PDE-5 Restore Cognitive and Metabolic Function in Patients with Alzheimer’s Disease (AD)

Given that life expectancy is increasing and the human population is constantly aging, the quest for new, effective diagnostic methods and therapies in the context of cognitive decline is wide open. The present review was based on the pde-5 restore cognitive and metabolic function in patients with Alzheimer's disease (AD). PDE5 inhibitors, often known as PDE5i, are frequently given medications for the treatment of pulmonary arterial hypertension (PAH) and erectile dysfunction (ED). Their known mechanism in these disorders is to increase vasodilation that is dependent on nitric oxide by obstructing the breakdown of cyclic guanosine monophosphate (cGMP) in vascular myocytes that is mediated by PDE5. One well-known natural PDE5 inhibitor is the flavonoid icariin, which comes from Epimedium brevicornum. Given that it enhances learning and memory in APP/PS1 transgenic mice, it stands out among the other examples in this class. The NO/cGMP signaling pathway is probably stimulated in order to achieve this effect, which lessens the physio-pathological alterations in treated mice. Icarimin is an AChE inhibitor, which makes it an even more appealing possibility for the development of innovative AD treatments. Natural chemicals frequently operate through parallel processes. In conclusion, conflicting findings from clinical trials can be gleaned from PDE inhibitors, despite their extremely promising performances in vitro and in certain in vivo illness models.