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Dietary folic acid prevents peripheral neuropathy in mouse models of neural tube defects and type 2 diabetes

GSE275111 Mus musculus (mouse) RNA-seq (gene expression) 25 samples Submitted 2025/12/17 Platform GPL24247
At a glance

RNA-seq (gene expression) · mouse · 25 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
25 samples
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
Dietary folic acid prevents peripheral neuropathy in mouse models of neural tube defects and type 2 diabetesProceedings of the National Academy of Sciences of the United States of America · 2026
Summary (written by the submitters)
Folate-mediated one-carbon metabolism is implicated in several pathologies including neural tube defects (NTDs), cancer and neurodegenerative disorders, whereas diabetes is associated with NTDs and peripheral neuropathy (PN). The development of peripheral neuropathy was assessed in Shmt1+/- and Shmt1 -/- mice, which are models of human folic acid-responsive NTDs, and diabetic (Leprdb) mice to determine if NTDs and PN have a shared etiology.
Read the full summary ↓
From 6 weeks of age, male and female mice with reduced Shmt1 expression exhibited PN, with greater severity in females compared to males. The neuropathic progression was distinct from diabetic peripheral neuropathy (DPN) observed in Leprdb mice. Excess dietary folic acid prevented PN in both Shmt1-/- and Leprdb/db mice, whereas dietary uridine caused demyelinating PN in mice independent of genotype and folate status. The transcriptome from L3-L5 dorsal root ganglia (DRG) exhibited distinct sex-specific differences in glial cell gene expression when comparing Shmt1+/+ and Shmt1-/- mice. DRG sensory neurons exhibited changes in the expression of solute carriers and ion channels involved in nociception, neurotransmission and structural support. We conclude that reduced thymidylate synthesis causes folic-acid responsive NTDs and PN in mice, and that diabetes sensitizes mice to folic acid-responsive PN. Diabetes induces a special nutritional requirement for high intake of folic acid to prevent PN.
Published in
Dietary folic acid prevents peripheral neuropathy in mouse models of neural tube defects and type 2 diabetes
Chakraborty J, Ghosh A, Awuah EB et al. · Proceedings of the National Academy of Sciences of the United States of America 2026 · PMID 41481435 · doi:10.1073/pnas.2528095123
This dataset
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.

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 GSE275111_RAW.tar (it can run to tens of gigabytes).

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.

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 PRJNA1149463 and SRA study SRP527200. Searching any of these in the dataset finder brings you back here.

Samples in this study

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