently, in a research report published in the international journal PNAS, researchers from the University of Alabama and others found through research that reducing natural lipid levels is directly related to brain aging. This lipid molecule exists in the human body and plays an important role in many biochemical reactions in the body. Researchers of fat-like molecules have discovered that this kind of fat-like molecules can cause the death of dopamine-producing neurons. When dopamine-producing neurons die or malfunction, the body will experience symptoms related to Parkinson's disease.

  researcher Professor Guy Caldwell (Guy Caldwell) said that this study reveals the molecular mechanism of the lipid-lipid molecule type that causes neurological malformations. In this article, the researchers mainly studied the phosphatidylethanolamine lipid molecule called PE. Researchers have shown how low levels of PE can increase the content of α-octane, which is directly related to Parkinson's disease. At the same time, researchers found that ethanolamine (ETA) can also increase PE content. In order for it to function properly, the intracellular proteins must be folded correctly. Accidental folding can lead to diseases, and the accumulation of misfolded proteins in cells can cause abnormalities and death of the nervous system. In previous studies, researchers found that excessive alpha-synuclein is an intracellular disease that may interfere with the transport of proteins, dopamine and other substances to the desired site. This interruption of transportation can cause severe mechanical damage. Researchers used yeast and Caenorhabditis elegans as laboratory models and found that increased levels of ETA can reverse the nutrient transport problems described above. Supplementing with ETA keeps neurons healthy, so if PE content can be restored, it will survive longer.

  Finally, the researcher Coldwell said that maybe one day he will develop an additive that can inhibit the decline in PE levels, or a new drug that can activate the function of the enzyme that converts ETA into PE.