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

Background Amyloid 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. Objective To 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. Methods This 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 18 F-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. Results Baseline 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. Conclusions In 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.