Published online Jun 22, 2016. doi: 10.5498/wjp.v6.i2.208
Peer-review started: March 1, 2016
First decision: March 22, 2016
Revised: April 24, 2016
Accepted: May 10, 2016
Article in press: May 11, 2016
Published online: June 22, 2016
Core tip: Patients with Alzheimer’s disease (AD) have not benefited from any disease-modifying drug until now. Multiple etiologic pathways have been explored and suggest promising solutions in the future. The iron chelator deferoxamine is one potential therapeutic solution around which future studies are being directed. Another potential therapeutic solution is related to thrombin inhibitors. In this minireview, a common pathophysiological pathway is suggested for the pathogenesis of AD that is initiated by the presence of vascular risk factors inducing brain tissue hypoxia and endothelial cell activation. In predisposed individuals, this can lead to thrombin activation and iron decompartmentalization. The resulting oxidative stress will eventually lead to neuronal and glial cell death.