Krabbe disease is an inherited neurological disorder caused by galactosylceramidase deficiency in children. Castelvetri et al. focused on psychosine in this study as a potential etiological agent of Krabbe disease since psychosine (galactosylsphingosine) has been shown to be an etiological agent of the pathological condition found in the nervous system of patients with Krabbe disease. They supported the role of psychosine as a potential causal agent in Krabee's disorder by discussing the important role played by psychosine in this disease. Castelvetri et al. stated that psychosine accumulation is recognized as a causative lipid for loss of oligodendrocytes and myelin sheath in Krabbe disease. Therefore, psychosine is highly cytotoxic and responsible for the extensive pathology of the disease. Furthermore, psychosine has been shown to be responsible for the loss of function in lysosomal galactosylceramidase activity resulting in demyelination and vulnerability of several neurons. Furthermore, by examining free myelin in vitro, he demonstrated that psychosine was able to inhibit fast axonal transport (FAT) by activating axonal PP1 and GSK3β in the axon. Defects in the FAT are indicated by the formation of localized swelling of the axon. Castelvetri et al. demonstrated FAT defects present in cellular and animal models of Krabbe disease, and the sphingolipid psychosine was demonstrated as an inhibitor of FAT. Therefore, psychosine is highly cytotoxic and responsible for the broad pathology of the disease that is capable of blocking fast axonal transport. Furthermore, this is the first study to show the molecular mechanism of dying degeneration in this inherited genetic disease. To examine whether the sphingolipid psychosine is capable of... half of the article ......n et al. 2012).Castelvetri et al. indicated that due to the interference of different pathogenic mechanisms with each other, this affects the efficiency of hematogenous replacement therapy. Furthermore, the results showed that the use of psychosine as a FAT inhibitor was able to activate the PP1-GSK3β pathway, which could be used as a potential therapy for Krabbe disease neurodegeneration by reversing FAT defects. Interestingly, they stated that the drug treatment used in their study was not associated with any metabolic correction. Therefore, the mutants treated in their research were able to demonstrate neurological symptoms of the disease. For all these reasons, they concluded that neuroprotective treatments could be used with traditional hematogenous replacement as a potential therapy for Krabbe disease and other leukodystrophies...