ReviewInternational journal of molecular sciences2013
Gene expression profiling as a tool to investigate the molecular machinery activated during hippocampal neurodegeneration induced by trimethyltin (TMT) administration.
Review in International journal of molecular sciences, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 35 citations in OpenAlex.
- Effects of Continuous Theta Burst Stimulation on Behavior and NMDA Receptor Subunits in the Trimethyltin-Induced Alzheimer's-like Disease Model.Biomedicines · 2026Article
- Combined exercise and Hawthorn protect against learning impairments and hippocampal damage from trimethyltin neurotoxicity in rat.Scientific reports · 2025Article
- Multi-Omics Analysis of Hippocampus in Rats Administered Trimethyltin Chloride.Neurotoxicity research · 2025Article
- Feasibility study of PET/CT for the detection and localization of nervous system damage caused by trimethyltin chloride.Scientific reports · 2025Article
- Article
- Neuroprotective effects of ex vivo-expanded regulatory T cells on trimethyltin-induced neurodegeneration in mice.Journal of neuroinflammation · 2022Article
- Intermittent Theta Burst Stimulation Ameliorates Cognitive Deficit and Attenuates NeuroinflammationFrontiers in aging neuroscience · 2022Article
- Therapeutic Effects of Hydrogen Gas Inhalation on Trimethyltin-Induced Neurotoxicity and Cognitive Impairment in the C57BL/6 Mice Model.International journal of molecular sciences · 2021Article
- Prenatal Trimethyltin Exposure Induces Long-Term DNA Methylation Changes in the Male Mouse Hippocampus.International journal of molecular sciences · 2021Article
- KIF5A-dependent axonal transport deficiency disrupts autophagic flux in trimethyltin chloride-induced neurotoxicity.Autophagy · 2021Article
- Autophagy in trimethyltin-induced neurodegeneration.Journal of neural transmission (Vienna, Austria : 1996) · 2020Review
- Expression of mGlu Receptor Genes in the Hippocampus After Intoxication with Trimethyltin.Journal of molecular neuroscience : MN · 2019Article
- The Neuroprotective Effects of 17β-Estradiol Pretreatment in a Model of Neonatal Hippocampal Injury Induced by Trimethyltin.Frontiers in cellular neuroscience · 2018Article
- Ginsenoside Rd as a potential neuroprotective agent prevents trimethyltin injury.Biomedical reports · 2017Article
- Association Between Microglia, Inflammatory Factors, and Complement with Loss of Hippocampal Mossy Fiber Synapses Induced by Trimethyltin.Neurotoxicity research · 2016Article
- Estrogen administration modulates hippocampal GABAergic subpopulations in the hippocampus of trimethyltin-treated rats.Frontiers in cellular neuroscience · 2015Article
- Cellular targets for neuropeptide Y-mediated control of adult neurogenesis.Frontiers in cellular neuroscience · 2015Review
- Article
- Article
- Promising Therapeutic Potential of miR-220-3p Mimic Against Murine Trimethyltin Hippocampal Injury.Iranian journal of pharmaceutical research : IJPRArticle
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Trimethyltin (TMT) is an organotin compound exhibiting neurotoxicant effects selectively localized in the limbic system and especially marked in the hippocampus, in both experimental animal models and accidentally exposed humans. TMT administration causes selective neuronal death involving either the granular neurons of the dentate gyrus or the pyramidal cells of the Cornu Ammonis, with a different pattern of localization depending on the different species studied or the dosage schedule. TMT is broadly used to realize experimental models of hippocampal neurodegeneration associated with cognitive impairment and temporal lobe epilepsy, though the molecular mechanisms underlying the associated selective neuronal death are still not conclusively clarified. Experimental evidence indicates that TMT-induced neurodegeneration is a complex event involving different pathogenetic mechanisms, probably acting differently in animal and cell models, which include neuroinflammation, intracellular calcium overload, and oxidative stress. Microarray-based, genome-wide expression analysis has been used to investigate the molecular scenario occurring in the TMT-injured brain in different in vivo and in vitro models, producing an overwhelming amount of data. The aim of this review is to discuss and rationalize the state-of-the-art on TMT-associated genome wide expression profiles in order to identify comparable and reproducible data that may allow focusing on significantly involved pathways.
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Registered trials
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.