ABSTRACT
Cranberry extract (CBE) rich in polyphenols are potent to delay paralysis induced by alleviating β-amyloid (Aβ) toxicity in C. elegans model of Alzheimer's disease (AD). In order to better apply CBE as an anti-AD agent efficiently, we sought to deterrmine whether preventive or therapeutic effect contributes more prominently toward CBE's anti-AD activity. As the level of Aβ toxicity and memory health are two major pathological parameters in AD, in the present study, we compared the effects of CBE on Aβ toxicity and memory health in the C. elegans AD model treated with preventive and therapeutic protocols. Our results revealed that CBE prominently showed the preventive efficacy, providing a basis for further investigation of these effects in mammals.
Subject(s)
Animals , Female , Humans , Male , Alzheimer Disease , Drug Therapy , Genetics , Metabolism , Psychology , Amyloid beta-Peptides , Metabolism , Toxicity , Caenorhabditis elegans , Metabolism , Dietary Supplements , Disease Models, Animal , Fruit , Chemistry , Memory , Plant Extracts , Vaccinium macrocarpon , ChemistryABSTRACT
As the disease modifying therapies against Alzheimer’s disease (AD) continue to exist as a major challenge of this century, the search for newer drug leads with lesser side effects is on the rise. A large number of plant extracts and phytocompounds are being actively pursued for their anti-Alzheimer effects. In the present study, the antioxidant activity, cholinesterase inhibition, anti-amyloidogenic potential and neuroprotective properties of methanolic extract of dry ginger (GE) have been evaluated. The extract contained 18±0.6 mg/g gallic acid equivalents of total phenolic content and 4.18±0.69 mg quercetin equivalents/g of dry material. GE expressed high antioxidant activity with an IC50 value of 70±0.304 µg/mL in DPPH assay and 845.4±56.62 μM Fe(II) equivalents/g dry weight in FRAP assay respectively. In Ellman’s assay for the cholinesterase inhibitory activity, GE had an IC50 value of 41±1.2 µg/mL and 52±2 µg/mL for inhibition of acetyl- and butyrylcholinesterase respectively. Also, GE increased the cell survival against amyloid β (Aβ) induced toxicity in primary adult rat hippocampal cell culture. Aggregation experiments with the thioflavin T binding studies showed that GE effectively prevented the formation of Aβ oligomers and dissociated the preformed oligomers. These findings suggest that methanolic GE influences multiple therapeutic molecular targets of AD and can be considered as an effective nontoxic neutraceutical supplement for AD.