P-glycoproteins in the Pathology and Treatment of Alzheimer's Disease

Alzheimer's disease (AD), a central cause of dementia, is characterized by the accumulation of amyloid beta- peptide (A beta) peptides in the brain. P-glycoprotein (P-gp), a highly expressed protein in the BBB, plays a fundamental role in transporting A beta from the brain to the blood and protecting the blood-brain barrier (BBB). The dysfunction or decreased abundance of this transporting protein is associated with the accumulation of A beta, leading to dementia and cognitive deficits. In this review article, we consolidate the existing literature on the impact of P-gp in the pathophysiology and therapy of AD. Current evidence claims that p-gp is involved in AD pathology and that enhancing the activity of this transporter may be a promising therapeutic approach to hinder AD progression. There is also a growing interest in P-gp as a potential therapeutic target for AD. Hence, ongoing clinical trials and research should investigate P-gp inhibitor efficacy as a therapeutic approach for improving AD drug delivery to the brain and treatment outcomes.