a b s t r a c t b-Amyloid (Ab) may play an important role in the pathogenesis of Alzheimer's disease. However, a causal relationship between Ab oligomers and layer-specific neurodegeneration has not been clarified. Here we show up-regulation of calsyntenin (Cst)-3 in cultured neurons treated with Ab oligomers and in Tg2576 mice. Cst-3 is distributed in large neurons in layers 2-3 and 5 of the cerebral cortex, and accumulated in dystrophic neurites surrounding Ab-plaques. Overexpression of Cst-3 accelerates neuronal death. These results indicate that up-regulation of Cst-3 in cortical neurons in layers 2-3 and 5 by Ab oligomers may lead to increase in vulnerability of neurons.
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