Indirubin-3'-monoxime rescues spatial memory deficits and attenuates beta-amyloid-associated neuropathology in a mouse model of Alzheimer's disease

Neurobiol Dis. 2010 Aug;39(2):156-68. doi: 10.1016/j.nbd.2010.03.022. Epub 2010 Apr 8.

Abstract

Indirubin and its derivatives have been shown to possess potent inhibitory effects on cyclin-dependent protein kinase 5 and glycogen synthase kinase 3beta, two protein kinases involved in abnormal hyperphosphorylation of tau and amyloid precursor protein processing/beta-amyloid (Abeta) production. Here, we showed that systemic treatment of APP and presenilin 1 (PS1) transgenic mice, a robust Alzheimer's disease (AD) mouse model, with indirubin-3'-monoxime (IMX; 20mg/kg; 3 times weekly), for as little as 2months, significantly attenuated spatial memory deficits. This was accompanied by a marked decrease in several AD-like phenotypes, including Abeta deposition, tau hyperphosphorylation, accumulation of activated microglia and astrocytes around Abeta plaques, and loss of synaptophysin immunoreactivity. These findings suggest that IMX is a potential therapeutic agent to combat AD.

Publication types

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

MeSH terms

  • Alzheimer Disease / complications*
  • Alzheimer Disease / genetics
  • Alzheimer Disease / metabolism
  • Alzheimer Disease / pathology
  • Amyloid beta-Peptides / metabolism*
  • Amyloid beta-Protein Precursor / genetics
  • Analysis of Variance
  • Animals
  • Astrocytes / drug effects
  • Astrocytes / metabolism
  • Astrocytes / pathology
  • Cell Count / methods
  • Disease Models, Animal
  • Enzyme-Linked Immunosorbent Assay / methods
  • Glial Fibrillary Acidic Protein / metabolism
  • Hippocampus / metabolism
  • Humans
  • Indoles / pharmacology
  • Indoles / therapeutic use*
  • Maze Learning / drug effects
  • Memory Disorders / drug therapy*
  • Memory Disorders / etiology*
  • Mice
  • Mice, Transgenic
  • Microglia / drug effects
  • Microglia / metabolism
  • Microglia / pathology
  • Neocortex / metabolism
  • Neuropsychological Tests
  • Oximes / pharmacology
  • Oximes / therapeutic use*
  • Peptide Fragments / metabolism*
  • Presenilin-1 / genetics
  • Synaptophysin / metabolism
  • tau Proteins / metabolism

Substances

  • Amyloid beta-Peptides
  • Amyloid beta-Protein Precursor
  • Glial Fibrillary Acidic Protein
  • Indoles
  • Oximes
  • PSEN1 protein, human
  • Peptide Fragments
  • Presenilin-1
  • Synaptophysin
  • amyloid beta-protein (1-42)
  • indirubin-3'-monoxime
  • tau Proteins