Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2048353 | FEBS Letters | 2011 | 6 Pages |
Abstract
β-Amyloid (Aβ) may play an important role in the pathogenesis of Alzheimer’s disease. However, a causal relationship between Aβ oligomers and layer-specific neurodegeneration has not been clarified. Here we show up-regulation of calsyntenin (Cst)-3 in cultured neurons treated with Aβ 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 Aβ-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 Aβ oligomers may lead to increase in vulnerability of neurons.
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Authors
Yoko Uchida, Shun-ichirou Nakano, Fujiya Gomi, Hiroshi Takahashi,