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Hemoglobin is made up of Alpha globin and Beta globin, and thalassemia occurs when there is a mutation in a gene that helps control the production of one of these proteins. There are two main types of thalassemia: alpha-thalassemia and beta-thalassemia, each named for the respective protein that the mutated gene affects and include two forms, thalassemia major and thalassemia minor. The mutations that cause thalassemia disrupt normal production of hemoglobin, causing low hemoglobin levels and red blood cell destruction, causing anemia. There are four genes involved with the production of the alpha hemoglobin chain. In alpha-thalassemia, when one inherits one mutated gene, he or she will show no signs or symptoms of thalassemia, but he or she is a carrier and can pass it on to his or her children.
The Tau protein hypothesis states that a hyperphosphorylation of Tau inhibits its function of stabilizing the micro tubules in the brain thereby destroying its function of neuron transport. The Tau protein is a micro tubule associated protein with a high solubility that consists of 758 amino acid residues.. This protein has six active domains in humans out of which three have three binding domains and the other three have four of them. Under normal conditions, the protein gets phosphorylated on at least 30 of the potential 79 serine/threonine phosphorylating sites. This phosphorylated Tau protein then interacts with tubulin and effects a stabilization of the microtubules by causing the tubulin to interact with it.