Pathogenic mechanisms in Alzheimer's disease

Eur J Pharmacol. 2006 Sep 1;545(1):29-38. doi: 10.1016/j.ejphar.2006.06.078. Epub 2006 Jul 4.

Abstract

Alzheimer's disease is a progressive neurodegenerative disorder associated with aging and characterized by neurofibrillary tangles and amyloid plaques that deposit in the brain, triggering the neurodegenerative phenomena and leading to neuronal death. Amyloid plaques are primarily composed of beta-amyloid peptides, which derive from the Amyloid Precursor Protein (APP) upon the consequential action of beta- and gamma-secretase. This review discusses recent literature on beta- and gamma-secretase, and on those cellular factors, like cholesterol and phosphorylation of APP, that are involved in aging and may affect the function of both beta- and gamma-secretase.

Publication types

  • Review

MeSH terms

  • Aging / metabolism
  • Alzheimer Disease / metabolism*
  • Alzheimer Disease / pathology
  • Amyloid Precursor Protein Secretases / metabolism
  • Amyloid beta-Protein Precursor / metabolism
  • Animals
  • Aspartic Acid Endopeptidases / metabolism
  • Cholesterol / metabolism
  • Humans
  • Membrane Glycoproteins / metabolism
  • Membrane Proteins / metabolism
  • Phosphorylation
  • Presenilins / metabolism

Substances

  • Amyloid beta-Protein Precursor
  • Membrane Glycoproteins
  • Membrane Proteins
  • PSENEN protein, human
  • Presenilins
  • nicastrin protein
  • Cholesterol
  • Amyloid Precursor Protein Secretases
  • Aspartic Acid Endopeptidases
  • BACE1 protein, human