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Up‐regulation of calsyntenin‐3 by β‐amyloid increases vulnerability of cortical neurons
Author(s) -
Uchida Yoko,
Nakano Shun-ichirou,
Gomi Fujiya,
Takahashi Hiroshi
Publication year - 2011
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2011.01.025
Subject(s) - cortical neurons , vulnerability (computing) , amyloid (mycology) , neuroscience , chemistry , psychology , computer science , computer security , inorganic chemistry
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.