Print This PostSince moving to the University of Edinburgh, a large part of my research has shifted towards vascular dementia and small vessel disease. It is a natural progression for me after recent years focused on vascular neuropathology and dementia, and I wanted to use this blog to introduce the topic to anyone who, like me not so long ago, may not have given it the attention it deserves.
When we talk about dementia research, the conversation often gravitates towards amyloid and tau. These are the headline pathologies, the ones that attract the most funding and fill the most conference sessions. But there is another contributor to dementia that affects millions of people worldwide and arguably represents our best opportunity for prevention. Cerebral small vessel disease, or SVD, is the most important vascular contributor to cognitive decline and dementia.
What is Cerebral Small Vessel Disease?
SVD refers to a group of conditions that damage the small blood vessels deep within the brain. You cannot see these vessels on a standard scan, but what you can see are the consequences. White matter hyperintensities, lacunes, microbleeds and enlarged perivascular spaces are the hallmark imaging features that tell us something has gone wrong at the microvascular level. If you have ever looked at a brain MRI of someone over 65, chances are you have seen white matter hyperintensities. They are incredibly common in ageing populations, and their presence increases with age, hypertension, diabetes and smoking.
From an epidemiological perspective, SVD is not a rare condition. It accounts for approximately 25% of all ischaemic strokes and contributes to an estimated 45% of dementia cases globally. Those are not small numbers. Yet when we think of the landscape of dementia research, the proportion of attention SVD receives does not match the proportion of disease it causes.
SVD and Vascular Cognitive Impairment
Vascular dementia is the second most common form of dementia after Alzheimer’s disease. The World Stroke Organization’s 2026 fact sheet (Cai, Mok and Markus, 2026, International Journal of Stroke) reported that pure vascular dementia accounts for around 15% of all dementia cases, with mixed vascular and neurodegenerative pathology responsible for another 16%. Together, that represents approximately 17.6 million people worldwide. Under current trends, the global burden is projected to reach 42.7 million cases by 2050.
SVD sits at the centre of this. It is the primary driver of vascular cognitive impairment and the most common pathological substrate underlying vascular dementia diagnoses. From population neuropathology studies, including work from the Cognitive Function and Ageing Studies that I was involved with at Newcastle, we know that vascular pathology is one of the most prevalent findings in the ageing brain. Late life dementia is rarely caused by a single pathology. Mixed disease is the norm, and SVD is frequently part of that mix.
What is Driving the Damage?
Recent research has advanced our understanding of the mechanisms through which SVD leads to cognitive decline. A comprehensive review by Markus and colleagues (2025, Physiological Reviews) laid out the current understanding of SVD pathogenesis, identifying blood brain barrier disruption, endothelial dysfunction, neuroinflammation and impaired perivascular clearance as the central processes driving disease progression.
Very recently in a study by Leigh and colleagues (2026, Annals of Neurology), showed that disruption of the blood brain barrier within white matter hyperintensities was the strongest predictor of how much those lesions would expand over time. Disruption in the tissue surrounding existing lesions, the penumbra, was the best predictor of which patients would progress to worse disease. This is significant because it suggests we may be able to identify individuals at highest risk of cognitive decline before it happens, using imaging markers of blood brain barrier integrity.
Risk factors for SVD are largely the same one’s epidemiologists have been tracking for decades. Ageing, hypertension, hyperglycaemia and smoking all increase levels of reactive oxygen species and pro inflammatory cytokines, compromise vascular integrity and ultimately damage the brain parenchyma. These are modifiable risk factors, which brings us to perhaps the most important point.
Prevention and What Comes Next
The American Heart Association’s 2025 scientific statement (Smith et al., 2025, Stroke) described vascular contributions to cognitive impairment and dementia as potentially the most preventable cause of clinically significant cognitive decline. That is a bold statement, but the evidence supports it. Intensive blood pressure lowering has been shown to reduce white matter hyperintensity progression and delay cognitive impairment. There is also emerging evidence that B vitamins can lower homocysteine and may slow white matter lesion progression.
On the treatment side, there are currently no FDA approved therapies specifically for vascular cognitive impairment. However, clinical trials are underway. Isosorbide mononitrate and cilostazol, both modulators of endothelial function, have shown promise in reducing recurrent stroke, dependence and cognitive impairment after lacunar stroke. Newer therapeutic approaches targeting neuroinflammation, oxidative stress and endothelial dysfunction are also in development.
From an epidemiological standpoint, the challenge now is translating what we know about risk factors into effective population level prevention strategies. We have the knowledge. The question is whether we can implement it at scale to reduce the burden of SVD related dementia in the decades ahead. That is a question I am looking forward to working on in my new role at Edinburgh.
Why This Matters
SVD is not a niche topic. It is a major contributor to dementia worldwide, it overlaps with and worsens Alzheimer’s pathology, and it is driven by risk factors we already know how to target. If we are serious about reducing the global burden of dementia, giving SVD the research attention and funding it warrants is not optional. It is essential.
Dr Connor Richardson
Author
Dr Connor Richardson is a Neuro-epidemiology Research Associate at The University of Edinburgh. His research interests lie in using advanced statistical modelling and machine learning to measure dementia risk. Connor blogs about his research, Equality, Diversity and Inclusion and sometimes his Pomapoo’s.
Dementia Researcher
Hi,i have small vessel disease along with white matter problems.this showed up on a scan. My doctor hasnt offered treatment or advice.I would like to know if thdre is anything i can do.I do have memory problems.I am not a diabetic blood pressure generally not high. I have high colesterol but take statins then come off them because of leg cramps and muscle problems. My doctor just told me the findings, that was it. I do suffer from stress anxiety and I am going through a divorce. I know my memory is worsening.What can i do to help myself. Thank you
Thank you for getting in touch. I’m sorry you were given the scan findings without a proper explanation or advice about what should happen next.
We cannot interpret individual scan results or provide medical advice, but worsening memory problems should be assessed. Please arrange another appointment with your GP and specifically ask:
– what the scan findings mean in your case;
– whether you need a memory assessment or referral to a memory clinic or neurologist;
for a review of your blood pressure, cholesterol and other factors affecting blood-vessel health;
– to discuss the muscle problems caused by statins. Do not keep stopping and restarting them without advice, as a different statin, dose or cholesterol-lowering medicine may suit you better.
Stress and anxiety can affect memory, particularly during something as difficult as a divorce, but they should not be assumed to be the only cause. It may help to write down examples of what you are forgetting and take someone you trust to the appointment.
Regular physical activity, a balanced diet, not smoking, limiting alcohol and staying socially active can support both heart and brain health, but these do not replace a medical review.
If you develop sudden facial weakness, weakness or numbness in an arm, difficulty speaking, loss of vision, severe confusion or a sudden severe headache, call 999 immediately.
If you are in the UK, you can also find NHS guidance on memory assessment and statin side effects.