Dr. Peeyush Pandit is an Assistant Professor of Neurosurgery at UTHealth Houston, where his laboratory investigates the genetic and signaling mechanisms that govern cerebral vascular development and maintenance and target this mechanisms to achieve neurovascular repair . Trained as a postdoc at Harvard Medical School under Dr. Anju Vasudevan, he co‑discovered endothelial GABA signaling as a key guidance cue for developing interneurons. Since launching his lab in 2021, Dr. Pandit has unveiled an epigenetic “brake” on angiogenesis and blood–brain barrier formation—mediated by HDAC2 and PRC2—in adult CNS endothelial cells. By deleting HDAC2, his team reactivated vascular growth programs, generating stable, functional vessels in the adult brain and driving neuronal regeneration in stroke models. His ongoing collaborations with clinical stroke research are extending these findings into aging and neurodegenerative contexts. With over 50 peer‑reviewed publications Dr. Pandit is committed to translating developmental vascular pathways into regenerative therapies and mentoring the next generation of neurovascular scientists.

Please tell us your background, where you are from, schooling, etc.

I was born and raised in India, where I completed my undergraduate studies before earning a Ph.D. in Neuroscience from Cochin University of Science and Technology. Afterward, I moved to the United States for postdoctoral training—first in the Department of Psychiatry at Harvard Medical School, where I explored neurovascular signaling pathways, and then at the University of Wisconsin Department of Neuroscience, where I focused on developmental vascular biology. In 2016, I joined UTHealth Houston. I promoted as a tenure‑track Assistant Professor of Neurosurgery in 2021, where I lead a lab dedicated to uncovering and harnessing the genetic and epigenetic mechanisms that drive brain angiogenesis and neuronal regeneration.

What led you to become involved with brain aneurysm research?

I first became involved in subarachnoid hemorrhage (SAH) research through my collaboration with clinician‑scientist Dr. Spiros Blackburn, who specializes in SAH surgeries. Working alongside him, I saw firsthand that the primary injured tissue in SAH is the cerebral vasculature—and that even after securing the aneurysm, blood–brain barrier disruption and downstream vascular dysfunction drive much of the poor neurological outcome. Recognizing that these vascular and BBB injuries represent critical, yet under‑addressed, pathways to recovery sparked my interest in applying my expertise in endothelial epigenetics and angiogenesis to develop therapies aimed at stabilizing and repairing damaged brain vessels in SAH patients.

In the simplest terms, what is the purpose of your project?

After bleeding in the brain (subarachnoid hemorrhage), blood vessels and brain cells are damaged, leading to problems with memory and thinking. My project tests a cancer drug to help regrow healthy blood vessels and new brain cells so patients can recover their cognitive abilities, and I’ll also check its effects on human blood vessels to speed up bringing this treatment to people.

In the simplest terms, what do you hope will change through your research findings?

I hope my research will lead to a treatment that helps people rebuild healthy brain blood vessels and grow new nerve cells after a brain bleed, so they can regain cognitive skills they’ve lost after SAH.

Why is the funding you are receiving through the Brain Aneurysm Foundation so important?

The Brain Aneurysm Foundation’s support is vital because it enables us to pursue a high‑risk, high‑reward strategy—repurposing an existing cancer drug to repair damaged brain vessels and promote neuronal recovery after subarachnoid hemorrhage—that traditional funding sources often overlook. This targeted funding provides the “proof of concept” we need in both animal models and human vessel studies, establishes the preclinical data required for larger clinical trials, and accelerates the path toward FDA approval. It also fosters crucial interdisciplinary collaboration with clinicians and access to patient samples and advanced imaging technologies. Without the Foundation’s investment, our project would lack the resources and clinical partnerships necessary to de‑risk the approach and translate these findings from the laboratory to real‑world treatments that can improve cognitive outcomes for SAH patients.