A more thorough understanding of systemic dysregulation of CREB in AD will facilitate the search for a biomarker of cognitive function in AD, and also aid in the understanding of the mechanisms underlying cognitive decline in AD.
Importantly, hippocampal cyclic adenosine monophosphate (cAMP), p-PKA, p-CREB and BDNF levels were significantly increased in the APP/PS1 mice after RJ treatment, indicating that the cAMP/PKA/CREB/BDNF pathway might be related to the ameliorative effect of RJ on cognitive decline.
We also discuss the development of novel therapeutic strategies based on CREB targeting to ameliorate cognitive decline in aging and cognitive disorders.