Aim: To explore the effect of beta-amyloid (A beta) on metabolism of cytoskeletal protein neurofilament, and search for effective cure to the lesion.
Methods: Wild type murine neuroblastoma N2a (N2awt) and N2a stably transfected with wild type amyloid precursor protein (N2aAPP) were cultured. Sandwich ELISA, immunocytochemistry, and Western blot were used respectively to measure the level of A beta, the expression and phosphorylation of neurofilament proteins.
Results: The immunoreactivity of neurofilament protein was almost abolished in N2aAPP, which beard a significantly higher level of A beta. Melatonin effectively decreased the level of A beta, and restored partially the level of phosphorylated and non-phosphorylated neurofilament in N2aAPP.
Conclusion: Overproduction of A beta inhibits neurofilament expression, and melatonin attenuates the A beta-induced lesion in cytoskeletal protein.