ArticleNeurotoxicity research
Changes in APP, PS1 and other factors related to Alzheimer's disease pathophysiology after trimethyltin-induced brain lesion in the rat.
Article in Neurotoxicity research. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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15 citing papers in PubMed, 42 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
- Beta-sitosterol mitigates cognitive deficit and hippocampal neurodegeneration in mice with trimethyltin-induced toxicity.Experimental animals · 2024Article
- 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
- Trimethyltin Increases Intracellular CaMolecular neurobiology · 2021Article
- Effects of Dizocilpine, Midazolam and Their Co-Application on the Trimethyltin (TMT)-Induced Rat Model of Cognitive Deficit.Brain sciences · 2021Article
- Autophagy is ActivatedInternational journal of molecular sciences · 2019Article
- Trimethyltin-induced cochlear degeneration in rat.Journal of otology · 2016Article
- Histopathological Analysis from Gallic Acid Administration on Hippocampal Cell Density, Depression, and Anxiety Related Behaviors in A Trimethyltin Intoxication Model.Cell journal · 2016Article
- Trimethyltin-Induced Microglial Activation via NADPH Oxidase and MAPKs Pathway in BV-2 Microglial Cells.Mediators of inflammation · 2015Article
- Gene expression profiling as a tool to investigate the molecular machinery activated during hippocampal neurodegeneration induced by trimethyltin (TMT) administration.International journal of molecular sciences · 2013Review
- Neuroprotective strategies in hippocampal neurodegeneration induced by the neurotoxicant trimethyltin.Neurochemical research · 2013Review
- Neurotoxins and neurotoxic species implicated in neurodegeneration.Neurotoxicity research · 2004Review
- Novel mechanisms and approaches in the study of neurodegeneration and neuroprotection. a review.Neurotoxicity research · 2003Review
- The vitamin-E analog trolox and the NMDA antagonist MK-801 protect pyramidal neurons in hippocampal slice cultures from IL-1beta-induced neurodegeneration.Neurotoxicity research · 2003Article
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Authors and funding
3 authors at 2 institutions in 2 countries.
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No grant is acknowledged in the PubMed record.
Abstract
Trimethyltin (TMT) chloride induces limbic system neurodegeneration, resulting in behavioral alterations including cognitive deficits. Different factors related to Alzheimer's disease (AD) were studied after TMT lesion in Sprague-Dawley rats. The expression of amyloid precursor protein (APP) containing 695 amino acids (APP695), APP containing the Kuniz protease inhibitor domain (APP- KPI), presenilin 1 (PS1), c- fos and IL- 1Beta was investigated at different timepoints after a single TMT injection (7 mg/kg i.p.) using in situ hybridization and immunohistochemistry. After the TMT treatment, extensive degeneration of pyramidal neurons was observed in the CA3 region of the hippocampus, concomitant with neurodegeneration in the outer layer of the CA1 region and layer II of entorhinal and piriform cortex. The affected regions showed abundant condensed eosinophilic and TUNEL-positive neuronal cells, that were apparent at day 4 after TMT, increasing to day 7 and subsequently disappearing. In the affected regions the levels of APP695 mRNA gradually declined with time after the TMT injection. While there was no apparent alteration in the overall expression of APP- KPI or PS1 mRNA, detailed analysis of the CA3c region showed that the mRNA expression shifted from neurons to glial cells. Three days after TMT, neurons in the piriform cortex, the CA3 region and DG expressed high levels of c-fos mRNA that slowly declined to become normalized when analyzed at day 28. At day 7 after TMT a few distinct IL- 1Beta mRNA expressing glial cells were observed in the CA3c region. Thus, TMT exposure leads to alterations in the expresson of APP, APP- KPI, PS1, c-fos and IL- 1Beta in the limbic system. These findings suggest that TMT lesions, not only share certain key features of AD symptomatology and regional neurodegeneration, but also induce effects on important factors related to the pathophysiology of AD.
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