Chinese researchers have explored the mechanism of how goji berry or wolfberry extract can protect against Alzheimer’s disease (AD).
Goji berry, a bright orange-red berry from a shrub native to China, has been eaten for generations for its health benefits. Today, it is widely used in traditional Chinese medicine and food preparation.
Previous studies have shown that the goji berry extract has antioxidant properties and protective effects against reactive oxygen species, a group of highly reactive chemicals related to a wide variety of human disorders, including neurodegenerative diseases, cardiovascular diseases, and cancer.
In the new study, researchers from the Institute of Biophysics under the Chinese Academy of Sciences studied the molecular mechanism under the goji berry’s benefits on the neuro system.
The researchers gave goji berry extract to C. elegans with AD. C. elegans is a type of worm with a simple and mapped genome. They found that the extract can break down the deposits of amyloid-beta protein, a key marker of AD. The protein tends to clump together to form plaques that affect brain function.
According to the results published in The FASEB Journal, the extract inhibited the production of reactive oxygen species, thereby inhibiting the generation of the amyloid-beta protein.
Meanwhile, the study also found that the extract can reduce deposits of amyloid-beta protein by activating mtUPR, the mitochondrial unfolded protein response. The researchers also located the gene related to the activation of mtUPR.
Mitochondrial function declines during aging. Cells activate mtUPR when mitochondrial integrity and function are impaired. The mtUPR promotes cell survival and the recovery of the mitochondrial network to ensure optimal cellular function. The mtUPR manipulations are taken as potential therapeutic targets for treating many diseases associated with mitochondrial dysfunction.
The researchers said that their study reveals a new mechanism of how goji berry extracts protect against AD and identifies a novel strategy for treating AD by enhancing the mtUPR.