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STING–IFN–CH25H lipid axis links innate immune activation to tau pathology [scRNA-seq]

GSE313021 Mus musculus (mouse) Single-cell RNA-seq 16 samples Submitted 2025/12/09 Platform GPL24247
At a glance

Single-cell RNA-seq · mouse · 16 samples

What it is
Single-cell RNA-seqGene activity measured in thousands of individual cells, so cell types can be told apart.
Organism
Mus musculus (mouse)
Samples
16 samples: 16 × LG253-NYGroups 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.
Summary (written by the submitters)
Genetic risk for Alzheimer’s disease is strongly enriched in pathways governing microglial activation and cholesterol metabolism, yet how these processes converge to drive neurodegeneration remains unclear. Here, we identify the oxysterol 25-hydroxycholesterol (25-HC) as a pathogenic lipid downstream of the cGAS-STING–IFN pathway. In models of tau pathology, interferon signaling induces Cholesterol 25-hydroxylase (CH25H) expression in microglia.
Read the full summary ↓
Ch25h deletion in female P301S mice suppressed tau aggregation, preserved synapses, prevented brain atrophy, and rescued memory. Mechanistically, loss of CH25H disrupted STING trafficking, attenuated IFN activation, dampened self-perpetuating microglial inflammation. Strikingly, 25HC directly accelerated tau propagation in human iPSC derived neurons. It also disrupted lysosomal and mitochondrial lipid composition, driving cholesteryl ester accumulation and promoting apoptosis under tau-induced stress. These findings define a STING–IFN–CH25H lipid axis that bridges innate immune activation to tau pathology and toxicity, offering a tractable therapeutic pathway for inflammation-driven neurodegenerative conditions.
This dataset
Open GSE313021 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 GSE313021_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: Single-cell studies usually ship their counts as 10x files (matrix.mtx, barcodes.tsv, features.tsv), an .h5 file, or an .rds / .h5ad object that Seurat or Scanpy can open. Look for those among the supplementary files.

Also filed as BioProject PRJNA1378145 and SRA study SRP653741. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗
Study design
16 × LG253-NY

Supports a between-group comparison across 16 samples.

How we read this: 1 replicated groups read from 16 sample titles; they account for 16 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

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