ArticleNaunyn-Schmiedeberg's archives of pharmacology2024
Agomelatine improves memory and learning impairments in a rat model of LPS-induced neurotoxicity by modulating the ERK/SorLA/BDNF/TrkB pathway.
Article in Naunyn-Schmiedeberg's archives of pharmacology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 9 citations in OpenAlex.
- Investigation of the Effects of Agomelatine in Rats with Experimental Cerebral Ischemia/Reperfusion Model.Biomedicines · 2026Article
- Agomelatine decreased cocaine-induced locomotor activity in rats; a dose-time response study.Frontiers in pharmacology · 2026Article
- Human neural stem cell-derived exosomes promote functional recovery in subarachnoid hemorrhage via bdnf/trkb pathway activation and astrocyte modulation.Acta neuropathologica communications · 2025Article
- Agomelatine Ameliorates Cognitive and Behavioral Deficits in Aβ-Induced Alzheimer's Disease-like Rat Model.Medicina (Kaunas, Lithuania) · 2025Article
- Agonism of MTNeurochemical research · 2025Article
- The Oxidative Stress in Epilepsy-Focus on Melatonin.International journal of molecular sciences · 2024Review
- Short-term high fat diet impairs memory, exacerbates the neuroimmune response, and evokes synaptic degradation via a complement-dependent mechanism in a mouse model of Alzheimer's disease.Brain, behavior, and immunity · 2024Article
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4 authors at 2 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
The mutual interplay between neuroinflammation, synaptic plasticity, and autophagy has piqued researchers' interest, particularly when it comes to linking their impact and relationship to cognitive deficits. Being able to reduce inflammation and apoptosis, melatonin has shown to have positive neuroprotective effects; that is why we thought to check the possible role of agomelatine (AGO) as a promising candidate that could have a positive impact on cognitive deficits. In the current study, AGO (40 mg/kg/day, p.o., 7 days) successfully ameliorated the cognitive and learning disabilities caused by lipopolysaccharide (LPS) in rats (250 μg/kg/day, i.p., 7 days). This positive impact was supported by improved histopathological findings and improved spatial memory as assessed using Morris water maze. AGO showed a strong ability to control BACE1 activity and to rein in the hippocampal amyloid beta (Aβ) deposition. Also, it improved neuronal survival, neuroplasticity, and neurogenesis by boosting BDNF levels and promoting its advantageous effects and by reinforcing the pTrkB expression. In addition, it upregulated the pre- and postsynaptic neuroplasticity biomarkers resembled in synapsin I, synaptophysin, and PSD-95. Furthermore, AGO showed a modulatory action on Sortilin-related receptor with A-type repeats (SorLA) pathway and adjusted autophagy. It is noteworthy that all of these actions were abolished by administering PD98059 a MEK/ERK pathway inhibitor (0.3 mg/kg/day, i.p., 7 days). In conclusion, AGO administration significantly improves memory and learning disabilities associated with LPS administration by modulating the ERK/SorLA/BDNF/TrkB signaling pathway parallel to its capacity to adjust the autophagic process.
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