Targeting the Akt signaling pathway is actually a possible therapeutic technique for treating neurodegenerative disorders. More over, many studies have confirmed the efficacy of drugs that inhibit lots of apoptotic pathways; these drugs include roscovitine and flavopiridol, inhibitors of cdk5 and the cell cycle, SB415286, a certain GSK 3 inhibitor, and CEP Flupirtine 1347, an competitive inhibitor of mixed lineage kinases. Many pro death pathways generally occur in the cytoplasm, activated prior to the release of cytochrome c. They are also extremely complex: for example, under normal physiological conditions cdk5 and its coactivator p35 show an expert success effect, while its break-down to cdk5/p25 and stimulation of cdk5/p35 induces apoptosis. Targeting the JNK pathway with certain drugs may possibly improve neuronal viability and constitute a potential target for the treating neurodegenerative diseases. In this respect, both in vitro and animal studies point-to the potential application of CEP 1347 like a potential drug for treating Parkinsons disease. Chromoblastomycosis Nevertheless, recent data suggest that CEP 1347 is useless in the treatment of Parkinsons disease. The failure of the drug in clinical studies may be a consequence of several causes. Subsequently, further research is necessary to identify the mechanisms underlying JNK signaling inhibition that causes neuroprotection. To the end, more particular JNK inhibitors including SP600125 have been developed. This substance is a reversible inhibitor of the JNK pathway that competes for ATP binding sites. The neuroprotective effects with this drug are due to it suppressing the expression of or by elimination of genes that control apoptosis, for example, Bax, Bim and Dp5. However, neuronal apoptosis is highly complex and multiple signals are activated. Hence the process of neuronal protection according to JNK inhibitors remains uncertain. Recent data suggest potential crosstalk between Akt and JNK. Since Akt activation LY2484595 posseses an important part in regulating neuronal survival, we examined whether the inhibition of JNK in CGNs with SP600125 results in an interaction with this professional survival pathway. We demonstrated that SP600125 maintains Akt service, which consequently has a result on targets downstream of Akt, like GSK 3 which is restricted. SP600125 also stops Rb phosphorylation that stops the expression of proteins active in the process of reentry to the cell cycle. More over, extra Akt substrates such as p FOXO1, p CREB and p35 were also affected after the specific inhibition of JNK by SP600125. Drugs found in this study contain propidium iodide from Sigma Chemical Co., SP600125, LY294002, MK 801, resveratrol, and 4 amino 4 amino 7 phenylpyrazolo pyrimidine and 5 7 pyrazolo pyrimidine from Calbiochem.