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Due to the involvement of the imbalance of Ca2+ homeostasis in neuronal cells in the pathogenesis of several neurodegenerative disorders such as Alzheimer’s Disease (AD), the use of drugs to prevent or attenuate this imbalance emerged as a new therapeutic perspective for this disease. Then, our recent discovery of the involvement of the interaction between intracellular signaling pathways mediated by Ca2+ and cAMP (Ca2+/cAMP signaling interaction) in the neurotransmission and neuroprotection, and also its pharmacological modulation, opens a large avenue for the drug development for cognitive deficit treatment in AD. This discovery emerged from several clinical studies performed since 1975 that reported that the use of L-type Ca2+ Channel Blockers (CCB) in the antihypertensive therapy decreased arterial pressure, but promoted typical symptoms of sympathetic hyperactivity such as tachycardia and increment of catecholamine plasma levels. Despite these adverse CCB-effects have been initially attributed to adjust reflex of arterial pressure, during almost four decades this enigmatic phenomenon remained unclear. We discovered in 2013 that these adverse effects resulted from increase of transmitter exocytosis from sympathetic neurons and adrenal chromaffin cells stimulated by CCB due to its modulatory action on the neural Ca2+/cAMP signaling interaction. In addition, we discovered that the pharmacological modulation of this signaling can attenuate neuronal death resulting from cytosolic Ca2+ overload due probably to activation of cellular survival pathways mediated by Protein Kinase cAMP-dependent (PKA) and cAMP-Response Element Binding protein (CREB). Then, our discovery of the role of Ca2+/cAMP signaling interaction in neurotransmission and neuroprotection could importantly contribute to the AD therapy.

New Therapeutic Perspectives for the Cognitive Deficit in Alzheimer's Disease: Pharmacological Modulation of Ca2+/cAMP Signaling Interaction