Experimental Research On The Effect Of NGF To The Expression Of Mutant APP In PC12 Cell

Objective:Alzheimer's disease (AD) is the commonly seen chronic degenerative neuropathy in elderly population. The main pathological change include the senile plaque (SP) and the neurofibrillary tangles (NFTs). The main component of amyloid sediment in SP is β-amyloid peptides (Aβ, including Aβ40 and Aβ42).The Aβpeptides are derived from the amyloid precursor protein (APP)which is considered very important for the AD pathogenesis. Present studies have proved that the accumulation of Aβ caused by the mutation of the APP genes, abnormal metabolism and over-expressiopn are the important reasons for the onset of AD. More and more studies have shown the genetic deficiencies in AD patients including APP, PS1, PS2, apoE4, ACT and ERAB genes, and have established many AD transgenic mouse models. Therefore, under different environmental influence and different experimental conditions, it's not convenient to explore the expression of AD characteristic products of APP and Aβ and their effects on the cell. Nowadays, the research on the pathogenesis of AD at abroad focused on the abnormal expression of APP in transgenic mouse models. There were no reports of the interference of NGF on transgenic AD cell models at home and abroad .The present work was focused on the construction of the plasmids which contain the mutant APP gene sequence, and the transfection to PC12 cells. We observe the expression of APP and Aβ and the changes in cellular morphology and cell cycles. Then interference was undertaken by the exposure to NGF to explore the molecular mechanism of APP and Aβ expression and the therapeutic effect of NGF on AD patients.