ArticleNeurotoxicity research2025
Multi-Omics Analysis of Hippocampus in Rats Administered Trimethyltin Chloride.
Article in Neurotoxicity research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Aerobic exercise significantly altersJournal of Alzheimer's disease : JAD · 2026Article
- Systematic Review: Proteomics-Driven Multi-Omics Integration for Alzheimer's Disease Pathology and Precision Medicine.Neurology international · 2025Review
- C3H mouse model of Alzheimer's disease: Blood markers, proteomic biomarkers, cognitive ability, and histopathology.Open veterinary journal · 2025Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Trimethyltin chloride (TMT) is a neurotoxicant that damages the central nervous system (CNS) and triggers neurodegeneration. This study used multi-omic data, including transcriptomics and proteomics of the rat hippocampus, to identify differentially expressed genes and proteins in TMT-induced neurotoxicity over time, related to neuro-axonal damage marked by plasma Neurofilament Light (NfL) levels. Data were collected at 12, 24, 48, 72, and 168 h post-TMT administration. NfL levels surged at 72 and 168 h, confirming neuro-axonal damage. Transcripts of genes in the chemokine signaling pathway (Cxcl10, Cxcl12, Cxcl14, Cxcl16), apoptosis pathway (Caspase-3, PARP1, CTSD), and TNF signaling pathway (TNFR1, MMP9, ICAM-1, TRAF3) showed significant differential expression starting from 48 h, preceding the NfL increase, suggesting their roles in neuro-axonal damage. Additionally, 11 Alzheimer's disease-related proteins, with significant changes from 72 to 168 h, were detected only in the proteomic dataset, indicating post-translational modifications might be crucial in neurotoxicity. Pathway analysis revealed that neurodegeneration and Alzheimer's disease pathways were among the top 15 affected by TMT-induced gene regulation, aligning with the involvement of TNF signaling, apoptosis, and chemokine signaling in neurodegeneration. This research highlighted the value of longitudinal omics studies, combined with pathway enrichment, gene-disease association, and neuro-axonal damage biomarker analyses, to elucidate neurotoxicant-induced neurodegeneration. Findings from this study could enhance the understanding of TMT-induced neurotoxicity, potentially informing future therapeutic strategies and preventive measures.
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Registered trials
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