Targeting Underlying Vascular Dysfunction in Cerebral Small Vessel Disease: Joanna Wardlaw, MD

Cerebral small vessel disease (cSVD) encompasses a range of pathological processes affecting the brain's small arteries, arterioles, capillaries, and venules, contributing to ischemic stroke, cognitive impairment, gait dysfunction, and dementia. Historically, clinical management has focused on controlling established vascular risk factors, including hypertension, diabetes, dyslipidemia, and smoking. Although these interventions remain essential for cardiovascular and cerebrovascular health, they do not fully prevent the development or progression of cSVD, highlighting the need for treatments that directly address underlying disease mechanisms.¹

Advances in neuroimaging, genetics, and neuropathology have expanded understanding of cSVD beyond traditional vascular risk factors. Emerging evidence implicates impaired cerebrovascular reactivity, blood-brain barrier dysfunction, endothelial injury, and inflammatory processes in disease development and progression.^1,2 Genetic studies have also identified inherited susceptibility that may influence how individuals respond to vascular risk exposures. Together, these findings have encouraged investigation of therapies aimed at preserving small vessel function and limiting ongoing brain injury.

“This isn't just a risk factor disease; it's something else going on, and we have to treat that something else, at least understand it better, because just treating the hypertension or the diabetes or stopping smoking, all of which are really important, is not going to solve the whole problem.”

At the 2026 World Stroke Congress (WSC) in Seoul, South Korea, Joanna Wardlaw, MD, presented a session titled New Treatments for Cerebral Small Vessel Disease: What Does the Future Hold. A professor of applied neuroimaging at the University of Edinburgh and group leader at the UK Dementia Research Institute, Wardlaw has contributed extensively to research examining the mechanisms, imaging characteristics, and clinical consequences of cSVD.

In an interview with NeurologyLive^®, Wardlaw discussed how growing recognition of the disease's biological complexity is influencing therapeutic development. She explained why traditional vascular risk management may be insufficient, highlighted emerging genetic and vascular mechanisms, and considered how treatments targeting blood-brain barrier integrity, inflammation, and cerebrovascular responsiveness could complement existing care.

For more coverage of WSC 2026, click here.