Dataset Information

Cross-Species Validation of the Cadmium-Induced Cognitive Impairment Prediction Model: Hippocampus-Specific Biomarker Assessment in a Chronic Cadmium-Exposed Rat Model

ABSTRACT: This dataset represents a hippocampus component of a multi-tissue proteomics study designed to validate the clinical prediction model for cognitive impairment identified through human clinical proteomics analysis. The rat model was exposed to cadmium (CdCl₂ 30 μg/kg/day, oral gavage) for 8 weeks to induce cognitive deficits mirroring human phenotypes.

ORGANISM(S): Rattus Norvegicus

SUBMITTER: Shaoxin Huang

PROVIDER: PXD069571 | iProX | Fri Oct 17 00:00:00 BST 2025

REPOSITORIES: iProX

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Project description:Background: Cadmium (Cd) is a heavy metal recognized as a neurotoxicant. However, the mechanisms underlying its neurotoxicity remain poorly understood. The gut-brain axis, a bidirectional communication pathway between the central nervous system and the gut microbiome, has been linked to various neurological disorders. Because the gut microbiome is a known target of Cd, it is important to investigate whether the gut-brain axis mechanistically contributes to the Cd-induced neurotoxicity. Objective: In our initial exploration of the role of the gut-brain axis in modulating Cd neurotoxicity on cognition, we investigated whether Cd exposure induces gut dysbiosis before the onset of cognitive deficits and explored the potential link between gut microbiome alterations and Cd-induced cognitive deficits. Methods: Adult male mice were exposed to 3 mg/L Cd via drinking water for nine weeks. Behavioral assessments were conducted throughout the exposure period to evaluate cognitive function. Fresh fecal pellets were collected weekly to monitor gut microbiome composition. The effects of Cd on the hippocampus and intestine were analyzed using transcriptomics and mass spectrometry (MS)-based metabolomics. Results: Cd exposure resulted in hippocampus-dependent learning and memory deficits, first observed at four weeks into exposure. RNA sequencing of the hippocampus at the terminal time point revealed reduced expression of genes involved in cognition and neuroinflammation in Cd exposed mice. Metagenomic shotgun sequencing showed that Cd-induced gut dysbiosis preceded the onset of cognitive impairments, with specific bacterial species associated with Cd-induced cognitive deficits, confirmed by using the cor.test function (Spearman correlation, p < 0.1) in R. Furthermore, Cd exposure compromised intestinal barrier integrity, increased inflammatory cytokines levels, and altered the levels of neuroactive microbial metabolites in mice, which may be linked to Cd-induced gut dysbiosis Conclusion: Our study is the first to show that Cd exposure triggers gut microbial shifts before the onset of cognitive deficits, accompanied by increased intestinal permeability and elevated proinflammatory biomarkers in both the intestine and brain at the terminal time point. These findings suggest a potential critical role of gut-brain axis in modulating Cd neurotoxicity and underscore the need for future research to elucidate the mechanistic involvement of gut microbiome as a potential target for mitigating Cd-induced cognitive decline.

Dataset Information

Cross-Species Validation of the Cadmium-Induced Cognitive Impairment Prediction Model: Hippocampus-Specific Biomarker Assessment in a Chronic Cadmium-Exposed Rat Model

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