Molecular biology of the amyloid of Alzheimer's disease. An overview

Biol Res. 1992;25(2):63-72.

Abstract

Alzheimer's disease is a progressive neurodegenerative disorder that affects a significant percentage of elderly individuals. Degenerative nerve cells express atypical proteins, and amyloid is deposited. The hallmark event of Alzheimer's disease is the deposition of amyloid as insoluble fibrous masses in extracellular neuritic plaques and around the walls of cerebral blood vessels. This review will focus on the advances on the knowledge of Alzheimer's amyloid, because it is becoming increasingly clear that the deposition of amyloid on neuritic plaques in the brain represents the earliest and most characteristic pathological feature of Alzheimer's disease. The main component of amyloid is a 4.2-4.5 KDa hydrophobic peptide, named amyloid beta-peptide, that is codified in chromosome 21 as part of a much larger precursor protein. The study of the mechanism by which the amyloid beta-peptide arises from the amyloid precursor protein is very important in order to understand the biological basis of amyloid deposition and its role in Alzheimer's disease.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Alzheimer Disease / genetics*
  • Alzheimer Disease / metabolism
  • Alzheimer Disease / pathology
  • Amyloid / genetics*
  • Amyloid / metabolism
  • Animals
  • Brain / metabolism
  • Brain / pathology
  • Humans
  • Molecular Biology / methods
  • Nerve Growth Factors / metabolism
  • Neurotoxins / metabolism
  • Prion Proteins
  • Prions
  • Protein Precursors / metabolism

Substances

  • Amyloid
  • Nerve Growth Factors
  • Neurotoxins
  • PRNP protein, human
  • Prion Proteins
  • Prions
  • Protein Precursors