Cuprizone causes the destruction of neuron myelin in the hippocampus through an oxidative stress-dependent process, yet it does not impair short-term spatial memory

Multiple Sclerosis (MS) is a demyelinating disease of the central nervous system that affects patients with many sensory, motor, and cognitive symptoms. This study aims to evaluate memory function and histopathology and measure the oxidative stress level in the hippocampus of the MS model in mice.

Mice were divided into two groups that received a normal diet (control) and one that received a diet containing 0.2% cuprizone (cuprizone) for six weeks. After measuring the animal's weight and behavioral memory test, the hippocampus was evaluated in terms of histopathology and biochemical markers to measure the level of oxidative stress parameters.

The weight gain of mice after 6 weeks of the cuprizone diet was significantly lower than the control group (p < 0.05). Although behavioral evaluations performed with the Y maze test did not have significant differences between the two groups, the hippocampus in the cuprizone group revealed obvious demyelination. Measuring the parameters related to the level of oxidative stress showed that the amount of lipid peroxidation in the cuprizone group increased significantly compared to the control group (p < 0.05). In addition, the reduced glutathione and catalase activity levels in the cuprizone group showed a significant decrease compared to the control group (p < 0.05).

The induction of acute demyelination with cuprizone, probably through the creation of oxidative stress in the hippocampus, was able to lead to demyelination in the tissue of this region, while it had no significant effect on the memory performance of the animals.