Decreased fractalkine and increased IP-10 expression in aged brain of APP(swe) transgenic mice.
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.
Duan
Rui-Sheng
RS
Division of Neurodegeneration Novum, plan 5, Department of Neurobiology, Care Sciences and Society Karolinska Institute, Karolinska University Hospital Huddinge, 141 86 Stockholm, Sweden.
Yang
Xin
X
Chen
Zhi-Guo
ZG
Lu
Ming-Ou
MO
Morris
Chris
C
Winblad
Bengt
B
Zhu
Jie
J
D000375:Aging / Q000502:physiology*; D000544:Alzheimer Disease / Q000378:metabolism; D016564:Amyloid beta-Protein Precursor / Q000235:genetics / Q000378:metabolism*; D000818:Animals; D001921:Brain / Q000033:anatomy & histology / Q000378:metabolism*; D054428:Chemokine CX3CL1 / Q000235:genetics / Q000378:metabolism*; D054357:Chemokine CXCL10 / Q000378:metabolism*; D005260:Female; D006801:Humans; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic
D016564:Amyloid beta-Protein Precursor; D054428:Chemokine CX3CL1; D054357:Chemokine CXCL10; C515539:Cx3cl1 protein, mouse