Background: Alzheimer’s disease (AD) is a neurodegenerative disease featured by memory
loss, neuroinflammation and oxidative stress. Overproduction or insufficient clearance of Aβ leads to its
pathological aggregation and deposition, which is considered the predominant neuropathological hallmark
of AD. Therefore, reducing Aβ levels and inhibiting Aβ-induced neurotoxicity are feasible therapeutic
strategies for AD treatment. Wolfberry has been traditionally used as a natural antioxidant and
anti-aging product. However, whether wolfberry species has therapeutic potential on AD remains unknown.
Method: The effects of fruitless wolfberry-sprout extract (FWE) on Aβ fibrillation and fibril disaggregation
was measured by thioflavin T fluorescence and transmission electron microscope imaging; Aβ oligomer
level was determined by dot-blot; Cell viability and apoptosis was assessed by MTT and TUNEL
assay. The levels of Aβ40/42, oxidative stress biomarkers and inflammatory cytokines were detected by
corresponding kits. 8-month-old male APP/PS1 mice and their age-matched WT littermates were treated
with FWE or vehicle by oral administration (gavage) once a day for 4 weeks. Then the cognitive performance
was determined using object recognition test and Y-maze test. The Aβ burden and gliosis was
evaluated by immunostaining and immunoblotting, respectively.
Results: FWE significantly inhibited Aβ fibrillation and disaggregated the formed Aβ fibrils, lowered
Aβ oligomer level and Aβ-induced neuro-cytotoxicity, and attenuated oxidative stress in vitro. Oral administration
of FWE remarkably improved cognitive function, reduced Aβ burden, decreased gliosis and
inflammatory cytokines release, and ameliorated oxidative stress in the brains of APP/PS1 mice.
Conclusion: These findings indicate that FWE is a promising natural agent for AD treatment.