GEO series

Single cell genomic and epigenomic analysis of mouse and human Alzheimer's disease (Human)

GSE288063 Homo sapiens (human) Single-cell RNA-seq 18 samples Submitted 2026/10/01 Platform GPL24676

At a glance

Single-cell RNA-seq · human · 18 samples

What it is: Single-cell RNA-seqGene activity measured in thousands of individual cells, so cell types can be told apart.
Organism: Homo sapiens (human)
Samples: 18 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.

Summary (written by the submitters)

Aging is the strongest risk factor for Alzheimer’s disease (AD), yet the mechanisms by which aging promotes AD progression remain incompletely understood. Chronic neuroinflammation is a hallmark of both brain aging and AD, with microglia undergoing progressive inflammatory and functional changes, but how these age-associated changes contribute to disease progression is unclear.

Read the full summary ↓

Here, we profiled gene expression and chromatin accessibility in the hippocampus across aging and amyloid-β (Aβ) pathology, and identified progressive activation of cGAS-STING pathway and interferon-responsive microglial states that are markedly accelerated in the process. Pharmacological inhibition of STING in aged mice improved spatial memory, reduced Aβ plaque burden and shifted microglia from interferon-responsive states towards a phagocytic program associated with enhanced Aβ clearance. Mechanistically, STING activation reduced MEF2 activity and occupancy at enhancers of phagocytosis-associated genes, whereas STING inhibition restored MEF2 activity. Human AD hippocampal microglia similarly exhibited elevated IRF3 activity together with reduced MEF2C activity and nuclear availability. STING inhibition failed to preserve Aβ phagocytosis in MEF2C-deficient human iPSC-derived microglia. Together, these findings identify a cGAS–STING–MEF2 regulatory axis through which aging-associated innate immune signaling impairs microglial Aβ clearance and suggest that targeting cGAS–STING may restore protective microglial function in AD.

This dataset

Open GSE288063 in finder → Find more human 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 GSE288063_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 PRJNA1215757 and SRA study SRP559920. Searching any of these in the dataset finder brings you back here.

NCBI GEO page ↗

Samples in this study

The sample list for this study is not cached yet. Press Load samples and it will be fetched from NCBI.

+ 18 more — browse all 18 samples with per-sample file links →

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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.