ArticleCell reports2024
Post-stroke hippocampal neurogenesis is impaired by microvascular dysfunction and PI3K signaling in cerebral amyloid angiopathy.
Article in Cell reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed.
- Exercise and Productive Hippocampal Neurogenesis After Stroke: From Niche Remodeling to Cognitive Recovery.Brain sciences · 2026Review
- 1,8-Cineole Promotes the Proliferation of Neural Stem Cells and Inhibits Oxidative Damage Induced by Ischemic Stroke via the Wnt/β-Catenin Signaling Pathway.Molecular neurobiology · 2026Article
- Research progress on blood therapy for anti-aging.Journal of advanced research · 2026Review
- Mertk promotes early microglial-mediated synaptic engulfment in Alzheimer's disease.Theranostics · 2026Article
- Breast Cancer Cell-Derived Exosomal miR-92b-3p Promotes Tumor Angiogenesis and Metastasis by Suppressing PTEN in Vascular Endothelial Cells.Oncology research · 2026Article
- Mechanobiology of hippocampal neurogenesis: directing neural stem cell fate through physical cues.Frontiers in molecular neuroscience · 2026Review
- Stroke Exacerbates Respiratory Disorder and Cognition Impairment in Mice with Cerebral Amyloid Angiopathy.Aging and disease · 2025Article
- Models and mechanisms of post-stroke dementia and cognitive impairment.Frontiers in stroke · 2025Article
- Vortioxetine alleviates motor, cognitive and emotional disorders in post-stroke rats by regulating the TLR-2/NF-Frontiers in pharmacology · 2025Article
Corrections and comments
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Authors and funding
19 authors.
Funding
Abstract
Ischemic stroke and cerebral amyloid angiopathy (CAA) pose significant challenges in an aging population, particularly in post-stroke recovery. Using the 5xFAD mouse model, we explore the relationship between CAA, ischemic stroke, and tissue recovery. We hypothesize that amyloid-beta accumulation worsens stroke outcomes by inducing blood-brain barrier (BBB) dysfunction, leading to impaired neurogenesis. Our findings show that CAA exacerbates stroke outcomes, with mice exhibiting constricted BBB microvessels, reduced cerebral blood flow, and impaired tissue recovery. Transcriptional analysis shows that endothelial cells and neural progenitor cells (NPCs) in the hippocampus exhibit differential gene expression in response to CAA and stroke, specifically targeting the phosphatidylinositol 3-kinase (PI3K) pathway. In vitro experiments with human NPCs validate these findings, showing that disruption of the CXCL12-PIK3C2A-CREB3L2 axis impairs neurogenesis. Notably, PI3K pathway activation restores neurogenesis, highlighting a potential therapeutic approach. These results suggest that CAA combined with stroke induces microvascular dysfunction and aberrant neurogenesis through this specific pathway.
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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.