Membrane biophysics and mechanics in Alzheimer's disease

Mol Neurobiol. 2010 Jun;41(2-3):138-48. doi: 10.1007/s12035-010-8121-9. Epub 2010 May 1.

Abstract

Alzheimer's disease is a chronic neurodegenerative disorder characterized by neuronal loss, cerebrovascular inflammation, and accumulation of senile plaques in the brain parenchyma and cerebral blood vessels. Amyloid-beta peptide (Abeta), a major component of senile plaques, has been shown to exert multiple toxic effects to neurons, astrocytes, glial cells, and brain endothelium. Oligomeric Abeta can disturb the structure and function of cell membranes and alter membrane mechanical properties, such as membrane fluidity and molecular order. Much of these effects are attributed to their capability to trigger oxidative stress and inflammation. In this review, we discuss the effects of Abeta on neuronal cells, astrocytes, and cerebral endothelial cells with special emphasis on cell membrane properties and cell functions.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Alzheimer Disease* / metabolism
  • Alzheimer Disease* / pathology
  • Amyloid beta-Peptides / metabolism
  • Amyloid beta-Peptides / toxicity*
  • Astrocytes / cytology
  • Astrocytes / drug effects*
  • Astrocytes / metabolism
  • Calcium / metabolism
  • Cell Membrane* / chemistry
  • Cell Membrane* / drug effects
  • Cell Membrane* / metabolism
  • Cerebrovascular Circulation
  • Cholesterol / metabolism
  • Endothelial Cells / cytology
  • Endothelial Cells / drug effects*
  • Endothelial Cells / metabolism
  • Mitochondria / metabolism
  • Neurons / cytology
  • Neurons / drug effects*
  • Neurons / metabolism
  • Oxidative Stress / physiology
  • Phospholipases A2 / metabolism

Substances

  • Amyloid beta-Peptides
  • Cholesterol
  • Phospholipases A2
  • Calcium