Possible role of glial cells in the progression of Alzheimer's disease pathology

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Here, we aimed to examine the possible role of astrocyte-derived S100B in the progression of Alzheimer's disease pathology. First, using Alzheimer's disease model mice, we showed that Alzheimer's disease-like pathology was significantly ameliorated by the treatment of arundic acid [(R)-(-)-2-propyloctanoic acid], which is known to negatively regulate astrocyte synthesis of S100B. Subsequently, to dissect the relationship between S100B and Alzheimer's disease-like pathology, we took a genetic approach by crossing transgenic mice expressing human S100B with Alzheimer's disease model mice. We demonstrated evidence that (over)-expression of S100B acts to accelerate Alzheimer's disease-like pathology. Taken together, these data suggest that inhibiting astrocytic activation by blocking S100B biosynthesis may be a promising therapeutic strategy to delay Alzheimer's disease progression.