Shock membrane electropotential drops and limited diffusive distance of beta-amyloids in cerebral neurons are detrimental enhancement to Alzheimer's diseases

Colloids Surf B Biointerfaces. 2009 Oct 15;73(2):339-45. doi: 10.1016/j.colsurfb.2009.06.004. Epub 2009 Jun 10.

Abstract

Molecular physicobiochemical calculations indicated that the metallic ion binding to beta-amyloids (Abeta) may induce production of hydrogen peroxide, which triggers the Ca ion redistribution from the extracellular to the intracellular compartmentation, resulting in a transient membrane electropotential drop by at least 208.06 mV. Moreover, using the Mark and Houwink empirical equation, we predicted that the diffusible distances of all Abeta identities would be confined in a very tiny region within a radius less than 3.96 x 10(-4)cm in brain at 192h after produced. Because of the inherent tendency of aggregation behaved by the Abetas, the maximum diffusion coefficient and inherent viscosity were 8.24 x 10(-15)cm(2)s(-1) and 72.15 cps for the 12 mers (40.8 kDa), the largest soluble form of ABs. Conclusively, we have quantitatively predicted that the shock membrane potential drop (Deltaphi>208.06 mV) and limited diffusible distance (<3.96 x 10(-4)cm) in the brain would contribute the major detrimental effects to the neurons in the Alzheimer's diseases.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease / physiopathology*
  • Amyloid beta-Peptides / toxicity*
  • Animals
  • Brain / drug effects*
  • Brain / pathology*
  • Calcium / metabolism
  • Chelating Agents / pharmacology
  • Diffusion
  • Electrolytes
  • Homeostasis / drug effects
  • Membrane Potentials / drug effects*
  • Models, Biological
  • Neurons / drug effects*
  • Neurons / pathology*
  • Organ Specificity / drug effects
  • Time Factors
  • Viscosity / drug effects

Substances

  • Amyloid beta-Peptides
  • Chelating Agents
  • Electrolytes
  • Calcium