Diverse compounds mimic Alzheimer disease-causing mutations by augmenting Abeta42 production

Nat Med. 2005 May;11(5):545-50. doi: 10.1038/nm1235. Epub 2005 Apr 17.

Abstract

Increased Abeta42 production has been linked to the development of Alzheimer disease. We now identify a number of compounds that raise Abeta42. Among the more potent Abeta42-raising agents identified are fenofibrate, an antilipidemic agent, and celecoxib, a COX-2-selective NSAID. Many COX-2-selective NSAIDs tested raised Abeta42, including multiple COX-2-selective derivatives of two Abeta42-lowering NSAIDs. Compounds devoid of COX activity and the endogenous isoprenoids FPP and GGPP also raised Abeta42. These compounds seem to target the gamma-secretase complex, increasing gamma-secretase-catalyzed production of Abeta42 in vitro. Short-term in vivo studies show that two Abeta42-raising compounds increase Abeta42 levels in the brains of mice. The elevations in Abeta42 by these compounds are comparable to the increases in Abeta42 induced by Alzheimer disease-causing mutations in the genes encoding amyloid beta protein precursor and presenilins, raising the possibility that exogenous compounds or naturally occurring isoprenoids might increase Abeta42 production in humans.

Publication types

  • Comparative Study
  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Alzheimer Disease / metabolism*
  • Amyloid Precursor Protein Secretases
  • Amyloid beta-Peptides / biosynthesis*
  • Anti-Inflammatory Agents, Non-Steroidal / chemistry
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology
  • Aspartic Acid Endopeptidases
  • Brain / metabolism*
  • Celecoxib
  • Cell Line
  • Cyclooxygenase Inhibitors / chemistry
  • Cyclooxygenase Inhibitors / pharmacology
  • Endopeptidases / metabolism*
  • Enzyme Activation / drug effects
  • Enzyme-Linked Immunosorbent Assay
  • Female
  • Fenofibrate / chemistry
  • Fenofibrate / pharmacology
  • Humans
  • Hypolipidemic Agents / chemistry
  • Hypolipidemic Agents / pharmacology
  • Immunoprecipitation
  • Intracellular Signaling Peptides and Proteins
  • Mass Spectrometry
  • Protein Serine-Threonine Kinases / metabolism
  • Pyrazoles / chemistry
  • Pyrazoles / pharmacology
  • Sulfonamides / chemistry
  • Sulfonamides / pharmacology
  • Transfection
  • rho-Associated Kinases
  • rhoA GTP-Binding Protein / metabolism

Substances

  • Amyloid beta-Peptides
  • Anti-Inflammatory Agents, Non-Steroidal
  • Cyclooxygenase Inhibitors
  • Hypolipidemic Agents
  • Intracellular Signaling Peptides and Proteins
  • Pyrazoles
  • Sulfonamides
  • Protein Serine-Threonine Kinases
  • rho-Associated Kinases
  • Amyloid Precursor Protein Secretases
  • Endopeptidases
  • Aspartic Acid Endopeptidases
  • BACE1 protein, human
  • rhoA GTP-Binding Protein
  • Celecoxib
  • Fenofibrate