SCD5 expression alters the homeostatic control of Wnt proteins, at this early stage in the investigation, the questions of whether SCD5-mediated modification of Wnt synthesis and secretion is related to a potential change in their acylation, and whether changing levels of Wnt are responsible for the alterations in the activation of Wnt pathways in SCD5-expressing cells await further experimental confirmation. Finally, given the mounting evidence suggesting a mechanistic association of abnormal Wnt signaling with Alzheimer’s and Parkinson’s diseases, our findings suggest that SCD5 may be a molecular link between signaling and lipogenic pathways mechanisms and these neurodegenerative conditions. In conclusion, the present study provides the first evidence that human SCD5 activity is implicated in the regulation of critical biological functions in neuronal cells. Our findings imply that, by modulating fatty acid composition, lipogenesis and intracellular signaling, SCD5 controls the rate of replication and differentiation of neuronal cells. We observed that the Lomitapide Mesylate constitutive expression of human SCD5 promotes a shift in the fatty acid composition in lipids of neuronal cells, which was characterized by elevated levels of n-7 MUFA with a concomitant reduction in SFA. These modifications in the fatty acid pattern were accompanied by lipogenic alterations, such as the change in the rate of synthesis of phospholipids, which are known to affect cell growth, survival and differentiation. Remarkably, SCD5 expression promotes a profound deregulation of EGF’s intracellular signaling mechanisms. We observed that SCD5 expression suppresses the ligand-induced activation of the EGFRAkt/ERK signaling platform. SCD5 activity also reduces the activation of canonical Wnt signaling whereas it stimulates the non-canonical branch of the Wnt pathway. These activity changes could be directly related to the perturbations in the synthesis and secretion of Wnt proteins observed in SCD5-expressing neuronal cells. We also found that SCD5 expression accelerates cell cycle progression while suppressing the program of differentiation, indicating that the fate of neuronal cells is, ultimately, determined by the activity of the desaturase. Lastly, our studies suggest a value for SCD5 as a potential target for clinical interventions in poorly-treated neurological diseases such as brain cancer, Alzheimer and other neurodegenerative conditions. Despite the extensive electrophysiological studies regarding the effects of inhaled anesthetics on membrane ion channels and receptor proteins the exact molecular mode of action of anesthetics remains uncertain. In addition to altering the function of membrane ion channels and Gomisin-D receptors in vitro, the inhaled anesthetics are known to affect enzymes as well as many cytoplasmic proteins in the mammalian central nervous system, providing multiple targets for their actions including side effects. Among these cytoplasmic proteins is tubulin, the component protein of cytoskeletal microtubules. Tubulin proteins polymerize to form microtubules, nanoscale cylindrically shaped protein polymers that are part of the cellular cytoskeleton. The neuronal MT cytoskeleton, in particular, possesses a unique architecture, responsible for maintaining highly asymmetric neuron morphology and the intracellular transport of vesicles. Unlike MTs in all other cells, the MTs in dendrites are interrupted and oriented in local networks of mixed polarity.