OBJECTIVE To provide reference for improving relevant policies of health insurance reimbursement management for off-label drug use in China. METHODS The institutional framework and core mechanisms of public health insurance reimbursement for off-label drug use in the United States were systematically reviewed. Experiences were summarized and optimization suggestions for health insurance reimbursement of off-label drug use in China were proposed. RESULTS & CONCLUSIONS The United States has established a clearly defined institutional framework with division of responsibilities between drug regulation and health insurance reimbursement： FDA is responsible for marketing approval and promotional regulation， while the Centers for Medicare & Medicaid Services （CMS） is responsible for formulating reimbursement policies， distinguishing between “whether a drug can be used” and “whether a drug can be reimbursed”. Reimbursement management is built on an evidence-based decision-making foundation， primarily relying on dynamically updated authoritative drug compendia， supplemented by published medical literature. CMS dynamically updates the list of authoritative drug compendia through an annual public application and evaluation process. Additionally， prior authorization mechanisms are employed to conduct prospective reviews of high-cost， high-risk off-label drug uses， thereby controlling the risk to health insurance funds. It is recommended that China pilot evidence-based reimbursement for off-label drug use in disease areas with prominent clinical needs， relying on real-world research evidence and selecting drugs with certain evidence-based support to explore reimbursement pathways for off-label drug use. Meanwhile， prior authorization mechanisms should be introduced， combined with health insurance information platforms to achieve standardized reviews， so as to enhance the controllability of health insurance fund expenditures while ensuring rational drug use and safeguarding patients’ health rights and interests.

Objective: To investigate the role of HIV-1 envelope protein gp120 in cognitive impairment induced by neuronal damage. Methods: Western blot and immunofluorescence assay were used to detect microglia activation, inflammatory factor expression and neuronal damage after gp120 treatment. Neuronal damage and neurocognitive performance in gp120-transgenic mice were evaluated using immunohistochemical staining and behavioral analysis, respectively. Results: In vivo and in vitro experiments showed that HIV-1 gp120 significantly induced the expression of caspase-1 and IL-1β, and indirectly caused neuronal synaptic shortening and neuronal damage (P<0.05). Compared with wild-type mice, gp120-transgenic mice showed significant cortical and hippocampal glial activation, neuronal loss, dendritic damage and neurocognitive disorders. Conclusions HIV-1 gp120 might cause neuronal damage through activating the release of inflammatory factor by microglia and involve in neurocognitive impairment.