Alzheimer's disease (AD) is a neurodegenerative disease and the leading cause of dementia. In APP, the amyloid beta (Aβ) peptide is produced by two membrane-bound endoproteases, β-secretase and γ-secretase, and abnormal accumulation of Aβ42 among them affects neuronal function and connectivity, causing AD. There are several types of AD diagnostic methods, among which the method using biomarkers is diagnosed using the concentration of Aβ peptide in cerebrospinal fluid or plasma, which is difficult to distinguish between non-patient and MCI, and is known to be less accurate. In a previous study on Aβ42 phagocytosis have shown elevated Aβ42 phagocytosis of macrophage treated with decursinol, suggesting an increase in the specific ligand recognition rate of macrophage and Aβ42 caused by decursinol. In this study, we will use the results of increased specific ligand recognition rates to measure Aβ42 concentrations in plasma to discuss diagnostic methods for differentiating between non-patient and MCI, as well as the binding affinity of decursinol to Aβ42 and structural changes in the binding of decursinol to Aβ42.