Copper-containing enzymes perform fundamental functions by activating dioxygen (O2) and therefore allowing chemical energy-transfer for aerobic metabolism. The copper-dependence of O2 transport, metabolism and production of signalling molecules are supported by molecular systems that regulate and preserve tightly-bound static and weakly-bound dynamic cellular copper pools. Disruption of the reducing intracellular environment, characterized by glutathione shortage and ambient Cu(II) abundance drives oxidative stress and interferes with the bidirectional, copper-dependent communication between neurons and astrocytes, eventually leading to various brain disease forms. A deeper understanding of of the regulatory effects of copper on neuro-glia coupling via polyamine metabolism may reveal novel copper signalling functions and new directions for therapeutic intervention in brain disorders associated with aberrant copper metabolism.
Kardos, J., Héja, L., Simon, Á., Jablonkai, I., Kovács, R., & Jemnitz, K. (2018, October 22). Copper signalling: Causes and consequences 06 Biological Sciences 0601 Biochemistry and Cell Biology. Cell Communication and Signaling. BioMed Central Ltd. https://doi.org/10.1186/s12964-018-0277-3