Alzheimer′s disease（AD）is a common form of neurodegenerative disease. Oxidative stress plays an important role in the pathogenesis and development of AD. Researchers found that aging，the mutation of presenilin 1（PS1） gene and environment may lead to excessive oxidative stress，and then promote the formation of Aβ in the brain. At the same time，the imbalance between the production and elimination of oxygen radicals can lead to the abnormal autophagy function in hippocampal neurons and induce cells from autophagy to death. The possible mechanism is that the disorder of Notch 1 pathway leads to the loss of antioxidant capacity and the increase of （Aβ）deposition，which result in the development of AD pathology. Further study of its underlying mechanism will provide strong theoretical support for multiple therapeutic treatments of AD including the regulation of oxidative stress response and autophagy balance through the Notch 1 pathway as well as timely use of γ-secretase modulator.