How does zinc regulate communication between brain cells?

In the average adult human body contains nearly 2 g of total zinc content, equivalent to half the amount of iron and 10 - 15 times the amount of copper. In the brain, zinc and iron are the two most concentrated metals. The highest levels of zinc are found in the hippocampus, as well as in the choroidal layer of the retina - an extension of the brain.
Zinc plays an important role in axial and synaptic transmission, which is essential for nucleic acid metabolism. Zinc deficiency can impair DNA, RNA and protein synthesis during brain development. For these reasons, zinc deficiency during pregnancy and lactation has been shown to be associated with many congenital abnormalities in the infant's nervous system.
Furthermore, children with insufficient zinc intake may experience reduced learning ability, lethargy and mental retardation. Hyperactive children may be deficient in zinc and vitamin B6, as well as in excess of lead and copper. Alcoholism, schizophrenia, Wilson's disease, and Pick's disease are brain disorders associated with zinc levels. Zinc has been used successfully to treat Wilson's disease, dermatitis, and specific types of schizophrenia.

Zinc is responsible for the DNA-binding ability of many transcription factors through the “zinc finger” (ZnF) protein. These proteins directly regulate gene expression, as well as communicate with RNA and facilitate protein interactions. The structure of ZnFs is centered around the zinc ion and gives the molecule the ability to form a finger-like structure, capable of tightly binding to specific DNA sequence domains.
In brain development, ZnF proteins not only play a role in embryogenesis and neurogenesis, but also in region-specific developmental selection. For example, zinc finger proteins are involved in the development of the olfactory region, neurons in the cerebellum, and the CA1 region of the hippocampus.
Other zinc-finger transcription factors are also involved in neuronal function, including the thyroid hormone receptor that plays a role in nerve cell growth and development, the retinoic acid receptor, and the retinoic acid receptor. Vitamin D is involved in neuronal differentiation.

Zinc transporters and binding proteins are key regulators of zinc homeostasis in neurons. The two protein zinc transporters ZnT and Zip function to regulate intracellular zinc levels, which are responsible for the accumulation of free zinc in the hippocampus and cerebral cortex. Metallothionein, a family of proteins with high binding affinity to zinc, not only plays a role in zinc homeostasis, but also in cell protection against oxidative stress.
Most of the zinc in the CNS is tightly bound to enzymes, but about 10% of the zinc in the brain is unbound and is therefore characterized as "free" zinc. The main function of free zinc is to modulate a variety of postsynaptic receptors.
Under pathological conditions, neurotoxic concentrations of free zinc can accumulate in neurons. Scientists agree that excess zinc accumulation leads to nerve cell damage. There are three main hypotheses currently being explored, that is, an excess of zinc causes excitability, induces oxidative stress, and impairs cellular energy generation. In fact, there is compelling evidence that all three of these mechanisms of zinc may work together to induce neuronal damage.
Children need to provide enough elemental zinc/day for them to eat well, reach the correct height and weight and exceed the standard. Zinc plays a role in affecting most biological processes taking place in the body, especially the breakdown of nucleic acids, proteins... Organs in the body when zinc deficiency can lead to a There are a number of diseases such as neurological disorders, irritability, etc. Therefore, parents need to learn about the role of zinc and guide them to appropriate zinc supplements for their children.
In addition to zinc, parents also need to supplement their children with other important vitamins and minerals such as lysine, chromium, B vitamins,... errands.
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References: pubmed.ncbi.nlm.nih.gov, ncbi.nlm.nih.gov