Cardiovascular drugs and triazole based kinase inhibitors as a new strategies for the treatment of Alzheimer disease

Abstract

Atherosclerosis and stroke (including cerebrovascular atheroand arteriosclerosis with neurological consequences such as Alzheimer disease (AD)) are two leading causes of ageassociated disability, dementia, and death. Five million people suffer from AD only in the United States and this figure will balloon to 16 million persons, mostly the elderly, by the year 2040. Conventional wisdom for the last 20 years has decreed that AD is a "neurodegenerative" disorder caused primarily by the abnormal deposition of a brain tissue protein called amyloid beta. Neurodegenerative disorders are characterized by an entire loss of cognitive function and inappropriate death of nerve cells in the brain areas that control such functions as memory and language. The goal of this review is to determine the fact that there is a tight relationship between atherosclerosis and stroke-induced vascular lesions in AD pathology. We have also analyzed current status of the potential possibility of the therapeutics effects of such cardiovascular drugs as atorvastatin, simvastatin, and candesartan, as well as nitric oxide synthase (NOS) inhibitors 7-nitroindazole (a selective inhibitor of neuronal NOS), aminoguanidine (a selective inhibitor of inducible NOS), 1-nitroimidazole ornithine (a selective inhibitor of endothelial NOS), and purine-triazole based kinase inhibitors as a completely new treatment strategy in animal models that mimics cholesterol induced AD and/or AD-like pathology, which deserves special attention.