Dr Beard completed his PhD (Human Physiology) in 2015 in the Translational Stroke Laboratory of Professor Neil Spratt at the University of Newcastle, Australia. His PhD thesis investigated the mechanisms regulating collateral blood flow after stroke. He found that changes in intracranial pressure (ICP) profoundly reduced collateral blood flow to the ischaemic brain during stroke. This work generated the novel hypothesis, that changes in ICP in human stroke may be the cause of the previously identified, but poorly understood phenomenon of collateral vessel failure and neurological deterioration in a subset of stroke patients. This work provided the stimulus for clinical investigations to the test this novel hypothesis.
In September 2016, Dr Beard took up a postdoctoral position in the Laboratory of Cerebral Ischaemia of Professor Alastair Buchan at the University of Oxford. In this role he is continuing to research the important role of the cerebral vasculature in determining stroke outcome. Specifically, he is now focusing on cytoprotective therapies that can protect the cells that make up the capillaries of the brain as a means of improving microvascular perfusion, reducing blood brain barrier disruption and ultimately improving neurological outcome after stroke. As well as his research pursuits, Dr Beard has continued to develop his expertise as a university educator. He is currently a tutor in physiology at Corpus Christi College and Harris Manchester College.
I am interested in both cardiovascular physiology and neuroscience, in particular how the cardiovascular system affects the functioning of the nervous system. This lead me to my current field of research in ischaemic stroke, a disease in which disruption of blood flow to the brain (by a clot) has a profound and often devastating affect on brain function leading to death and disability. I am particularly interested in how the function of the blood vessels in the brain influences brain function and ultimately neurological outcome after stroke.
During my doctoral studies I investigated a set of so called “bypass” or collateral vessels in the brain. These vessels allow blood to flow around the clot towards the compromised but still saveable tissue of the brain called the penumbra. The degree of flow through these vessels is a very important predictor of stroke outcome. I identified that an increase in pressure within the skull after stroke severely reduces flow through these vessels (termed collateral failure), which may lead to neurological deterioration in stroke patients in which the clot is unable to be removed.
Fortunately for stroke patients there are treatments available to dissolve (with a drug known as tPA) or remove (with intra-arterial clot retrieval devices) the clot. Unfortunately for some stroke patients, reopening the occluded vessel affords no-improvement, as adequate restoration of blood flow to the capillaries of the brain is not achieved, termed “no-reflow phenomenon”.
Very recent evidence suggests that constriction and subsequent death of pericytes that surround the capillaries is responsible for this lack of blood flow to the capillaries. Furthermore, death of pericytes, endothelial cells and astrocytes compromises the blood brain barrier, which can further complicate reperfusion therapies due to increased risk of vessel rupture and bleeding.
My current research at the University of Oxford is investigating novel therapies with cytoprotective effects in multiple cells types within the cerebral capillaries. I am particular interested in therapies that can reduce the constriction and subsequent death of pericytes as a means of improving capillary blood flow and reducing blood brain barrier disruption following stroke.
Rapamycin in ischemic stroke: Old drug, new tricks?
Hadley G. et al, (2019), J Cereb Blood Flow Metab, 39, 20 - 35
The role of the endoplasmic reticulum stress response following cerebral ischemia.
Hadley G. et al, (2018), Int J Stroke, 13, 379 - 390
Intracranial Pressure and Collateral Blood Flow
Beard DJ. et al, (2016), Stroke, 47, 1695 - 1700
Intracranial Pressure Elevation 24 h after Ischemic Stroke in Aged Rats Is Prevented by Early, Short Hypothermia Treatment
Murtha LA. et al, (2016), Frontiers in Aging Neuroscience, 8
Ischemic penumbra as a trigger for intracranial pressure rise – A potential cause for collateral failure and infarct progression?
Beard DJ. et al, (2016), Journal of Cerebral Blood Flow & Metabolism, 36, 917 - 927