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A Model of the Role of Cholesterol in the Development of Alzheimer’s Disease

  • Gizelle Kupac Vianna
  • Artur E. Reis
  • Luís Alfredo V. de Carvalho
  • Roseli S. Wedemann
Part of the Lecture Notes in Computer Science book series (LNCS, volume 3991)

Abstract

We present a mathematical-computational model of the development of Alzheimer’s disease, based on the assumption that cholesterol plays a key role in the formation of neuropathological lesions that characterize the disease: the senile amyloid plaques and neurofibrillary tangles. The final model, conceived as a system of equations, was simulated by a computer program.

Keywords

High Cholesterol Diet Neuropathological Lesion Neuropathological Alteration Dietary Lipid Composition Cholesterol Domain 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

References

  1. 1.
    Howland, D., et al.: Modulation of Secreted β-Amyloid Precursor Protein and Amyloid β-Peptide in Brain by Cholesterol. The J. of Biological Chemistry 273(26), 16576–16582 (1998)CrossRefGoogle Scholar
  2. 2.
    Illenberger, S., et al.: The Endogenous and Cell Cycle-Dependent Phosphorylation of Tau Protein in Living Cells: Implications for Alzheimer’s Disease. Molecular Biology of the Cell 9, 1495–1512 (1998)Google Scholar
  3. 3.
    Ji, S.R., Wu, Y., Sui, S.F.: Cholesterol is an Important Factor Affecting the Membrane Insertion of β-Amyloid Peptide (Aβ-40), which Potentially Inhibit the Fibril Formation. The J. of Biological Chem. 277(8), 6273–6279 (2001)CrossRefGoogle Scholar
  4. 4.
    Murray, R.K.: The Biochemical Basis of Some Neuropsychiatry Disorders. In: Murray, R.K., Granner, D.K., Mayers, P.A., et al. (eds.) Harpers Biochemistry, Int. Edition, 23th edn., pp. 750–752. Prentice-Hall, Englewood Cliffs (1993)Google Scholar
  5. 5.
    Pappolla, M.A., Smith, M.A., et al.: Cholesterol, Oxidative Stress, and Alzheimer’s Disease: Expanding the Horizons of Pathogenesis. In: Smith, M.A., Perry, G. (eds.) Serial Review: Causes and Consequences of Oxidative Stress in Alzheimer’s Disease. Free Radical Biology and Medicine, vol. 33(2), pp. 173–181. Elsevier, Amsterdam (2002)Google Scholar
  6. 6.
    Rissman, R.A., Poon, W.W., Jones, M.B., et al.: Caspase-cleavage of Tau is an early event in Alzheimer’s disease tangle pathology. The J. of Clinical Investigation 114(1), 121–130 (2004)Google Scholar
  7. 7.
    Selkoe, D.J.: Toward a Comprehensive Theory for Alzheimer’s Disease. Hypothesis: Alzheimer’s Disease is Caused by the Cerebral Accumulation and Cytotoxicity of Amyloid β-Protein. Annals of the New York Academy of Science 924, 17–25 (2000)CrossRefGoogle Scholar
  8. 8.
    Wood, W.G., et al.: Brain Membrane Cholesterol Domains, Aging and Amyloid Beta-Peptides. Neurobiology of Aging (23), 685–694 (2002)Google Scholar
  9. 9.
    Vianna, G.K.: Um Modelo Neurocomputacional do Papel do Colesterol no Desenvolvimento da Doença de Alzheimer. Ph.D. Dissertation, Prog. Eng. de Sistemas e Computação, Universidade Federal do Rio de Janeiro, Brazil (2005) (in Portuguese)Google Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 2006

Authors and Affiliations

  • Gizelle Kupac Vianna
    • 1
  • Artur E. Reis
    • 1
  • Luís Alfredo V. de Carvalho
    • 1
  • Roseli S. Wedemann
    • 2
  1. 1.COPPEUniversidade Federal do Rio de Janeiro, Prog. Eng. de Sistemas e ComputaçãoRio de JaneiroBrazil
  2. 2.Instituto de Matemática e EstatísticaUniversidade do Estado do Rio de JaneiroRio de JaneiroBrazil

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