Mending our blood vessels to combat dementia
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Mending our blood vessels to combat dementia
A new drug aims to repair blood vessels to fight dementia, with research linking poor vascular health to Alzheimer’s and deteriorating brain function.
Problem
Cardiovascular disease and Alzheimer disease: a critical connection
New approaches are essential given the growing incidence of dementia and its significant societal, medical and financial impact. In 2020, it was estimated that 55 million people were living with dementia globally. In Australia, it is estimated that by 2058, 1.1 million people will be living with dementia at an estimated cost of $36 billion annually.
Growth in Alzheimer’s is being driven by the ageing population, with declining cardiovascular health. We are seeing an increase in diabetes, hypertension, obesity and decreased physical activity, all risk factors for dementia and cardiovascular disease.
There is a growing recognition of the involvement of blood vessels in the development of dementia, with evidence now showing vascular leak as one of the earliest and most consistent vascular changes in Alzheimer disease – where the blood-brain barrier becomes compromised. This allows toxic substances to enter the brain and inhibits clearance of toxic material from the brain, triggering inflammation, amyloid accumulation, and neurodegeneration. These amyloids are abnormal protein deposits, which pack together, forming hard, sticky plaques that disrupt cell function, causing neuronal cell death and progressive cognitive decline.
Vascular leak is also a complication of anti-amyloid treatment and is a feature of the small vessel disease, cerebral amyloid angiopathy (CAA) – a major contributor to dementia of the elderly.
Solution
Mending the leaky blood vessels offers hope
This project is developing a novel, orally active small molecule therapy that targets the underlying vascular dysfunction seen early in the progression of Alzheimer’s disease and other dementias.
The drug uses new molecular glue technology to stabilise VE-cadherin, a novel target and a key protein that is essential for maintaining the blood-brain barrier integrity. Our therapy aims to mend and inhibit leaky blood vessels in the brain, restore healthy vessel function and enhance clearance of toxic amyloid deposits from the brain.
This new approach not only has the potential to slow disease progression but also holds promise to mitigate cerebral amyloid angiopathy (CAA) and treat amyloid-related imaging abnormalities (ARIA), two vascular complications for which no current therapies exist.
Impact
A new frontier in dementia care with global, scalable impact
This vascular leak targeting therapy represents a transformative shift in dementia care: from managing late-stage symptoms to intervening early to modify the course of disease.
By repairing the blood-brain barrier and limiting vascular leaks, we aim to reduce cognitive decline, enhance the safety of amyloid therapies, and improve quality of life for millions. This could also significantly reduce hospitalisation, caregiving burden, and health system costs.
This is more than a drug – it's a paradigm shift in how we think about brain health, prevention, and longevity.
Meet the team
Supported by
It’s now becoming apparent that [dementia is] part of a cardiovascular disease. We have strong data to show that mending the leak and improving the function of the vasculature of the brain clears the amyloid from the brain.
Jennifer Gamble
Project Lead
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