Development, Optimization, and Physicochemical Characterization of Fluorescent Carbon Dot‐ Ginkgo biloba Extract Co‐Loaded Niosomes for Future Neurological Disease‐Relevant Evaluation

BACKGROUND: Alzheimer's disease (AD) is one of the major neurodegenerative diseases that affect the human brain and lead to memory loss. The present approaches to disease management have been relatively poor; the therapies provided do not arrest the disease process. This study aimed to develop and optimize dual-loaded niosomes containing Ginkgo biloba extract and CDOTs and to evaluate their physicochemical properties, formulation-level fluorescence, in vitro release, and preliminary cytocompatibility. The study did not assess blood-brain barrier transport, neuronal effects, Alzheimer's disease-specific mechanisms, or in vivo therapeutic efficacy. RESULTS: Niosomes were prepared based on non-ionic surfactants and cholesterol for the encapsulation of Ginkgo and CDOTs. The response surface methodology (RSM) was used to optimize niosomal formulations through a Box-Behnken design. The formulations were evaluated for vesicle size, entrapment efficiency, and release profile. Field Emission Scanning Electron Microscopy (FESEM) research indicated that the average diameters of the free niosomes and CDOT@Ginkgo@Niosomes were 69.56 nm and 72.19 nm, respectively. HFF cell viability remained high at lower concentrations, whereas significant reductions in viability were observed at 10 and 50 μg/mL after 48 h, indicating concentration-dependent cytocompatibility. The formulation exhibited acceptable preliminary cytocompatibility at lower concentrations, whereas reduced viability was observed at higher concentrations. For both CDOT and Ginkgo, CDOT@Ginkgo@Niosomes showed a delayed release profile over 72 h, with near-complete release observed at the final time point. CONCLUSIONS: CDOT@Ginkgo@Niosomes showed successful co-loading, preserved formulation-level fluorescence, delayed release, and acceptable cytocompatibility at lower concentrations in HFF cells. These findings support further formulation optimization and subsequent evaluation in disease-relevant neuronal, blood-brain barrier, and in vivo models. The present results do not demonstrate neuroprotection, diagnostic performance, blood-brain barrier transport, or the prevention or treatment of neurodegenerative disease.