Conclusion
In conclusion, we report that cdk5-based signaling could lead to tau hyperphosphorylation and polycylitol derivatives (SR4-02 and SR4-04) as ARM adjunctives effectively restore learning and memory functions, reducing active tau levels and improve hippocampal neuronal density in the experimental model of CM. Initially, long-term, short term memory and novelty based learning was studied by conducting Barnes maze, T-maze and novel object recognition task in animal models. Further studies with respect to cdk5/p25 and tau phosphorylation protein expression were carried out using western blotting, immunohistochemistry and Golgi-cox staining. Since polycyclitol derivatives have shown the potential to alleviate tau levels and restore cognition in experimental models of CM and drugs targeting chronic hypoxia and altered vascular remodeling may restore tau levels in neurodegenerative diseases, more in depth studies which focus on molecular signaling pathways associated with tau hyperphosphorylation and cognitive functions in animal models of Alzheimer’s and depression must be carried out to further understand the role of SR4-02 and SR4-04.