The Fundamental Neurobiological Mechanism of the Oxidative Stress-Related Deamidation Reaction in the 4E-BP2 Protein

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4E-BP2 deamidation significantly alters protein production in the brain and nervous system. It maintains the balance of protein production required for a healthy nervous system. Any imbalance in protein production in the brain and nervous system causes all neurodegenerative diseases. Discovering what causes 4E-BP2 deamidation only in neurons will make it possible to control this balance of protein production and cure neurodegenerative diseases such as memory loss, Alzheimer's, and Parkinson's. Alzheimer’s disease is caused by the absence of 4E-BP2 protein in the brain's neurons. This protein undergoes deamidation spontaneously only in the neurons and, in this way, controls the production of proteins in the neurons. This, in turn, determines whether or not Alzheimer’s and Parkinson’s disease start or progress. The purpose of this work is to discover the neurobiological mechanism that causes the deamidation reaction in the 4E-BP2 protein by performing immunoblotting in the retinal ganglia, the optic nerve, the dorsal root ganglia, the sciatic nerve, and the whole brain, extracted via dissection from 2-month-old, Wild-type male mice. The results showed that deamidation mainly occurs in the axons or axon-enriched regions of the optic nerve, the whole brain, and the sciatic nerve, confirming conclusively that axons are the critical factors behind the neurobiological mechanism of 4E-BP2 protein deamidation. The results confirm that they are also the reason why 4E-BP2 deamidation occurs only in neural tissue.

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