The cognitive deficit induced by Al nanoparticle ingestion is associated with hippocampal inflammation in mice

Abstract Background Although, both environmental and genetic factors are known as the predispositions to AD development, each of these factors are suggested to acts via increasing the Al content of brain tissue. Al nanoparticles are newer nanomaterials that have been significantly exposed to the human body. When Al reaches the nanosize, it may display different characteristics from natural Al, and its potential influence on body function is an interesting aspect of research as these particles might have more negative impact on human health. Activation of microglia and expression of the inflammatory cytokine IL‐1 (interleukin‐1) in the brain have been used as hallmarks of brain inflammation. Our recent findings suggest that administration of nano‐Al for a short period of 5 days can cause memory impairment. Given the importance of neuroinflammation in Alzheimer’s pathology, the question was whether 5‐day nano‐Al intake could lead to inflammatory changes in the hippocampus. Method Adult male NMRI mice were treated with nano‐Al in doses 5 and 10 mg/kg/oral gavage for 5 days. The test session of novel object recognition (NOR) task was performed on day 5. Following the NOR test, the hippocampi were isolated. Considering the key roles of microglia activation and IL‐1β in neuroinflammation, the levels of hippocampal iba‐1 (as the speciefic marker of microglial activation) and IL‐1β were determined using western blot studies. Result The results showed that nano‐Al oral gavage in doses of 5 and 10 mg/kg impairs NOR memory in mice. Moreover, the memory impairing effect of nano‐Al coincided with a dose dependent increase in hippocampal iba‐1. It also increased the content of IL‐1 in the hippocampus. Conclusion This study showed that nano‐Al in doses as low as 5 and 10 mg/ kg ingested for 5 days impairs memory and induces neuroinflammation in the hippocampus.