The data demonstrated that tryptamine plays a role in Alzheimer's disease as a substrate and inhibitor of the key enzymes. Tryptamine reveals increased electron flow in the late-onset Alzheimer's disease (LOAD) cells compared to controls. In our study, FDG PET utilization increased in whole brain (control 0.94 ± 0.11 versus tryptamine-treated 0.95 ± 0.18) but reduced in specific areas of the brain involved in neurodegeneration in tryptamine-treated mice compared to control mice. Glucose loading can increase tryptamine, while tryptamine can alter the glucose uptake by brain. Glucose transporter Glut1 is reduced in neurodegeneration and increased in cancer. The increased tryptamine metabolic activity revealed in the reprogrammed cells from Alzheimer's disease patients likely supported by the complex reaction mechanisms. The Pictet−Spengler reaction, which yields either a β-carboline or a tetrahydroquinoline product from an aromatic amine such as tryptamine and an aldehyde, is widely utilized in plant alkaloid biosynthesis. The tryptamine biotransformation can be instrumental for reducing concentrations of tryptamine in humans.
Elsevier, Tryptamine Microbiota-Deregulated Aminoacyl-tRNA Biosynthesis: A Conceptual Evolution of the Role of Microbiota Tryptamine in Human Diseases, 2024, pp 253-267
