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Blood-brain barrier dysfunction in response to Alzheimer's disease mutations and aged serum in a tissue-engineered microvascular model

GSE272179 Homo sapiens (human) RNA-seq (gene expression) 54 samples Submitted 2024/09/01 Platform GPL24676
At a glance

RNA-seq (gene expression) · human · 54 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
Homo sapiens (human)
Samples
54 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
Mutations associated with Alzheimer's disease and aged serum synergistically elicit blood-brain barrier dysfunction in a tissue-engineered modelFluids and barriers of the CNS · 2026
Summary (written by the submitters)
Alzheimer’s disease is a disease of neurodegeneration and aging that affects millions of Americans, and is expected to impact millions more without significant advancement in our understanding of the disease. An emerging focus in Alzheimer’s study is the role of the cerebrovasculature in the initiation, progression, and exacerbation of symptomatic disease.
Read the full summary ↓
Disruption of the blood-brain barrier, which tightly controls any exchange between systemic circulation and brain tissue, has manifested in post-mortem and in vivo studies of late-stage Alzheimer’s disease as microbleeds, dysfunctional glucose transport, and impaired efflux of toxins; additional animal studies have indicated that some vascular dysfunction precedes neuronal degeneration in the progression of the disease. Thus, to understand the drivers and progression of Alzheimer’s disease in hopes of identifying therapeutic breakpoints, the role of blood-brain barrier dysfunction must be investigated. Here, we utilize a tissue-engineered model of the blood-brain barrier with high spatiotemporal resolution to assess its dysfunction with cell-intrinsic mutations associated with Alzheimer’s (APP(Swe) and PSEN1(M146V)) and the systemic influence of aged blood components (exposure to aged vs. young human serum).
Published in
Mutations associated with Alzheimer's disease and aged serum synergistically elicit blood-brain barrier dysfunction in a tissue-engineered model
Chung TD, Liang L, Wang L et al. · Fluids and barriers of the CNS 2026 · PMID 41699702 · doi:10.1186/s12987-026-00773-x
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 GSE272179_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 PRJNA1135453 and SRA study SRP519704. Searching any of these in the dataset finder brings you back here.

Samples in this study

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