RESUMEN
The generation of ßamyloid protein (Aß) is considered a key step in the pathogenesis of Alzheimer's disease (AD) and the regulation of its production is an important therapeutic strategy. It was hypothesized in the present study that NogoA may be involved in AD and may regulate the generation of Aß. NogoA is known to act as a major inhibitor of neuron regeneration in the adult central nervous system. A recent study indicated that NogoA is associated with AD; however, the underlying effect and molecular mechanisms remain largely elusive. In the present study, the potential effects of NogoA on AD were investigated. ELISA was used to detect the levels of Aß, enzymatic activity detection kits were used to determine the activity of secretase enzymes in amyloid precursor protein (APP) metabolism, and western blot analysis was used to detect the expression levels of proteins associated with the APP processing and NogoA/Nogo66 receptor (NgR) signaling pathways. The results revealed that Nogo66, the major inhibitory region of NogoA, promoted neuronal Aß secretion by increasing the activity of ßsecretase 1 via the NgR/Rhoassociated coiledcoil containing kinases pathway in a dosedependent manner. The present data suggested that NogoA may facilitate the onset and development of AD by promoting Aß secretion, providing information on a potential novel target for AD therapy.