ArticleToxicology reports2024
Reciprocal crosslink among MeCP2/BDNF /CREB signaling pinpointed in autism spectrum disorder.
Article in Toxicology reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 4 citations in OpenAlex.
- Iron dysregulation in the central nervous system: implications for autism spectrum disorder.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Review
- Montelukast Ameliorates Antimony-Induced Neurotoxicity Accompanied by Alterations in Oxidative Stress, Neuroinflammation, and Mitochondrial Function.Biological trace element research · 2026Article
- Cerebroprotective potential of ceftriaxone against cadmium chloride-induced cerebral inflammatory changes and oxidative insult.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autism spectrum disorder, or individual disability (ID), is a condition characterized by complications in social interaction, restricted repetitive behavior, and difficulties in social communication. Neuquinon (NQ) possess a powerful therapeutic potential in various neurodegenerative disease. Nevertheless, contributing to NQ's low water solubility and bioavailability, its medicinal use has been constrained. Liposomes were supposed to be prospective drug-delivering agents for NQ, crossing the blood-brain barrier (BBB), and reaching the target organs. The current investigation aims to track the signaling pathways that govern NQ and liposomal neuquinon (LNQ) action in autistic models generated by ethyl formic acid. The neurotransmitters gamma amino-butyric acid (GABA), acetylcholine (ACh), and acetylcholinesterase (AChE) in addition to, the gene expressions of brain-derived neurotrophic factor (BDNF), cAMP response element-binding protein (CREB), and methyl-CpG-binding protein 2 (MeCP2) and the DNA damage COMET analysis at different time intervals of the study, were assessed. EFA in a dose of 500 mg/kg BW was used to induce autism in rats, and then NQ and LNQ were administered in 10 mg/kg and 2 mg/kg BW, respectively. The results revealed that NQ and LNQ significantly down-regulated BDNF, GABA, and AChE; on the other hand, they up-regulated MeCP2, CREB gene expressions, and ACh action. NQ and LNQ displayed improvement in DNA damage in almost all brain regions after EFA alterations; even better results were noticed post-LNQ therapy. Therefore, it may be concluded that neuquinon and liposomal-loaded neuquinon have a therapeutic index versus EFA-induced autism in a rat model.
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Registered trials
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