Agalliu Lab

I’m excited to announce that this collaboration with the Konofagou laboratory to examine the cell biological mechanisms and transcriptome changes at the BBB after Focused Ultrasound with Microbubbles-mediated BBB opening is now published. nature.com/articles/s4417…

Drs. Dritan Agalliu (Columbia), Madeleine Cunningham (Univ of OK), Russell Dale (Univ of Sydney, AU), & Jennifer Frankovich (Stanford) present their research & discuss whether PANS & PANDAS are best understood as autoimmune, autoinflammatory, or both. ➡️#video" target="_blank" rel="nofollow noopener">pandasppn.org/neuroimmune-ep…

Finally - It is official. Thank you @atvbahajournals for highlighting the amazing work of Aomeng Cui in the @AgalliuLab and Sproul labs to generate IPSC-derived human brain endothelial cells and build a 3D iPSC - derived neurovascular unit for studying neurological diseases.

Breakthroughs happen many times when you're able to re-imagine your project as a different form of puzzle. NYC Postdocs: Join us on Wednesday at Columbia University for this exciting Night Science session on puzzle switching! Registration is free and we have a few spots left.

According to Columbia neurologist Dr. Joshua Willey, strokes are becoming more common in younger adults. Patent foramen ovales (PFOs) and other underlying conditions, including clotting disorders and some autoimmune diseases, can increase a younger person’s stroke risk. columbiamed.link/3XjMSZG

I thank the @atvbahajournals editors for providing a fair, unbiased and honest review of our paper unlike some other journals that either refused to review the paper or provided an unfair review process.

Finally, we show that the APPLon/Lon mutation, a genetic risk factor for familial Alzheimer’s disease, has distinct effects on the rBMEC physiology compared to Ab exposure suggesting that the mutation does more than affect Ab processing and generation of the toxic Ab form.

Second we generate a 3D hiPSC-derived neurovascular unit with rBMECs, pericytes and astrocytes using the MIMETAS platform with flow which mirrors the brain 3D architecture.

In this study, first we describe a new protocol to generate human iPSC-derived brain endothelial cells (rBMECs) with the correct molecular and organotypic identity and robust blood-brain barrier properties.

I am very excited that our paper, a collaboration between Dr. Andrew Sproul and my laboratories, is finally published in @atvbahajournals. I want to thank expecially a very MSTP talented student, Aomeng Cui, from @AgalliuLab who led the study. ahajournals.org/doi/10.1161/AT…

This is a beautiful paper by Jeremy Nathans group!

Interactive effects of blood–brain barrier breakdown and Alzheimer's disease biomarker status on cognitive decline in older adults without dementia alz-journals.onlinelibrary.wiley.com/doi/10.1002/al…

I am looking forward to discussing with several PANS researcher the contribution of neuroimmune vs neurodevelopmental factors in triggering PANDAS/PANS on Dec 2, 2025. I encourage the physicians to join the webinar organized by PPN & PANDAS Network to learn more about it.

A postdoc position is open in the @AgalliuLab for a scientist with a strong PhD background in Neuroscience, Neuroimmunology or Vascular Biology and interest in neurovascular / BBdysfunction in CNS disorders. Please contact me with your CV and cover letter if you are interested.

@DAgalliu Yay! Congrats to Azzurra and Danny! Go Agalliu lab !! 🍾🍾🥂🥂

Here is the manuscript published online today outlining the role of Rab7a in regulation of BBB junctions after ischemic stroke! link.springer.com/article/10.118…

I am very happy to report that our manuscript describing the requirement of Rab7a to degrade select BBB junctional proteins during acute BBB breakdown after stroke is accepted at Acta Neuropathologica Communications! The final paper will be available soon biorxiv.org/content/10.110…

We identify a unique brain endothelial cell (BEC) type one interferon (IFN1) signature in human and mouse ischemic stroke tissue. We show that deletion of endothelial IFN1 receptor (Ifnar1) exacerbates post-stroke BBB disruption and expands angiogenic and immature BBB features .

Vascular normalization [stabilization of aberrant angiogenesis and restoration of blood-brain barrier (BBB)] is critical for reducing long-term sequelae after ischemic stroke. How immune and developmental signaling pathways coordinate these processes is poorly understood.

Conversely, IFNβ administration immediately after stroke reduces acute BBB disruption. Activation of IFN1 signaling in mouse BECs in vitro promotes junctional stabilization and reduces VEGF signaling to enhance barrier properties, but suppress angiogenic features.