Neuroprotective Effects Of Fruitless Wolfberry-sprout Extract On Alzheimer’s Disease Transgenic Mice

Alzheimer’s disease(AD),the most common form of dementia,chronic and progressive neurodegenerative disease associated with memory and cognition impairment ultimately leading to death.Despite the great efforts to find a cure,current treatments have low efficacy.Epidemiological and experimental data show that natural antioxidant have an important role in the prevention of AD and other nervous system degenerative diseases.Our laboratory analysis demonstrates that Fruitless wolfberry-sprout tea contains flavonoids and polyphenols,which suggests that if FWE have anti-AD activity,to prevent Alzheimer’s disease by drinking it.Based on the above assumption,we conducted the following study to examine whether the Fruitless wolfberry-sprout has the role of prevention and treatment of Alzheimer’s disease.Experimental results demonstrated that FWE strongly disaggregated formed Aβ fibrils and inhibited the formation of AP fibrillation and Aβ oligomer toxic,by using Thioflavin T fluorescence assay,western-blot assay and Transmission electron microscope imaging.In vitro AD cell models were used to detect the protective effects against Aβ42-induced neuronal cell death.Results demonstrated FWE could inhibit Aβ42-induced cytotoxicity and apoptosis of hippocampal neurons(HT22)by MTT assay,TUNEL,and reduced the levels of Aβ40 and Aβ42 secreted in 7PA2 cells,as well as the Aβ-induced oxidative stress in SH-SY5Y cell.Ethology task demonstrated that FWE improved memory and cognitive performance of AD transgenic mice,decreased microgliosis,astrogliosis,oxidative stress,Aβ levels,inflammatory cytokines and senile plaques in the brains of AD mice.Reduced the level of senile plaques in cerebral cortex and hippocampus of AD mice.These results indicate that FWE may be a promising natural product for the prevention of AD,The neuroprotective effects against AD are related to the reduction of Aβ production,clearance of Aβ,inhibition of Aβ-induced oxidative stress and inflammatory response to reduce cytotoxicity and reduce neuronal apoptosis.Specific mechanisms of action need to be studied further.