The maintenance of the neuronal survival and function needs simultaneous support from a variety of neural survival factors, which form an information network through signal transduction pathways in nerve cells, and generate an amplified effect via intracellular generalization (Poo, 2001). Therefore, we examined two other neurotrophic factors, CNTF and GDNF. CNTF is a member of a cytokine family (Duff & Baile, 2003), and is known for its neuroprotective effects, being as a survival factor for sympathetic, sensory and hippocampal neurons. Garcia et al. reported that CNTF reduced the impairments of synaptic and cognitive functions in the Tg2576 AD mouse model, and rescues neurons from degeneration induced by Aβ in vitro and in vivo (Pasquin, Sharma & Gauchat, 2015; Garcia et al., 2010). GDNF family and its different receptor systems are now recognized as one of the major neurotrophic networks in the nervous system, which are important for the development, maintenance and function of neurons and glial cells. GDNF signaling through NCAM can result in the activation of kinases MAP and Src-like kinases, and contributes to the regulation of several different processes, including synapse formation and neurite outgrowth (Allen et al., 2013). In hippocampal neuronal cultures, GDNF has been found to increase the number of synapses. Although most studies on the function of GDNF and its receptors has been concentrated on midbrain dopaminergic neurons, the receptors of GDNF are observed in many other brain regions. A study analyzed 250 blood plasma samples of AD patients, and identified GDNF as one of 18 signaling proteins. GDNF level was lower in AD patients than the controls. It is not difficult to envision how a signaling molecule such as GDNF, which has potent effects on neuronal maturation, cell survival and synapse formation, can effect cognitive functions; and if aberrantly or insufficiently expressed or secreted, contribute to cognitive decline (Ibáñez & Andressoo, 2016; Pertusa et al., 2008). Our study also found DNLA can significantly increase the expression of CNTF and GDNF. The results indicated that the ability of DNLA to prevent neuronal and synaptic loss may be attributed to increase the expression of BDNF, CNTF and GDNF.