ArticleHuman cell2021
The protective effects of Agomelatine against Aβ1-42 oligomers-induced cellular senescence mediated by SIRT6 and Agomelatine's potential in AD treatment.
Article in Human cell, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- Senescence as a Central Node in Alzheimer's Disease: Molecular Triggers, Cellular Effectors, and RNA-Based Interventions.Neurochemical research · 2026Review
- Agomelatine Ameliorates Cognitive and Behavioral Deficits in Aβ-Induced Alzheimer's Disease-like Rat Model.Medicina (Kaunas, Lithuania) · 2025Article
- Exercise mitigates Alzheimer's disease by targeting ferroptosis driven by cellular senescence.Frontiers in cell and developmental biology · 2025Review
- METTL14 inhibits Aβ1-42-induced neuronal injury through regulating the stability of CBLN4 mRNA in Alzheimer's disease.Journal of bioenergetics and biomembranes · 2024Article
- Article
- Inflammation and aging: signaling pathways and intervention therapies.Signal transduction and targeted therapy · 2023Review
- Sirtuins in osteoarthritis: current understanding.Frontiers in immunology · 2023Review
- Midazolam alleviates cellular senescence in SH-SY5Y neuronal cells in Alzheimer's disease.Brain and behavior · 2023Article
- Luteolin suppresses TNF-α-induced inflammatory injury and senescence of nucleus pulposus cells via the Sirt6/NF-κB pathway.Experimental and therapeutic medicine · 2022Article
- The Long-Term Culture of Human Fibroblasts Reveals a Spectroscopic Signature of Senescence.International journal of molecular sciences · 2022Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is a vicious degenerative disease commonly observed in the elderly population, and the deposition of Amyloid β (Aβ) is regarded as the principal pathological inducement of AD. Severe oxidative stress, inflammatory reactions, and cell senescence in neurons can be induced by Aβ1-42 oligomers, which further contribute to the damage on neurons. Agomelatine is an antidepressant that is recently claimed to have promising anti-oxidative stress and anti-inflammatory effects. The present study aims to explore the potential therapeutic function of Agomelatine on AD and the possible mechanism. Aβ1-42 oligomers were used to induce an in vitro injury model in SH-SY5Y neuronal cells. First, we found that exposure to Aβ1-42 oligomers significantly exacerbated oxidative stress by increasing hydrogen peroxide production and reducing glutathione peroxidase (GPx), which were partially rescued by Agomelatine. Also, Agomelatine attenuated Aβ1-42 oligomers-induced inflammatory response by decreasing the expression of TNF-α and IL-1β. Notably, Agomelatine improved cellular senescence by reducing senescence-associated β-galactosidase (SA-β-Gal) staining and mitigating Aβ1-42 oligomers-induced reduction of telomerase activity. In addition, the upregulated p16
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.