A mild dose of aspirin promotes hippocampal neurogenesis and working memory in experimental ageing mice

Abstract

Abstract Aspirin treatment is the most widely used preventive measure against cardiovascular diseases. Aspirin is also expected to provide beneficial effects on the brain. However, the association between aspirin treatment and neurocognitive functions is a subject of debate. Ample reports strongly advocate that a mild dose of aspirin positively modulates hippocampal plasticity responsible for memory. Aspirin is a selective cyclooxygenase (COX)-2 inhibitor but the underlying mechanism through which aspirin modulates neuroplasticity remains unclear. Adult neurogenesis in the hippocampus has been established as an underlying basis of learning and memory. Therefore, aspirin treatment might be linked to the regulation of hippocampal neurogenesis. Thus, this study revisited the effect of low-dose aspirin on learning and memory in correlation with the regulation of hippocampal neurogenesis in the brains of ageing experimental mice. Results from the novel object recognition (NOR) test, Morris water maze (MWM), and cued radial arm maze (cued RAM) revealed that aspirin treatment enhances working memory in experimental ageing mice. Further, the co-immunohistochemical assessments on the brain sections indicated an increased number of doublecortin (DCX) positive immature neurons and bromodeoxyuridine (BrdU)/neuronal nuclei (NeuN) double-positive newly generated neurons in the hippocampi of mice in aspirin-treated group compared to the control group. Recently, enhanced activity of acetylcholinesterase (AChE) in circulation has been identified as an indicative biomarker of dementia. The biochemical assessment in the blood of aspirin-treated mice showed decreased activity of AChE than that of the control group. This study supports the procognitive effects of aspirin which can be translated to treat dementia.