Abstract
Alzheimer's disease (AD), a central cause of dementia, is characterized by the accumulation of amyloid β-peptide (Aβ) peptides in the brain. P-glycoprotein (P-gp), a highly expressed protein in the BBB, plays a fundamental role in transporting Aβ 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 Aβ, 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.
