ArticleMolecular psychiatry2023
VEGF-A in serum protects against memory impairment in APP/PS1 transgenic mice by blocking neutrophil infiltration.
Article in Molecular psychiatry, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 22 citations in OpenAlex.
- Neutrophil Extracellular Traps Mediate in vitro and in vivo Degradation of α-Synuclein Amyloid Fibrils.Journal of inflammation research · 2026Article
- Association of choroid plexus volume with white matter microstructure, glymphatic function, and peripheral systemic inflammation in Alzheimer's disease.Translational psychiatry · 2025Article
- Correlation study of 5-HT in brain with cognitive function and anxious-like behavior in APP/PS1 transgene mice.Sleep and biological rhythms · 2025Article
- Neutrophils from Alzheimer's disease mice fail to phagocytose debris and show altered release of immune modulators with age.Frontiers in immunology · 2025Article
- Blockage of VEGF function by bevacizumab alleviates early-stage cerebrovascular dysfunction and improves cognitive function in a mouse model of Alzheimer's disease.Translational neurodegeneration · 2024Article
- CD8 positive T-cells decrease neurogenesis and induce anxiety-like behaviour following hepatitis B vaccination.Brain communications · 2024Article
Corrections and comments
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Authors and funding
18 authors at 2 institutions in 2 countries.
Funding
Abstract
Activation of innate immunity in the brain is a prominent feature of Alzheimer's disease (AD). The present study investigated the regulation of innate immunity by wild-type serum injection in a transgenic AD mouse model. We found that treatment with wild-type mouse serum significantly reduced the number of neutrophils and microglial reactivity in the brains of APP/PS1 mice. Mimicking this effect, neutrophil depletion via Ly6G neutralizing antibodies resulted in improvements in AD brain functions. Serum proteomic analysis identified vascular endothelial growth factor-A (VEGF-A) and chemokine (C-X-C motif) ligand 1 (CXCL1) as factors enriched in serum samples, which are crucial for neutrophil migration and chemotaxis, leukocyte migration, and cell chemotaxis. Exogenous VEGF-A reversed amyloid β (Aβ)-induced decreases in cyclin-dependent kinase 5 (Cdk5) and increases in CXCL1 in vitro and blocked neutrophil infiltration into the AD brain. Endothelial Cdk5 overexpression conferred an inhibitory effect on CXCL1 and neutrophil infiltration, thereby restoring memory abilities in APP/PS1 mice. Our findings uncover a previously unknown link between blood-derived VEGF signaling and neutrophil infiltration and support targeting endothelial Cdk5 signaling as a potential therapeutic strategy for AD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.