Abstract
Pharmacological modulation of neural Ca2+/camp signaling interaction as therapeutic goal for treatment of Alzheimer´s disease
Highlights
Since 1970 ́s, several clinical studies have reported that acute and chronic administration of L-type Ca2+ channel blockers (CCBs) in hypertensive patients, such as nifedipine and verapamil, decreased arterial pressure but produced typical symptoms of sympathetic hyperactivity such as tachycardia, and increment of catecholamine plasma levels [1]
In 2013, we discovered that this paradoxical sympathetic hyperactivity produced by L-type CCBs is due to its modulatory action on the interaction between the intracellular signalling pathways mediated by Ca2+ and cAMP (Ca2+/cAMP signalling interaction)
Our studies have showed that the pharmacological modulation of the Ca2+/cAMP signalling interaction by combined use of L-type CCBs and compounds which increase cytosolic cAMP concentration ([cAMP]c), named cAMP-enhancer compounds, could be useful to increase neurotransmission, and neuroprotection in neurological and psychiatric disorders, such as Alzheimers diseases (AD) [5,6,7,8]
Summary
Since 1970 ́s, several clinical studies have reported that acute and chronic administration of L-type Ca2+ channel blockers (CCBs) in hypertensive patients, such as nifedipine and verapamil, decreased arterial pressure but produced typical symptoms of sympathetic hyperactivity such as tachycardia, and increment of catecholamine plasma levels [1]. Our studies have showed that the pharmacological modulation of the Ca2+/cAMP signalling interaction by combined use of L-type CCBs and compounds which increase cytosolic cAMP concentration ([cAMP]c), named cAMP-enhancer compounds, could be useful to increase neurotransmission, and neuroprotection in neurological and psychiatric disorders, such as Alzheimers diseases (AD) [5,6,7,8].
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
