IMS 2026 | Mitochondrial dysfunction, immune senescence and frailty in multiple myeloma

So my translational group has been studying immune senescence now for a number of years and one of the potential drivers of immune senescence is mitochondrial dysfunction. Immune senescence is where the biological aging process has affected the immune system that drives a sterile chronic inflammation. That in itself drives the diseases of old age and ultimately results in loss of independence and frailty. So it’s all part of the mixture. Now, our aim with our work is to identify what mediators are produced by myeloma that can actually drive that mitochondrial dysfunction with an aim of trying to rectify that. For example, we have an early phase trial in design where we’re using nicotinamide riboside, which is actually a dietary supplement, not a therapeutic agent. But what it can do in health is improve mitochondrial function. So the question is, can it actually do anything to reverse the mitochondrial dysfunction we see? We see mitochondrial dysfunction in frail patients. Is it independent of age and comorbidities? That’s quite difficult to dissect at the moment because of the patient numbers. We are working our way through that but for example looking at senescent CD8 cells which is one of our starting areas we do see that independent of age and comorbidities but there’s a distinct sex mismatch there a difference in the senescence immune senescence between males and females so we are still learning a lot but the aim is not just to have an understanding, the aim is to develop either a biomarker or more realistically develop an assay that will allow us to test already licensed drugs in the space to try and mitigate the dysfunction.

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