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Model for the Transfer of Ca2+ from Outside the Cell to Inside the Cell with Bovine Milk Component to Justify Its Use as an Alzheimer’s Treatment

Received: 24 December 2019     Accepted: 30 December 2019     Published: 28 May 2020
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Abstract

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.

Published in Journal of Family Medicine and Health Care (Volume 6, Issue 2)
DOI 10.11648/j.jfmhc.20200602.15
Page(s) 56-61
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2020. Published by Science Publishing Group

Keywords

Bovine Milk, Mass Spectrometry, ms and ms2, Alzheimer’s Disease Treatment, Model of Ca2+ Transport

References
[1] Madson, M.; Method of testing for a milk trisaccharide patent US 8,993,226 B2 (2015).
[2] Christus, J.; Madson, M.; Possible Treatment for the arresting of progression of Parkinson’s disease from bovine milk, accepted for publication in World Journal of Food Science and Technology (2019).
[3] Ahlijanian, M.; Striessnig, J.; Caterall, W.; Phosphorylation of alpha-1-like subunit of an omega conotoxin-sensitive brain calcium channel by c-AMP dependent protein kinase and protein kinase Journal of Biological Chemistry 266 (30) 20192-20197 (1991).
[4] Curtis, B.; Caterall, W.; Phosphorylation of the calcium antagonist receptor of the voltage sensitive calcium channel by c-Amp dependent protein kinase Proceedings of the National Academy of Sciences USA 82 (8) 2528-2532 (1985).
[5] Goligorsky, M.; Colflesh, D.; Gordeiesko, D.; Moore, L.; Branching points of renal resistance arteries are enriched in L-tyr calcium channel and initiate vasoconstriction American Journal of Physiology-Renal Physiology 28 (2) F251-F257 (1995).
[6] Moni, Y.; Friedrich, T.; Kim, M.-S.; Mikami, A.; Nak, S.; Eva, P.; Primary structural and functional expression of a brain calcium channel Nature 350 (6317) 398 (1991).
[7] Hou, X.; Pedi, L.; Diver, M.; Long, S.; Crystal structure of the calcium channel Orai Science 3381 (6112) 1305-1313 (2012).
[8] Cataldi, M.; Perez-Reyes, E.; Tsien, R.; Differences in apparent size of low and high voltage activated Ca2+ channels Journal of Biological Chemistry 237 (48) 45959-45976 (2002).
[9] Bezrukov, S.; Kasianowicz, J.; The charge state of an ion channel controls neutral polymer pore European Biophysics Journal 26 (6) 471-476 (1997).
[10] Tsien, R.; Hess, P.; MecClesky, G.; Rosenberg, R.; Calcium channels: mechanism of selectivity, permeation and block, Annual Reviews of Biophysics and Biophysical-Chemistry 16 (1) 265-290 (1987).
[11] Pahlsson, P.; Shakin-Eshleman, S.; Spitaluik, S.; N-linked glycosylation of beta amyloid precursor protein Biochemical and Biophysical Research Communications 189 (3) 1667-1673 (1992).
[12] Christus, J.; Madson, M.; Treatment of Mycobacterium lepromatous with bovine milk World Journal of Food Science and Technology 2 (3) 55-61 (2018).
[13] Lewis, R.; Cahalan, M.; Potassium and calcium channels in lymphocytes Annual Reviews of Immunology 13 (1) 633-653 (1995).
[14] Di Pasquale, E.; Fantini, J.; Chaninian, M.; Maresca, M.; Taieb, N.; Altered ion channel formation by the Parkinson’s disease-linked E46K mutant of alpha synuclein is corrected by GM3 but not by GM1 Journal of Molecular Biology 397 (1) 202-2018 (2010).
[15] Angulo, E.; Noe’, V.; Casado, V.; Mallol, J.; Gomex-Isla, T.; Up-regulation of the Kv3.4 potassium channel subunit in early stages of Alzheimer’s disease Journal of Neurochemistry 9 (3) 549-557 (2004).
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    Jesus’ Christus, Michael Arden Madson. (2020). Model for the Transfer of Ca2+ from Outside the Cell to Inside the Cell with Bovine Milk Component to Justify Its Use as an Alzheimer’s Treatment. Journal of Family Medicine and Health Care, 6(2), 56-61. https://doi.org/10.11648/j.jfmhc.20200602.15

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    ACS Style

    Jesus’ Christus; Michael Arden Madson. Model for the Transfer of Ca2+ from Outside the Cell to Inside the Cell with Bovine Milk Component to Justify Its Use as an Alzheimer’s Treatment. J. Fam. Med. Health Care 2020, 6(2), 56-61. doi: 10.11648/j.jfmhc.20200602.15

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    AMA Style

    Jesus’ Christus, Michael Arden Madson. Model for the Transfer of Ca2+ from Outside the Cell to Inside the Cell with Bovine Milk Component to Justify Its Use as an Alzheimer’s Treatment. J Fam Med Health Care. 2020;6(2):56-61. doi: 10.11648/j.jfmhc.20200602.15

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  • @article{10.11648/j.jfmhc.20200602.15,
      author = {Jesus’ Christus and Michael Arden Madson},
      title = {Model for the Transfer of Ca2+ from Outside the Cell to Inside the Cell with Bovine Milk Component to Justify Its Use as an Alzheimer’s Treatment},
      journal = {Journal of Family Medicine and Health Care},
      volume = {6},
      number = {2},
      pages = {56-61},
      doi = {10.11648/j.jfmhc.20200602.15},
      url = {https://doi.org/10.11648/j.jfmhc.20200602.15},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.jfmhc.20200602.15},
      abstract = {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.},
     year = {2020}
    }
    

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    AB  - 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.
    VL  - 6
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Author Information
  • Research and Development, BioLogistics Limited Liability Company, Ames Iowa, United States of America

  • Research and Development, BioLogistics Limited Liability Company, Ames Iowa, United States of America

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