← BioTransfer GEO Dataset Finder
GEO series

Cadmium-induced gut dysbiosis precedes the onset of hippocampus-dependent learning and memory deficits in mice

GSE293538 Mus musculus (mouse) RNA-seq (gene expression) 10 samples Submitted 2026/04/01 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 10 samples

What it is
RNA-seq (gene expression)Gene activity measured by sequencing. The summary does not mention single-cell work, so this is most likely bulk: one average per sample, the usual starting point for comparing groups.
Organism
Mus musculus (mouse)
Samples
10 samples: 5 × C57BL/6 mouse hippocampus, vehicle vs 5 × C57BL/6 mouse hippocampus, CdGroups are read from the sample names, not from the paper. Check the list below.
Data you can get
A processed table (series matrix) and supplementary files from NCBI; the raw sequencing reads from ENA. Which of these hold counts depends on the study, so check the file list.
Paper
Cadmium-induced gut dysbiosis precedes the onset of hippocampus-dependent learning and memory deficits in miceToxicology · 2025
Summary (written by the submitters)
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.
Read the full summary ↓
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.
Published in
Cadmium-induced gut dysbiosis precedes the onset of hippocampus-dependent learning and memory deficits in mice
Wang H, Lim JJ, Gu H et al. · Toxicology 2025 · PMID 40850461 · doi:10.1016/j.tox.2025.154265
This dataset
Open GSE293538 in finder → Find more mouse RNA-seq datasets →
Download · which file do I need?

Direct links to NCBI and ENA, no account and no request form. Pick by what you want to do: take the small processed table to look, the supplementary files to re-analyse, or the original raw data to start over.

1 · Just have a look

Processed table

The series matrix: one table of values per sample as the submitters processed it. The smallest download, and it opens in Excel or R. Start here to see what the data look like.

Series matrix ↓
2 · Re-analyse it

Supplementary files

The count tables and other files the authors uploaded. Take only the samples you need, or the whole study as GSE293538_RAW.tar (it can run to tens of gigabytes).

All supplementary files ↗ Whole study · RAW.tar ↓
3 · Start from the raw reads

Raw sequencing reads

The original FASTQ files, straight from the sequencer, held at ENA. Large, and you align them yourself, so only choose this if you need to re-process the study from scratch.

Raw reads on ENA ↗

What the files usually look like: For RNA-seq the counts are usually a table among the supplementary files (look for 'counts', 'expression', 'FPKM' or 'TPM' in the file name). The series matrix of a sequencing study is sometimes nearly empty.

Also filed as BioProject PRJNA1244899 and SRA study SRP575733. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗ Paper (PMID 40850461) ↗
Study design
5 × C57BL/6 mouse hippocampus, vehicle vs 5 × C57BL/6 mouse hippocampus, Cd

Supports a between-group comparison across 10 samples.

How we read this: 2 replicated groups read from 10 sample titles; they account for 10 of them. These groups are guessed from the sample names, not taken from the paper, so check them against the sample list below before relying on them.

Samples in this study
Datasets on a similar topic

Search all mouse RNA-seq datasets in GEO →

Share this dataset

Metadata from NCBI GEO, cached and refreshed periodically — the NCBI page above is authoritative. Downloads link straight to NCBI/ENA; nothing is proxied through BioTransfer.