ESOC 2025 | The potential targeting of TNF-alpha signaling for secondary prevention of ischemic stroke
John McCabe, MB, BCh, BAO, MRCPI, PhD, Mater Misericordiae University Hospital, Dublin, Ireland, comments on the potential of tumor necrosis factor alpha (TNF-alpha) as an inflammatory biomarker for predicting major vascular recurrence after ischemic stroke. Dr McCabe highlights that elevated TNF-alpha levels after a stroke are independently associated with recurrence, suggesting that TNF-alpha signaling may be a specific target for secondary prevention. This interview took place at the 11th European Stroke Organisation Conference (ESOC) in Helsinki, Finland.
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Transcript
So specifically in terms of inflammatory biomarkers, we also have some recent unpublished data that will be presented at the European Stroke Conference, which has shown that elevated tumor necrosis factor alpha measured after an ischemic stroke is also independently associated with major vascular recurrence including recurrent stroke and we have shown that these associations are robust after adjusting for cardiovascular risk factors and secondary prevention medication and the reason why this is also interesting is that the associations between TNF-alpha and recurrence were robust even after adjustment for other inflammatory markers, such as interleukin-6 and high-sensitivity CRP, which suggests that TNF-alpha signaling may represent a specific target independent of IL-6 CRP signaling...
So specifically in terms of inflammatory biomarkers, we also have some recent unpublished data that will be presented at the European Stroke Conference, which has shown that elevated tumor necrosis factor alpha measured after an ischemic stroke is also independently associated with major vascular recurrence including recurrent stroke and we have shown that these associations are robust after adjusting for cardiovascular risk factors and secondary prevention medication and the reason why this is also interesting is that the associations between TNF-alpha and recurrence were robust even after adjustment for other inflammatory markers, such as interleukin-6 and high-sensitivity CRP, which suggests that TNF-alpha signaling may represent a specific target independent of IL-6 CRP signaling. The reason why we’re quite excited about this work is that as we enter the phase of implementation of anti-inflammatory therapies in clinical practice. We do need more drugs that we can repurpose for secondary prevention. And thankfully, there are many TNF-alpha inhibitors readily available that have been used for a very long time in clinical practice and have been demonstrated to be safe. And these drugs are typically used for rheumatoid arthritis and our hope is that the research may lead ultimately to trialing of these agents as potential treatment options in patients with ischemic stroke.
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