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

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

Author information

1
Centre de Recherche du CHU de Québec, 2705, Boulevard Laurier, Québec, QC G1V 4G2, Canada. Frederic.Calon@pha.ulaval.ca.

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.

PMID:
24655894
PMCID:
PMC3997966
DOI:
10.1186/1742-2094-11-54
[Indexed for MEDLINE]
Free PMC Article

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