Model for the Transfer of Ca<sup>2+</sup> from Outside the Cell to Inside the Cell with Bovine Milk Component to Justify Its Use as an Alzheimer’s Treatment

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A model of Ca²⁺ channel function rescue via treatment with a milk component is suggested. This molecule’s structure is shown by ms and ms² evidence, from an NH₄⁺ form cation exchange cartridge effluent. This model includes the participation of phospho-protein in the shuttling of Ca²⁺ through a path of anionic moieties from an N-acetamido neuraminyl group to a sulfate group. It suggests the rescue of Ca²⁺ function with bovine milk oligosaccharide dipeptide component in the treatment of Alzheimer’s disease. Ca²⁺ is proposed to end at a sulfo-tyrosine then extended inside the cell internally. The rolling of the Ca²⁺ from N-acetamido neuraminyl group is thought to be due to the interaction of doubly charged calcium cation with a series of negatively charged ions, sequestered and transported via the molecule from bovine milk oligosaccharide dipeptide. Excess K⁺ availability in early Alzheimer’s disease is known and may cause interference in the transport of Ca²⁺ in this disease. This model predicts that K⁺ can seize the Ca²⁺ channel rescue because it has no excess charge driving it forward to the end of the bovine milk component. The location of phosphate on the galactosyl group of the molecule from which the drawn structures is obtained by ms and ms², is described here. A pathway for the Ca²⁺ transfer along this structure is depicted here. The goal is to provide a rationale for using bovine milk as a low cost treatment for Alzheimer’s disease which would allow treatment of this disease for people in the third world who cannot afford high cost treatments.