C<sub>3</sub>N nanodots inhibits Aβ peptides aggregation pathogenic path in Alzheimer's disease.
basic_science · Level V
Where this comes from
- Record sourced from PubMed, PMID 37714837.
- Also identified by DOI 10.1038/s41467-023-41489-y and PMC identifier 10504243.
- Licence recorded as CC BY.
- The licence permits redistribution, so the abstract is shown in full and the full text is available from the publisher.
Abstract
Despite the accumulating evidence linking the development of Alzheimer's disease (AD) to the aggregation of Aβ peptides and the emergence of Aβ oligomers, the FDA has approved very few anti-aggregation-based therapies over the past several decades. Here, we report the discovery of an Aβ peptide aggregation inhibitor: an ultra-small nanodot called C<sub>3</sub>N. C<sub>3</sub>N nanodots alleviate aggregation-induced neuron cytotoxicity, rescue neuronal death, and prevent neurite damage in vitro. Importantly, they reduce the global cerebral Aβ peptides levels, particularly in fibrillar amyloid plaques, and restore synaptic loss in AD mice. Consequently, these C<sub>3</sub>N nanodots significantly ameliorate behavioral deficits of APP/PS1 double transgenic male AD mice. Moreover, analysis of critical tissues (e.g., heart, liver, spleen, lung, and kidney) display no obvious pathological damage, suggesting C<sub>3</sub>N nanodots are biologically safe. Finally, molecular dynamics simulations also reveal the inhibitory mechanisms of C<sub>3</sub>N nanodots in Aβ peptides aggregation and its potential application against AD.
Medical subject headings
- Alzheimer Disease
- Nanoparticles
- Amyloid beta-Peptides