Dexamethasone ameliorates Alzheimer’s pathological condition via inhibiting Nf-κB and mTOR signaling pathways

Alzheimer’s disease (AD) is one of the severe neurodegenerative disorders among the elderly population, so early interventions play an important role in AD progression. The deposition of amyloid-beta(Aβ) plaques and the accumulation of tau tangles within microglia and astrocytes which leads to inflammatory response due to the production of inflammatory mediators such as nitric oxide (NO), reactive oxygen species (ROS), tumor necrosis factor (TNF)-alpha that trigger the neuronal death. In the present study, we performed that dexamethasone as a synthetic anti-inflammatory agent can affect the progression of Alzheimer’s dementia via nuclear factor-κB(Nf-κB) and its downstream pathways. Literature review concentrated on Nf-κB, and the mammalian target of rapamycin(mTOR) pathway was executed in addition to looking for the molecular biology aspects in the Kyoto Encyclopedia of Genes and Genomes (KEGG). According to our hypothesis, it could be suggested that dexamethasone participates in reducing oxidative stress, inflammation, insulin resistance, and deposition of Aβ through inhibiting several pathways such as Nf-κB and mTOR signaling pathways. The present hypothesis proposes that dexamethasone could be a probable candidate to improve the pathological condition of AD. It should, however, be noted that due to little evidence for dexamethasone administration in AD patients, further investigations are required.