Allan Herndon Dudley syndrome (AHDS) is a severe psychomotor retardation disorder characterized by neurological impairments and abnormal thyroid hormone (TH) levels. THs regulate metabolism, embryonic development and neurogenesis. Mutations in the TH transporter, monocarboxylate transporter 8 (MCT8), are associated with AHDS; however, the function of this gene and the mechanism of the disease remain elusive. Similar to human patients, MCT8-knockout mice exhibit impaired TH levels; however, they lack neurological defects. We utilized the zebrafish model to study MCT8 function and psychomotor retardation. This transparent vertebrate has emerged as a promising model to study neurobiology and development because it combines the advantage of high-throughput genetics of invertebrates with mammalian-like conserved genome and brain structure. Importantly, in contrast to mice, MCT8 mutant (mct8-/-) zebrafish exhibit impaired neurogenesis and altered behavioural performances. Here, we studied the development of myelination in mct8-/- zebrafish. We used the myelin basic protein (mbp) as a marker for mature oligodendrocytes in the CNS. The levels of expression of mbp mRNA were reduced in mct8-/- larvae. Furthermore, time-lapse live imaging of mbp:EGFP transgenic fish showed a decrease in the number of oligodendrocytes in different brain regions of mct8-/- larvae during development. In order to test potential treatments, the effect of a few drugs on myelination was determined during several developmental stages in live mct8-/- larvae. These treatments resulted in partial to full recovery of myelination. These results suggest that, similar to humans, loss of MCT8 affects the development of myelin in zebrafish larvae. It also suggests a putative pharmacological treatment for AHDS patients. Altogether, the mct8-/- zebrafish provide a model to study the mechanism and treatment of psychomotor retardation, and may help to understand other myelination disorders such as multiple sclerosis.