Authors
Dongsheng Ji, Jing Zhao, Xinhui Huang, Xuan Liu, Qirong Yang, Xinfeng Li, Lei Yan, Debo Gao, Yuliang Xiao
Published in
Frontiers in pharmacology. Volume 17. Pages 1936198. Epub Sep 15, 2026.
Abstract
Alzheimer's disease (AD) is a severe neurodegenerative disorder characterised by progressive memory loss and cognitive decline. Because of the lack of effective treatment modalities for AD, novel therapeutics that could delay the progression of AD are urgently required. In this study, the neuroprotective effects and mechanisms of chondroitin sulphate nano-selenium (CS@Se) were investigated by using APPSwe, PSEN1dE9 (APP/PS1) transgenic mice. We found CS@Se to exhibit potent multi-targeted anti-AD effects, and it showed excellent ability to effectively alleviate neuropathy and cognitive dysfunction. Behavioural experiments showed that CS@Se improved learning and memory capacity and enhanced motor activity. Mechanistically, CS@Se upregulated A disintegrin and metalloproteinase domain-containing protein 10 (ADAM10) expression while downregulating the levels of amyloid precursor protein (APP) and beta-secretase 1 (BACE1). Further studies revealed that CS@Se could reduce β-amyloid (Aβ) deposition and inhibit tau phosphorylation by promoting APP hydrolysis and inhibiting the glycogen synthase kinase (GSK)-3β signalling pathway in APP/PS1 mice. Additionally, CS@Se could alleviate oxidative stress damage, neuroinflammation, and cholinergic damage. In conclusion, CS@Se confers substantial neuroprotective effects by modulating several key pathological pathways, providing evidence for its multi-target therapeutic strategy against AD.
PMID:
42812304
Bibliographic data and abstract were imported from PubMed on 18 Oct 2026.
Read full publication at:
Please sign in
to see all details.
Advertisement
Stats
- Recommendations n/a n/a positive of 0 vote(s)
- Views 9
- Comments 0