Abstract: Remyelination and need to access it: A range of diseases such as Guillain-Barre syndrome, Pelizaeus Merzbacher disease, relapsing-remitting and secondary progressive multiple sclerosis is associated with various degrees of nerve demyelination. These diseases present with various degrees of demyelination and different clinical manifestations. Treatments leading to remyelination are important for the restoration of functionality in these diseases with various clinical outcomes. Obtaining proper remyelination remains one of the current limitations for the treatment of demyelinating conditions. Establishing normal nerve function after axonal regeneration also necessitates proper myelination (Franklin et al., 2020). The process of remyelination is in many aspects very similar to the events that occur during development, with the exception that remyelination often does not reach the same myelin sheath thickness as observed during development. Therefore, understanding how these two processes (remyelination versus normal myelination after regeneration) differ can help develop novel translational applications in the field of regenerative medicine. With the scientific exploration of pharmacological compounds and therapies that can induce remyelination, there has been a surge of drugs with the potential to promote remyelination (Wooliscroft et al., 2019). Several of these are currently under clinical trials and include monoclonal antibody therapies, myelin protein stimulants, and non-selective G protein coupled receptor antagonists to name a few (Wooliscroft et al., 2019). However, the question arises as to whether these compounds are promoting remyelination or preventing demyelination. Thus, creating a need to identify newly synthesized myelin from previously existing myelin.