IVIg protects the 3xTg-AD mouse model of Alzheimer's disease from memory deficit and Aβ pathology

J Neuroinflammation. 2014 Mar 22:11:54. doi: 10.1186/1742-2094-11-54.

Abstract

Background: Intravenous immunoglobulin (IVIg) is currently in clinical study for Alzheimer's disease (AD). However, preclinical investigations are required to better understand AD-relevant outcomes of IVIg treatment and develop replacement therapies in case of unsustainable supply.

Methods: We investigated the effects of IVIg in the 3xTg-AD mouse model, which reproduces both Aβ and tau pathologies. Mice were injected twice weekly with 1.5 g/kg IVIg for 1 or 3 months.

Results: IVIg induced a modest but significant improvement in memory in the novel object recognition test and attenuated anxiety-like behavior in 3xTg-AD mice. We observed a correction of immunologic defects present in 3xTg-AD mice (-22% CD4/CD8 blood ratio; -17% IL-5/IL-10 ratio in the cortex) and a modulation of CX3CR1+ cell population (-13% in the bone marrow). IVIg treatment led to limited effects on tau pathology but resulted in a 22% reduction of the soluble Aβ42/Aβ40 ratio and a 60% decrease in concentrations of 56 kDa Aβ oligomers (Aβ*56).

Conclusion: The memory-enhancing effect of IVIg reported here suggests that Aβ oligomers, effector T cells and the fractalkine pathway are potential pharmacological targets of IVIg in AD.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Alzheimer Disease / complications*
  • Alzheimer Disease / drug therapy
  • Alzheimer Disease / genetics
  • Alzheimer Disease / pathology
  • Amyloid beta-Peptides / metabolism
  • Amyloid beta-Protein Precursor / genetics
  • Animals
  • Anxiety / drug therapy
  • Anxiety / etiology
  • Brain / drug effects
  • Brain / metabolism
  • Brain / pathology*
  • CX3C Chemokine Receptor 1
  • Cytokines / metabolism
  • Disease Models, Animal
  • Flow Cytometry
  • Humans
  • Immunoglobulins, Intravenous / therapeutic use*
  • Immunologic Factors / therapeutic use*
  • Memory Disorders / etiology*
  • Memory Disorders / genetics
  • Memory Disorders / prevention & control*
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Mutation / genetics
  • Peptide Fragments / metabolism
  • Presenilin-1 / genetics
  • Receptors, Chemokine / metabolism
  • tau Proteins / genetics

Substances

  • Amyloid beta-Peptides
  • Amyloid beta-Protein Precursor
  • CX3C Chemokine Receptor 1
  • Cx3cr1 protein, mouse
  • Cytokines
  • Immunoglobulins, Intravenous
  • Immunologic Factors
  • PSEN1 protein, human
  • Peptide Fragments
  • Presenilin-1
  • Receptors, Chemokine
  • amyloid beta-protein (1-40)
  • amyloid beta-protein (1-42)
  • tau Proteins