CCL2 accelerates microglia-mediated Abeta oligomer formation and progression of neurocognitive dysfunction.

ABSTRACT:

Background

The linkages between neuroinflammation and Alzheimer's disease (AD) pathogenesis are well established. What is not, however, is how specific immune pathways and proteins affect the disease. To this end, we previously demonstrated that transgenic over-expression of CCL2 enhanced microgliosis and induced diffuse amyloid plaque deposition in Tg2576 mice. This rodent model of AD expresses a Swedish beta-amyloid (Abeta) precursor protein mutant.

Methodology/principal findings

We now report that CCL2 transgene expression accelerates deficits in spatial and working memory and hippocampal synaptic transmission in beta-amyloid precursor protein (APP) mice as early as 2-3 months of age. This is followed by increased numbers of microglia that are seen surrounding Abeta oligo

SUBMITTER: Kiyota T 

PROVIDER: S-EPMC2703798 | biostudies-literature | 2009 Jul

REPOSITORIES: biostudies-literature