Chemotherapy-induced cognitive impairment (CICI), also known as "chemobrain," is a range of neurocognitive deficits experienced during and after cancer chemotherapy. It is also one of the significant factors affecting the quality of life of cancer patients. Due to patients' subjective feelings, the definition of cognitive impairment, the variety of testing scales, and the lack of pre-chemotherapy cognitive function measurements, it is difficult to determine its incidence rate. Consequently, the diagnosis and treatment of this condition are delayed. Existing studies report a high incidence of CICI, affecting 17% to 78% of survivors, and it may persist for years after chemotherapy cessation, leading to more severe progressive manifestations. Its main clinical presentations include deficits in attention, memory, reasoning, multi-tasking ability, decision-making ability, as well as learning and language impairments. These significantly affect patients' functional independence, imposing a heavy burden on families and society. Numerous studies have proposed several potential mechanisms and etiologies for CICI, including direct neurotoxicity of chemotherapeutic drugs, blood-brain barrier disruption, reduced hippocampal neurogenesis, white matter abnormalities, secondary neuroinflammatory responses, and increased oxidative stress. However, the exact underlying mechanisms remain unclear. Currently, there is no clear and effective diagnosis or treatment method for CICI. How to effectively diagnose and treat cognitive impairment caused by chemobrain remains a key focus and challenge in current research.
Previous studies indicate that in the treatment of ischemic stroke, Edaravone exerts its effects by scavenging oxygen free radicals, reducing inflammatory responses, mitigating neuronal and endothelial cell damage, and inhibiting excitatory neurotoxicity. It also inhibits neuronal lipid peroxidation and alleviates brain tissue damage and cerebral edema caused by cerebral ischemia and hypoxia. Dexborneol, as a bicyclic monoterpenoid compound, can also inhibit inflammatory responses, protect blood-brain barrier permeability, and reduce cell apoptosis. The combination of these two active ingredients can exert multiple mechanisms of action, including free radical scavenging, anti-inflammation, and blood-brain barrier protection, significantly reducing neuronal damage caused by acute ischemic stroke and exerting neuroprotective effects. Clinically, it effectively reduces infarct volume and improves neurological function.
The aforementioned pathogenesis of CICI precisely involves increased neuroinflammation and oxidative stress, as well as damage to the blood-brain barrier. Furthermore, the sublingual tablet dosage form offers advantages in convenience compared to injections. Based on this, we hypothesize that Edaravone Borneol sublingual tablets may also have considerable efficacy in treating chemotherapy-related cognitive impairment.
This study addresses a clinical cross-disciplinary event in neurology and oncology. It aims to evaluate the efficacy of Edaravone Dexborneol sublingual tablets for CICI and conduct preliminary exploration of early diagnostic biomarkers for CICI by collecting clinical patient imaging data, blood samples, and neuropsychological scale results. This will ultimately help optimize chemotherapy regimens to the greatest extent.