Multitarget Effects of Coconut Oil (Virgin Type) on Aβ-Induced Alzheimer’s Disease Animal Model

Almost 5% of people over 65 and 35% of those over 80 years of age have Alzheimer's disease (AD). The current study evaluated the neuroprotective effects of virgin coconut oil (VCO) on amyloid beta (Aβ)-induced cell injury. The total phenolic content (TPC) and total flavonoid content (TFC), 1,1-diphenyl-2-picrylhydrazyl (DPPH) radical scavenging and total antioxidant activity were measured. Rats were randomly divided into six groups: control; sham; sham receiving normal saline; Alzheimer’s rats (received Aβ 1 - 40); Alzheimer’s rats + 8% VCO and Alzheimer’s rats + 10% VCO. After 8 weeks, the levels of TNF-α protein, TNF-α and iNOS gene expression in the hippocampus, the nitric oxide level, thiol group, catalase, superoxide dismutase (SOD) and glutathione peroxidase (GPx) activity were measured. The morphological changes in the regions of the hippocampus and Aβ plaque formation were determined. Phosphorylated tau proteins were also determined by immunohistochemistry. VCO showed potential antiradical and antioxidant activity after in vitro treatment. VCO also significantly increased the thiol content, catalase, SOD and GPx activity and decreased the cholinesterase and nitric oxide levels. TNF-α and iNOS gene expression and protein levels decreased significantly after administration of VCO. Different areas of the hippocampus showed a significant change in the number of neurons in hippocampus, amount of phosphorylated tau and count of amyloid beta plaque in the Alzheimer’s rats that had been markedly restored by VCO. VCO showed neuroprotective effects in conjunction with various anti-Alzheimer’s medications (antioxidant, anti-inflammatory, cholinesterase inhibitors and reduced phosphorylated tau).