Brendan Gongol

This paper identifies metformin as a potential drug for long-term treatment of cerebral cavernous malformations using AI, high-throughput screening, and animal models.

This study shows that oxidative stress modifies miR-483 to 8OH-G miR-483, leading to endothelial dysfunction and increased atherosclerosis risk through altered targetomes.

This study identifies neuroinflammatory astrocytes and CCM endothelium interactions that drive leukocyte recruitment and immunothrombosis in cerebral cavernous malformations, while showing that targeting endothelial NF-kB may have harmful effects.

The paper shows that astrocytes contribute to cerebral cavernous malformations (CCMs) through VEGF production driven by endothelial NO, highlighting non-cell-autonomous mechanisms.