Alzheimer’s disease is a common type of dementia in people 65 years of age and older. Tens of millions of people worldwide are living with AD, and the number continues to grow. To date, there are several hypotheses about the pathogenesis of AD, the most widely studied of which is related to the accumulation of Aβ. Currently, there are five drugs in clinical treatment, most of which are inhibitors, as well as monoclonal antibody drugs such as Aducanumab that target Aβ. These drugs can effectively reduce the accumulation of Aβ. However, these drugs have significant side effects and are generally significantly reduced by the end of AD symptoms. This review will summarize the pathogenesis of AD related to Aβ, such as APP and neuroinflammation. This article will also discuss the progress and problems of existing Aβ-based therapies. In addition, this paper will also compare Aβ and Tau proteins to explore better AD treatment methods. These are the basis for further study of the pathogenesis of AD related to Aβ and the development of drugs based on it. Future studies could focus on the direction of immunotherapy targeting Aβ, and apply these drugs to therapies targeting Tau protein.
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