Small molecule, non-peptide p75 ligands inhibit Abeta-induced neurodegeneration and synaptic impairment

PLoS One. 2008;3(11):e3604. doi: 10.1371/journal.pone.0003604. Epub 2008 Nov 3.

Abstract

The p75 neurotrophin receptor (p75(NTR)) is expressed by neurons particularly vulnerable in Alzheimer's disease (AD). We tested the hypothesis that non-peptide, small molecule p75(NTR) ligands found to promote survival signaling might prevent Abeta-induced degeneration and synaptic dysfunction. These ligands inhibited Abeta-induced neuritic dystrophy, death of cultured neurons and Abeta-induced death of pyramidal neurons in hippocampal slice cultures. Moreover, ligands inhibited Abeta-induced activation of molecules involved in AD pathology including calpain/cdk5, GSK3beta and c-Jun, and tau phosphorylation, and prevented Abeta-induced inactivation of AKT and CREB. Finally, a p75(NTR) ligand blocked Abeta-induced hippocampal LTP impairment. These studies support an extensive intersection between p75(NTR) signaling and Abeta pathogenic mechanisms, and introduce a class of specific small molecule ligands with the unique ability to block multiple fundamental AD-related signaling pathways, reverse synaptic impairment and inhibit Abeta-induced neuronal dystrophy and death.

Publication types

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

MeSH terms

  • Amyloid beta-Peptides / pharmacology*
  • Animals
  • Animals, Newborn
  • Cell Death / drug effects
  • Cells, Cultured
  • Hippocampus / drug effects
  • Ligands
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Nerve Degeneration / chemically induced
  • Nerve Degeneration / prevention & control*
  • Neurons / drug effects
  • Organ Culture Techniques
  • Peptide Fragments / metabolism
  • Peptide Fragments / pharmacology*
  • Rats
  • Rats, Wistar
  • Receptors, Nerve Growth Factor / agonists*
  • Receptors, Nerve Growth Factor / genetics
  • Synaptic Transmission / drug effects*

Substances

  • Amyloid beta-Peptides
  • Ligands
  • Peptide Fragments
  • Receptors, Nerve Growth Factor
  • Ngfr protein, mouse