Omics · study · 2026
APP-deficiency impairs GLUT1 through defective growth factor signaling.
Listed in NCBI GEO
Cerebral glucose hypometabolism predicts progression from mild cognitive impairment to Alzheimer’s disease (AD).
Description
An important contributor to hypometabolism are decreased glucose transporter 1 (GLUT1) levels in the cerebral endothelium through unknown mechanisms. Because the amyloid precursor protein (APP) is causatively linked to AD, understanding its functions is essential.
Here we report that GLUT1 levels were reduced in three APP knockout (KO) models. RNA-seq data on APP KO MEFs revealed extensive changes in soluble and deposited extracellular matrix (ECM) encoding transcripts. Proteomics revealed a downregulation of secreted growth factors and glucose metabolism regulators in the absence of APP, which account for the GLUT1 defect.
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In cerebrospinal fluid from cognitively unimpaired individuals at risk for AD (PResymptomatic EValuation of Experimental or Novel Treatments for AD (PREVENT-AD) cohort), a positive correlation was observed between these factors and APP levels. Genetic APP variants associated with altered cerebral glucose uptake in the Alzheimer’s Disease Neuroimaging Initiative (ADNI) cohort. Our findings posit APP as a major modulator of GLUT1, likely via ECM and growth factor regulation.
Links
Get the data
- GEO FTP directory ftp.ncbi.nlm.nih.gov/geo/series/GSE344nnn/GSE344092 ↗
download · from NCBI GEO
Where it is published
- GEO accession page ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE344092 ↗
landing page · from NCBI GEO
Documentation and papers
- PRJNA1514623 ncbi.nlm.nih.gov/bioproject/PRJNA1514623 ↗
project · from NCBI GEO
Topics
- Stated by source
- Expression profiling by high throughput sequencing · Mus musculus
- From keywords
- Life Sciences
- Inferred from text
- Disease 75% · Mass spectrometry 65% · RNA sequencing 65%
Provenance · 1 source records, 10 field assertions
| Source | Key | Last seen | Raw |
|---|---|---|---|
| NCBI GEO | GSE344092 | 12 d ago | JSON v1 |
| Field | Assertion | Extractor | Evidence |
|---|---|---|---|
| access_level | source · NCBI GEO | connector:ncbi_geo@1.0.0 | |
| concepts[disease].local:disease:disease | enrichment · NCBI GEO | keyword-concept-rules@1.0.0 | title+description (75%) |
| concepts[field].local:field:life-sciences | mapping · NCBI GEO | connector:ncbi_geo@1.0.0 | |
| concepts[method].geo_series_type:expression-profiling-by-high-throughput-sequencing | source · NCBI GEO | connector:ncbi_geo@1.0.0 | /gdstype |
| concepts[modality].local:modality:mass-spectrometry | enrichment · NCBI GEO | keyword-concept-rules@1.0.0 | title+description (65%) |
| concepts[modality].local:modality:rna-seq | enrichment · NCBI GEO | keyword-concept-rules@1.0.0 | title+description (65%) |
| concepts[organism].NCBITaxon:10090 | source · NCBI GEO | connector:ncbi_geo@1.0.0 | /taxon |
| description | source · NCBI GEO | connector:ncbi_geo@1.0.0 | /summary |
| publication_date | source · NCBI GEO | connector:ncbi_geo@1.0.0 | |
| title | source · NCBI GEO | connector:ncbi_geo@1.0.0 | /title |