Silver-functionalized carbon dots regulate amyloid aggregation and microbial infection

Chao Wang1, Xu Shao1, Xiuyun Cao1

  • 1Department of Chemistry, School of Chemistry and Chemical Engineering, Northwestern Polytechnical University, 127 Youyi Road, Xi'an 710072, China. xinwang@nwpu.edu.cn.

Nanoscale
|November 7, 2025
PubMed

Insights

This study introduces silver-functionalized carbon dots (Ag@TACDs) as a novel Alzheimer's disease (AD) treatment. Ag@TACDs target both amyloid aggregation and microbial infections, offering a multi-faceted therapeutic approach.

Area of Science:

  • Neuroscience
  • Materials Science
  • Biotechnology

Background:

  • Alzheimer's disease (AD) is linked to amyloid accumulation and microbial infections.
  • Current single-target therapies for AD show limited clinical efficacy.
  • A multi-targeted strategy is needed to address AD's complex pathology.

Purpose of the Study:

  • To develop a novel multi-targeted therapeutic agent for Alzheimer's disease.
  • To investigate the efficacy of silver-functionalized carbon dots (Ag@TACDs) against amyloid aggregation and microbial infections.
  • To evaluate the biocompatibility and cellular effects of Ag@TACDs.

Main Methods:

  • In vitro experiments were conducted to assess the impact of Ag@TACDs on amyloid-beta 42 (Aβ42) misfolding and fibril depolymerization.
  • Antimicrobial activity of Ag@TACDs against bacterial infections was evaluated.
  • Cell viability and cytotoxicity assays were performed to determine biocompatibility and effects on Aβ42 oligomer-induced toxicity.

Main Results:

  • Ag@TACDs significantly inhibited Aβ42 misfolding and depolymerized mature Aβ42 fibrils at low concentrations (10 μg mL-1).
  • Ag@TACDs demonstrated potent antimicrobial properties against bacterial infections.
  • The novel agent exhibited good biocompatibility, enhanced cell activity, and reduced cytotoxicity from Aβ42 oligomers.

Conclusions:

  • Ag@TACDs represent a promising multi-targeted strategy for Alzheimer's disease treatment.
  • This approach effectively targets key pathological hallmarks of AD, including amyloid aggregation and infection.
  • The findings support the development of Ag@TACDs as potential multi-target inhibitors for AD therapy.