Many pathologies once believed to be incurable can now be definitively cured. However, ischemic and degenerative diseases of the central nervous system and traumatic injuries of the spine still lack a therapeutic approach capable of restoring lost function. Therefore, identification of cells capable of neuronal differentiation is of marked interest (Reynolds & Weiss 1992; Richards et al. 1992). Safford et al. (2002) reported neuronal differentiation by ADSCs, showing that murine and human ADSCs differentiate into neuronal tissue when cultured with valproic acid, forskolin, hydrocortisone, and insulin. Under these conditions, murine ADSCs expressed the neural tissue markers nestin, neuronal nuclei (NeuN), and glial fibrillary acidic protein. In human ADSCs, pretreatment with basic fibroblast growth factor (bFGF) and epidermal growth factor (EGF) for 7 days enhanced immunohistochemical changes observed during neuronal induction, causing adoption of a bipolar neuronal phenotype with strong IF-M, NeuN, and nestin expression (Safford et al. 2002). ADSCs from adult donors were treated with EGF and bFGF as neurospheres. The spheres were able to proliferate and induce Schwann and glial-like cells (Zavan et al. 2010). Ashjian et al (2003) reported that human ADSCs differentiate into cells resembling early neurons and glia in neural induction medium containing fetal bovine serum (FBS), insulin, indomethacin (INDO), and isobutylmethylxanthine (IBMX). After 14 days of differentiation, human ADSCs transformed into tropomyosin receptor kinase-A-, vimentin-, NeuN-, and neuron-specific enolase (NSE)-positive cells, adopted a neuron-like morphology, displayed voltage-dependent outward currents active after a brief delay, and did not become inactive during depolarization. Moreover, their steady-state current–voltage relationship exhibited outward reflection, similar to classic, delayed rectifier K+ channels in the mammalian node of Ranvier (Ashjian et al. 2003). The neural induction medium contained three active ingredients: insulin, INDO, and IBMX. Insulin has been shown to promote the maturation of differentiating neocortical cells in rat brains. INDO, a cyclo-oxygenase inhibitor, promotes neural cell survival after ischemic central nervous system injury, and IBMX, a phosphodiesterase inhibitor, increases intracellular cyclic adenosine monophosphate (cAMP), a neural stimulant. However, Ashjian et al. (2003) did not explain the necessity of all three agents. Subsequently, Ning et al. (2006) demonstrated the effect of each of these agents and their respective roles. IBMX induced morphological changes in ADSCs, similar to those induced by all three agents, whereas insulin and IBMX combined had little or no effect. The combination of IBMX and INDO or insulin exerted an effect similar to that of IBMX alone, while the combination of INDO and insulin had little or no effect. ADSCs treated with IBMX alone expressed the neuronal marker NF70 (Ning et al. 2006). Furthermore, 35% of ADSCs treated with IBMX and platelet-poor plasma, a specific inhibitor of insulin-like growth factor 1 (IGF-I) signaling, assumed a neuron-like morphology compared with approximately 95% of cells treated with IBMX. IBMX causes phosphorylation of the IGF-I receptor (IGF-IR) at tyrosine 1136 (Y1136). These results suggest that IBMX-induced neuron-like ADSC differentiation is mediated by IGF signaling through phosphorylation of the IGF-IR receptor at Y1136 (Ning et al. 2008). There are several types of stem cells, including bone marrow derived mesenchymal stem cells (BMSCs), umbilical cord blood cells, and ADSCs. These are attractive stem cell sources for clinical therapies (Kern et al. 2006). Zhang et al. (2012) undertook a comparison of rat ADSCs and BMSCs isolated from the same donor in terms of their proliferation capacity, potential towards neural differentiation, and ability to secret neurotrophin. ADSCs and BMSCs were cultured in neurobasal medium supplemented with EGF, bFGF, and B27 to form neurospheres. The neurospheres were then cultured in neurobasal medium supplemented with all-trans retinoic acid, FBS, horse serum, and N2, on poly-L-lysin and lamina double-coated dishes. Under these conditions, the population of ADSCs expressing nestin protein was significantly greater than that of BMSCs under undifferentiated conditions. Moreover, the expression of neural and glial markers in ADSCs was significantly higher than that of corresponding markers in BMSCs following neural differentiation.