Functionalized carbon dots with guanidine salt ionic liquid regulate oxidative damage and amyloid aggregation.

An imbalance in the brain microenvironment, involving oxidative stress and β-amyloid (Aβ) accumulation, is thought to be one of the primary characteristics of early Alzheimer's disease (AD). To address the intricate pathophysiology of AD, therapeutic approaches that can concurrently control several diseases in the AD microenvironment are desperately needed. This study created a guanidine salt ionic liquid functionalized carbon dots (CDs@TGM-IL) to mitigate Aβ aggregation-induced cytotoxicity and scavenge reactive oxygen species (ROS) simultaneously. In vitro studies have shown that CDs@TGM-IL can effectively inhibit Aβ42 protein aggregation, disaggregate mature Aβ42 fibrils, and effectively remove ROS. In vivo studies have found that CDs@TGM-IL can cross the blood-brain barrier (BBB) and improve cognitive performance in AD mice. Just as importantly, CDs@TGM-IL has been shown to have unparalleled biocompatibility. This means that CDs@TGM-IL is expected to be a possible treatment for AD.