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.