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Huntington disease (HD) is a neurodegenerative disease known by progressive motor, behavioral, and cognitive decline that culminates in the death. HD therapy is yet unsatisfactory. Chorea and psychiatric symptoms usually respond to pharmacotherapy. Recent advances in pathogenesis and newer biomarkers have promoted some progresses in HD therapy. It was suggested that an imbalance in the intracellular calcium (Ca2+) homeostasis has a key role in neurodegenerative diseases. Recently, we showed that the interaction between intracellular signaling pathways mediated by Ca2+ and cAMP (Ca2+/cAMP signaling interaction) plays as a key role in several cellular responses in mammalians, including neurosecretion and cell survival. Our studies showed that the pharmacological modulation of the Ca2+/cAMP signaling interaction by the combined use of the Ca2+ channel blockers (CCB), and drugs that increase the intracellular concentration of cAMP (cAMP-enhancer compounds), increases synaptic neurotransmission and stimulates neuroprotective response. Thus, we have proposed that this new pharmacological strategy could open a new avenue for the drug development more effective and safer for treatment of the neurodegenerative diseases, including HD. Here, we discuss the perspectives of the pharmacological modulation of the Ca2+/cAMP signaling interaction as a new therapeutic strategy for HD.
