Frankincense Upregulates the FMR1 Gene and Alleviates AlCl3-Induced Memory Impairment in Rats

Alzheimer's disease (AD) is a multifactorial disorder that its progress and development are related to various genetic and environmental factors. The disease onset is affected by both genetic and environmental factors such as oxidative stress, inflammation, and mitochondrial dysfunction, and is remarkably related to age progress. Aluminum, a neurotoxic environmental factor, impairs memory performance and can cause neurodegenerative diseases such as AD. On the other hand, the regulatory RNA-binding product of Fragile X mental retardation (FMR1) gene exerts a translational inhibitory effect on the expression of amyloid precursor protein (APP), the main culprit in AD development. In the present study, we treated AlCl3-induced Alzheimer’s disease model rats with Frankincense and investigated its protective and therapeutic effects on the AlCl3-induced memory disturbance by behavioral and molecular assays. Also, Rivastigmine was used as a standard control. Morris Water Maze (MWM) was used to assay special memory working of the rats and quantitative real-time PCR (qRT-PCR) was applied to investigate the expression profile of the FMR1 gene in the hippocampus of the treated rats. MWM behavioral tests indicated that both Frankincense and Rivastigmine not only may prevent AlCl3-induced memory impairment but also may alleviate the memory declines induced by AlCl3 in the rats. Expression analysis showed significant upregulation of the FMR1 gene in response to both Frankincense and Rivastigmin treatments. Further, qRT-PCR results revealed that the AlCl3-induced downregulation of the FMR1 gene expression could significantly be reversed by both Frankincense and Rivastigmine, though Rivastigmine was more effective than Frankincense. In conclusion, our results highlighted that Frankincense might be effective both in the prevention and treatment of memory impairments, to some extent, by affecting the FMR1 gene expression.