Introduction: Myelin is a crucial substance for the proper functioning of the nervous system. It envelops nerve fibers and enables the rapid conduction of action potentials. Oligodendrocytes produce myelin in the CNS and can myelinate multiple axons, while Schwann cells perform this function in the PNS by myelinating a single axon, allowing for nerve regeneration in the PNS. Demyelination is the process of myelin loss. It most commonly occurs as a result of neurodegenerative diseases such as multiple sclerosis. Experimental mouse models that mimic human pathological conditions are used to conduct motor tests to assess the motor abilities of mice and evaluate their recovery after applied therapies, providing insights into potential therapeutic approaches for humans. B4Galnt1 KO and cuprizone models are among the more frequently used due to their similarity to neurodegenerative diseases. Objectives: To examine the motor ability and coordination of genetically modified B4Galnt1 mice and cuprizone-fed mice and compare them with wild-type mice. Materials and methods: The study was conducted on three types of mice: KO, WT, and WTCUP, aged 3 and 6 months. Motor ability was assessed using the rotarod test and the footprint test. Results: The analysis of the rotarod test data did not reveal a significant difference in motor ability among the groups. In contrast, the analysis of the footprint test data in the second measurement showed reduced motor ability in genetically modified and cuprizone-treated mice compared to wild-type mice. Conclusion: Congenital demyelination, compared to chemically induced demyelination, causes a more significant reduction in motor ability and coordination. Both models exhibit reduced motor ability compared to the wild-type.