Hypoxic ischemic brain injury (HIBI) is one of the most common clinical disorders, especially in neonates. The complex pathophysiology of HIBI is an important cause of disability and even death of patients, however, being without effective clinical treatments. Common anesthetics (such as isoflurane, propofol and sevoflurane) have an adverse impact on neuronal cells for HIBI via the regulation of p75 neurotrophic factor receptor (P75NTR). In order to protect the injured brains and study the effect of underlying treatments, it is particularly significant to understand and master the developmental mechanism of anesthetics for the occurrence of HIBI related molecular mechanisms. Therefore, this paper will mainly review the corresponding pathogenic and protective mechanisms about HIBI binding to the research progress of the role of P75NTR. In conclusion, the effects of neuroprotection and injured nerves are involved in the expression and activation of P75NTR, mainly increased P75NTR mRNA, protein levels and calpain‐dependent for propofol, and inducing neuronal apoptosis for isoflurane and sevoflurane, and we look forward to that connection with P75NTR, common anaesthetic and HIBI may be a new direction of research and gain perfect outcomes in the future.

Postoperative cognitive dysfunction (POCD) is a decrease in mental capacity that can occur days to weeks after a medical procedure and may become permanent and rarely lasts for a longer period of time. With the continuous development of research, various viewpoints in academic circles have undergone subtle changes, and the role of anesthesia depth and anesthesia type seems to be gradually weakened; Alzheimer's disease (AD) is a latent and progressive neurodegenerative disease in the elderly. The protein hypothesis and the synaptic hypothesis are well‐known reasons. These changes will also lead to the occurrence of an inflammatory cascade. The exact etiology and pathogenesis need to be studied. The reasonable biological mechanism affecting brain protein deposition, neuroinflammation, and acetylcholine‐like effect has a certain relationship between AD and POCD. Whereas there is still further uncertainty about the mechanism and treatment, and it is elusive whether POCD is a link in the continuous progress of AD or a separate entity, which has doubts about the diagnosis and treatment of the disease. Therefore, this review is based on the current common clinical characteristics of AD and POCD, and pathophysiological research, to search for their common points and explore the direction and new strategies for future treatment.