Alzheimer´s Disease: Fundamental Concepts, Novel Findings and Therapeutics Outcomes Coming from the Ca2+/cAMP Signalling Interaction

The evidences that a dysregulation of the intracellular Ca2+ homeostasis increases the incidence of the neurodegenerative diseases, such as Alzheimer´s disease (AD), have been increasing. Thus, several findings have been reinforcing the concept that a reduction of a cytosolic Ca2+ excess, achieved due to the L-type Ca2+ channel blockers (CCBs), could be an interesting pharmacological goal to alleviate the AD symptoms. In addition, aging along with a healthy brain can be endorsed by daily exercise, a self-control in caloric ingestion and participating in intellectually challenging events. Indeed, these lifestyle issues may alleviate the Ca2+ excess from neurons achieved through a Ca2+ homeostasis dysregulation. Furthermore, several studies have been indicating that increasing cAMP levels may produce neuroprotective effects, thus alleviating the AD symptoms. From these concepts in mind, we discovered that the manipulation by medicines of the Ca2+/cAMP signalling through the mutual therapy involving CCBs, and cAMP-accumulating compounds, could be a novel plausible target to treat the AD. Then, this chapter discusses the fundamental concepts and current therapies to treat AD, including therapeutics outcomes coming from the pharmacological interference on the interaction between Ca2+ and cAMP signalling.

Keywords: Alzheimer’s Disease, Ca2+/cAMP Signalling Interaction, Ca2+ Dysregulations Neurodegenerative Diseases, Rolipram.