# High-Resolution Tracking of Aging-Related Small Molecules: Bridging Pollutant Exposure, Brain Aging Mechanisms, and Detection Innovations

## TL;DR

This paper explores how pollutants accelerate brain aging by affecting small molecules and introduces new detection tools for early intervention.

## Contribution

The study introduces a novel cascade framework and highlights antioxidant quantum dots for real-time monitoring of aging-related molecules.

## Key findings

- Pollutants worsen brain aging by activating NLRP3 and inhibiting HIF-1α through small molecule imbalances.
- Antioxidant quantum dots (AQDs) offer superior real-time monitoring of ROS and oxidative damage.
- A multimodal approach combining detection tools and mechanism studies provides a foundation for early intervention.

## Abstract

Brain aging is a complex process regulated by genetic, environmental, and metabolic factors, and increasing evidence suggests that environmental pollutants can significantly accelerate this process by interfering with oxidative stress, neuroinflammation, and mitochondrial function-related signaling pathways. Traditional studies have focused on the direct damage of pollutants on macromolecules (e.g., proteins, DNA), while the central role of senescence-associated small molecules (e.g., ROS, PGE2, lactate) in early regulatory mechanisms has been long neglected. In this study, we innovatively proposed a cascade framework of “small molecule metabolic imbalance-signaling pathway dysregulation-macromolecule collapse”, which reveals that pollutants exacerbate the dynamics of brain aging through activation of NLRP3 inflammatory vesicles and inhibition of HIF-1α. Meanwhile, to address the technical bottleneck of small molecule spatiotemporal dynamics monitoring, this paper systematically reviews the cutting-edge detection tools such as electrochemical sensors, genetically encoded fluorescent probes and antioxidant quantum dots (AQDs). Among them, AQDs show unique advantages in real-time monitoring of ROS fluctuations and intervention of oxidative damage by virtue of their ultra-high specific surface area, controllable surface modification, and free radical scavenging ability. By integrating multimodal detection techniques and mechanism studies, this work provides a new perspective for analyzing pollutant-induced brain aging and lays a methodological foundation for early intervention strategies based on small molecule metabolic networks.