Curcumin can bind
senile plaques and promote disaggregation of existing
amyloid deposits and prevent aggregation of new
amyloid deposits.
Curcumin can also reverse distorted and curvy neurites around
senile plaques and repair the neuritic abnormalities. We hypothesized whether altered neurite morphologies resulting from Aβ production had anything to do with the changes of expression of
microtubule-associated protein 2 (MAP2), but
curcumin could reverse damaged neurites by upregulation of MAP2 expression. In present study we designed and chemically synthesized
curcumin and its six derivatives. After screening the protective effect of
curcumin and derivatives, we found that the viability of SK-N-SH cell model induced by Aβ1-42 was significantly increased by
curcumin and Cur1, and the expression of MAP-2
protein was obviously up-regulated in immunocytochemical staining and Western blot. The cell morphologies, including the number of neurites, neurite growth and neurite extension, were significantly improved. Cur1 showed more significant protective effect on SK-N-SH cells than
curcumin. Our study revealed for the first time that the
neuroprotective effect of
curcumin and
curcumin derivatives not only directly depends on their special chemical constitution, but they can resist to Aβ damage by up-regulation of MAP-2 expression. In view of the special advantages of
curcumin and Cur1, we reasonably believe that
curcumin and Cur1 may be considered as an ideal therapeutic agent for the treatment of AD.