When a brain blood vessel ruptures, the leaked blood releases iron from haemoglobin, causing severe oxidative damage to the brain. This iron overload sets off a chain reaction of stress on the brain cells, leading to their death and resulting in loss of brain function in the affected regions.
Historically, the detrimental effects of excess iron in the brain following a stroke have been well documented. Attempts to counteract this with iron-binding treatments have been made, with iron chelators -drugs used to treat iron overload from frequent blood transfusions- like deferoxamine being considered for their protective potential in stroke cases.
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Building on this concept, previous research conducted by IGTP’s Cellular and Molecular Neurobiology (CMN) group, led by Dr Teresa Gasull and Dr Octavi Mart-Sistac, demonstrated the protective effects of the protein apotransferrin in models of ischemic stroke. Unlike deferoxamine and other drugs with fleeting lifespans in the bloodstream, apotransferrin offers a prolonged protective window due to its extended half-life, marking a significant stride over transient treatments.
In their latest study in mice, the team have used this protein on the less-studied yet more devastating type of stroke: intracerebral haemorrhage. The study reveals the benefits of an apotransferrin-based treatment in mitigating the damaging effects of this cerebral event.
Researchers have found that apotransferrin’s role in guarding against ferropoptosis – an iron-dependent cell death process recently described – could represent a turning point in how strokes are treated in the early stages, especially en route to the hospital, providing critical intervention during the golden hour.
“The study paves the way for further research to determine the therapeutic potential and safety profile of apotransferrin in clinical studies in stroke patients”, concludes Alexia Garca-Serran, predoctoral researcher at IGTP and first author of the study.
Source: Eurekalert
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