Decreased Fractalkine and Increased IP-10 Expression in Aged Brain of APPswe Transgenic Mice

Abstract

Chemokines and their receptors have been strongly implicated in the inflammatory process and pathogenesis of the neurodegenerative disorders, such as Alzheimer's disease (AD). In the present study, we examined the expression of chemokines, fractalkine, interferon-inducible protein-10 (IP-10) and macrophage inflammatory protein-1alpha (MIP-1alpha) by immunohistochemistry in the brain of transgenic mice APP SWE (Tg2576) at ages of 9, 11, and 17 months, which over-express a mutated form of human amyloid precursor protein (APP). Decreased fractalkine and increased IP-10 expression in cerebral cortex and hippocampus were found at ages of 9 and 17 months in Tg2576 mice when compared with age-matched control mice. On the contrary, MIP-1alpha expression showed no difference between Tg2576 mice and aged controls and was not influenced by ages. beta-amyloid (Abeta) positive plaques were co-located with the intense IP-10 expression. The finding suggests fractalkine and IP-10 may participate in the pathogenesis of AD; and could be new therapeutic strategies for neuroprotection.