Amyloid at the cutting edge: activation of alpha-secretase prevents amyloidogenesis in an Alzheimer disease mouse model

J Clin Invest. 2004 May;113(10):1384-7. doi: 10.1172/JCI21746.

Abstract

The amyloid beta-peptide (A beta peptide) is assumed to play a crucial and early role in the pathogenesis of Alzheimer disease. Thus, strategies for a pharmacotherapy aim at reducing A beta peptide generation, which proteolytically derives from the amyloid precursor protein (APP). The main targets so far have been beta- and gamma-secretase, the two proteases that cleave APP at the N- and C-terminus of the A beta peptide and are thus directly responsible for A beta peptide generation. A different strategy, namely the activation of alpha-secretase, has barely been investigated for its therapeutic potential. alpha-Secretase cleaves within the A beta peptide domain and thus precludes A beta peptide generation. Now, new results demonstrate that activation of alpha-secretase indeed reduces A beta peptide generation and toxicity in vivo.

Publication types

  • Kommentar
  • Review

MeSH terms

  • Alzheimer Disease / drug therapy
  • Alzheimer Disease / etiology
  • Alzheimer Disease / metabolism*
  • Amyloid / metabolism*
  • Amyloid Precursor Protein Secretases
  • Amyloidosis / drug therapy
  • Amyloidosis / metabolism
  • Amyloidosis / prevention & control*
  • Animals
  • Aspartic Acid Endopeptidases
  • Disease Models, Animal
  • Endopeptidases / metabolism*
  • Enzyme Activation
  • Humans
  • Mice

Substances

  • Amyloid
  • Amyloid Precursor Protein Secretases
  • Endopeptidases
  • Aspartic Acid Endopeptidases
  • BACE1 protein, human
  • Bace1 protein, mouse