The Polymer Society of Korea

Abstract

Alzheimer’s disease (AD) is marked by progressive neuronal and synaptic degeneration, leading to cognitive and motor decline and ultimately death. The pathology of AD arises from interconnected processes, including amyloid-β (Aβ) plaque formation, metal ion dyshomeostasis, oxidative stresss, and inflammation. Metals accumulate within Aβ plaques and intensify Aβ toxicity and oxidative stress, while ROS further accelerate Aβ aggregation. Although increasing evidence supports these interdependencies, their integrated contributions to AD pathogenesis remain poorly understood. To address this gap, we develop chemical tools that simultaneously target multiple pathogenic factors and elucidate the interaction networks governing their reactivity, providing a foundation for multi-target therapeutic strategies against AD.