Alzheimer's disease (AD) is a progressive degenerative disorder of the nervous system with an insidious onset. It is characterized clinically by a comprehensive dementia phenotype consisting of memory impairment, aphasia, apraxia, agnosia, impairment of visuospatial skills, executive dysfunction, and personality and behavioral changes with hitherto unknown etiology. Those with onset before 65 years of age, termed presenile dementia; Those with onset after 65 years of age said senile dementia. At present, there is no specific medicine that can cure or effectively reverse the course of the disease, only the combined use of drug treatment, non drug treatment and attentive care can reduce the symptoms and delay the progression of the disease. In the pre-existing literature, artemisinin has shown promising therapeutic effects on neuronal cells and is capable of pre - venting Alzheimer's disease. Artemisinin, as an anti malarial drug, was discovered by Prof. Tu You You. Now, it is widely practiced in a variety of diseases. Because of its ability to protect neuronal cells and its ability to rapidly pass the blood-brain barrier, artemisinin was discovered as a new drug for the treatment of Alzheimer's disease. However, the mechanism of action of artemisinin is not single. Epigenetic refers to heritable changes in gene function that occur in the absence of alterations in the DNA sequence of a gene and ultimately result in a change in phenotype. Among them, the modification of histones is closely related to the pathogenesis and targeted therapy of many diseases, especially with the acetylation of histones as the most. Therefore, we speculate that artemisinin may protect against Alzheimer's by regulating the acetylation levels of histones. So, this abstract provides a detailed description of this conjecture. First, we added artemisinin pretreatment followed by addition of aβ1-42 lesioning neural cells PC12 mimics Alzheimer's disease and determined the pre - protective effect of artemisinin on PC12 cells. Then, accompanied by a certain range of artemisinin's rising time of action and concentration of action, we found that at the acetylated histone 3 expression level gradually increased. Meanwhile, the dynamic balance of histone acetylation is co regulated by histone acetylases and deacetylases. Therefore, we added p300i, an inhibitor of acetylase, and TSA, an inhibitor of deacetylase, before the addition of artemisinin. When p300i was added, the expression of acetylation of histone 3 rose and blunted PC12 cell viability with increased apoptosis. When TSA is added, the activity of deacetylases is attenuated, allowing histone 3 deacetylation levels to be suppressed and thereby elevating the expression of acetylation. PC12 cells showed enhanced viability and decreased apoptosis. Therefore, we determined that artemisinin could pre protect PC12 cells by increasing the acetylation level of histone 3. At least, acetylation of histones is one such pathway by which artemisinin prevents Alzheimer's disease. Through the above experiments, we discovered a novel mechanism by which artemisinin protects neuronal cells, providing a new avenue for targeted therapy and a possibility for the development of new drugs