Department of Neurology, UCLA

Where the brain meets
its blood vessels.

A translational neuroscience laboratory at UCLA studying the molecular pathways that drive the two most common neurologic disorders: stroke and dementia.

Explore our research Meet the lab

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Peer-reviewed publications

Lab members

Lab established at UCLA

Core research programs

The Lab

Decoding the vascular roots of stroke and dementia

The Hinman Lab is a translational neuroscience laboratory exploring the molecular pathways behind the brain's two most common disorders. We work across scales — from single glial cells and the oligovascular niche to human blood biomarkers — to understand how cerebrovascular dysfunction injures white matter and drives cognitive decline.

Our discoveries span neurovascular signaling, remyelination after stroke, 3D models of intracranial atherosclerosis, and biomarkers that are reshaping how vascular contributions to dementia are measured in the clinic.

Our research programs

Principal Investigator

Jason D. Hinman, MD, PhD

Principal Investigator · Professor of Neurology · Director, UCLA Mary S. Easton Center for Alzheimer's Research & Care

Jason is a physician-scientist, trained in vascular neurology and neurorehabilitation, with clinical expertise in stroke, stroke recovery, vascular cognitive impairment, and dementia. In July 2026, he was appointed the Susan & David Wilstein Endowed Chair in Medicine at the David Geffen School of Medicine at UCLA. He also serves as Director of the Katherine and Benjamin Kagan AD Treatment Program and Director of the Easton Center Labs for Neurodegeneration. He co-directs the UCLA Neuroscience Physician-Scientist Training Program. He believes in fairness in education, science, and medicine.

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Research

Four programs, one question

We are a translational neuroscience lab studying the molecular pathways that drive the two most common neurologic disorders — stroke and dementia. Our work spans the vascular biology of the brain, from single glial cells to human clinical biomarkers, with the shared goal of protecting and repairing the brain's white matter.

Neurovascular mechanisms of white matter injury & repair

The oligovascular niche after stroke

White matter is exquisitely vulnerable to vascular injury. We study how signaling between blood vessels and oligodendrocyte lineage cells — the "oligovascular niche" — controls myelin loss and repair after ischemic stroke, including IL-17/CXCL5 chemokine signaling and SARM1-driven axonal degeneration.

IL-17/CXCL5 signaling in human and mouse white matter injury
Vascular regulation of remyelination
SARM1 as a target to limit axonal degeneration

Vascular contributions to cognitive impairment & dementia

How the failing neurovascular unit drives decline

An NIA-funded program investigating how vascular dysregulation contributes to neurodegeneration and Alzheimer's disease, including the interplay between neurovascular dysfunction and tau aggregation, and the angiogenic factor placental growth factor (PlGF) as a driver and marker of decline.

Placental growth factor (PlGF) and cognitive trajectories
Neurovascular dysfunction and tau pathology
Sex differences in brain aging

Intracranial atherosclerotic disease

Modeling diseased cerebral arteries in 3D

Intracranial atherosclerotic disease is a leading cause of stroke worldwide. We build flow-dependent, endothelialized 3D in vitro models of the cerebral vasculature to dissect disease mechanisms and test therapeutic and endovascular strategies.

Flow-dependent endothelialized 3D vascular models
Lesion location and clinical outcomes
Translational and endovascular therapy

Blood-based biomarkers & clinical translation

From the bench to the clinic

We develop and validate blood-based biomarkers of cerebral small vessel disease and post-stroke cognitive impairment, partnering in national consortia (MarkVCID) and contributing to AHA scientific statements that shape clinical practice — always with a commitment to equity in science and medicine.