Ginkgo biloba and longitudinal changes in amyloid PET and plasma amyloid-β oligomerization in amyloid-positive mild cognitive impairment: A retrospective analysis

BackgroundAmyloid PET-positive mild cognitive impairment (MCI) is a prodromal stage of Alzheimer's disease (AD), but its longitudinal clinical and biomarker trajectories vary considerably. Evidence linking oral interventions to amyloid-related biomarkers in this population remains limited.ObjectiveTo compare 18-month clinical outcomes and longitudinal changes in plasma amyloid-β (Aβ) oligomerization tendency and amyloid PET burden according to Ginkgo biloba use in amyloid PET-positive MCI.MethodsThis retrospective cohort study included 35 amyloid PET-positive MCI patients who underwent baseline and 18-month clinical evaluations, serial plasma Aβ oligomerization measurements using the Multimer Detection System-Oligomerized Aβ (MDS-OAβ) assay, and paired baseline and 18-month 18F-FC119S amyloid PET. Patients received Ginkgo biloba extract 240 mg/day (n = 21) or Non-Ginkgo cognitive enhancers (n = 14). Clinical stability, conversion to AD dementia (Korean Instrumental Activities of Daily Living ≥0.40), changes in MDS-OAβ, and changes in global cortical standardized uptake value ratio (SUVR) were assessed.ResultsBaseline characteristics were comparable between groups. At 18 months, all Ginkgo-treated patients remained clinically stable, whereas 57.1% of Non-Ginkgo patients showed cognitive decline. Conversion to AD dementia occurred in none of the Ginkgo group and in 28.6% of the Non-Ginkgo group. Plasma MDS-OAβ decreased with Ginkgo but increased without Ginkgo. Global amyloid PET SUVR remained stable in the Ginkgo group and increased in the Non-Ginkgo group.ConclusionsIn amyloid PET-positive MCI, Ginkgo biloba use was associated with sustained clinical stability, reduced plasma Aβ oligomerization tendency, and attenuation of amyloid PET progression over 18 months.