Ferroptosis: a potential therapeutic target for Alzheimer’s disease

Abstract

Abstract The most prevalent dementia-causing neurodegenerative condition is Alzheimer’s disease (AD). The aberrant buildup of amyloid β and tau hyperphosphorylation are the two most well-known theories about the mechanisms underlying AD development. However, a significant number of pharmacological clinical studies conducted around the world based on the two aforementioned theories have not shown promising outcomes, and AD is still not effectively treated. Ferroptosis, a non-apoptotic programmed cell death defined by the buildup of deadly amounts of iron-dependent lipid peroxides, has received more attention in recent years. A wealth of data is emerging to support the role of iron in the pathophysiology of AD. Cell line and animal studies applying ferroptosis modulators to the treatment of AD have shown encouraging results. Based on these studies, we describe in this review the underlying mechanisms of ferroptosis; the role that ferroptosis plays in AD pathology; and summarise some of the research advances in the treatment of AD with ferroptosis modulators. We hope to contribute to the clinical management of AD.