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Angiopoietin-2 aggravates Alzheimer’s disease by promoting BBB breakdown and neuroinflammation.

GSE286360 Mus musculus Expression profiling by high throughput sequencing 7 samples Submitted 2026/04/15 Platform GPL24247
Summary
Disruption of the blood-brain barrier (BBB) and increased vascular leakage contribute to neuroinflammation in Alzheimer’s disease (AD), driving disease pathogenesis and progression. However, the mechanisms underlying BBB dysfunction and neuroinflammation in AD remain unclear. Angiopoietin-2 (ANGPT2), a ligand for the TIE2 receptor, is known to destabilize blood vessels and compromise vascular integrity under inflammatory conditions. To investigate the role of ANGPT2 in AD pathology, we overexpressed ANGPT2 specifically in brain endothelial cells using an adeno-associated virus (AAV) system in 5xFAD transgenic mice. Single-nucleus RNA sequencing (snRNA-seq) revealed distinct transcriptional changes associated with ANGPT2 overexpression, pointing to multiple pathways through which ANGPT2 may exacerbate AD progression. These findings identify ANGPT2 as a key driver of BBB dysfunction and neuroinflammation in AD, highlighting it as a potential therapeutic target for mitigating disease progression.
Published in
Angiopoietin-2 aggravates Alzheimer's disease by promoting blood-brain barrier dysfunction and neuroinflammation
Lee E, Kim S, Zhu CL et al. · Cell reports 2026 · PMID 41529684 · doi:10.1016/j.celrep.2025.116621
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Also filed as BioProject PRJNA1208978 and SRA study SRP556499. Searching any of these in the dataset finder brings you back here.

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