Sodium propionate improves cognitive and memory function in mouse models of Alzheimer's disease

This study was designed to explore whether sodium propionate (SP) alleviates cognitive damage in a mouse model of Alzheimer's disease (AD). We evaluated behavioral and biochemical aspects in an animal model of AD made by intracerebroventricular injection of A beta 1-42 peptide. Two-month-old ICR mice were treated with SP or normal saline for 21 days (control group, A beta 1-42 group, A beta 1-42 + SP50 mg/kg group, A beta 1-42 + SP100 mg/kg group, and A beta 1-42 + SP200 mg/kg group). Behavioral tests showed that SP alleviated cognitive and memory impairments in AD mice. Moreover, SP treatment significantly suppressed the level of inducible nitric oxide synthase (iNOS) in the hippocampus. Concomitantly, the overexpression of interleukin-1 alpha (IL-1 alpha), interleukin-1 beta (IL-1 beta) and interleukin-6 (IL-6) in the hippocampus induced by A beta 1-42 was significantly reduced following treatment with SP. In addition, SP was able to increase the levels of synaptophysin (SYN) and postsynaptic dense protein 95 (PSD95). Our study shows that SP could significantly improve A beta 1-42-induced spatial learning and memory impairment by reducing neuroinflammation via inhibition of proinflammatory cytokines and iNOS activation and restoring synapse plasticity by increasing synaptically associated protein levels, suggesting that SP has a positive effect and potential for AD therapies.