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.
