Thank you for having me today, and we’re very excited to present at CTAD 2025 on our recent work on the plasma biomarkers for bone and senescence in AD and MCI patients. And then this was a cohort from the ROSMAP study from Rush Alzheimer’s Disease Center, that team, which comprises of bioinformatics students and Alzheimer’s experts. We did some analysis of these proteomics data from using Somalogic...
Thank you for having me today, and we’re very excited to present at CTAD 2025 on our recent work on the plasma biomarkers for bone and senescence in AD and MCI patients. And then this was a cohort from the ROSMAP study from Rush Alzheimer’s Disease Center, that team, which comprises of bioinformatics students and Alzheimer’s experts. We did some analysis of these proteomics data from using Somalogic. And we found that in Alzheimer’s disease, there was a significant alteration of the YKL40 as well as FGF19 proteins compared to the healthy controls. And this was seen in both males as well as females. And not just they contribute to the AD pathology, but they also contribute to osteo… For example, FGF19 contributes to osteogenesis and YKL40 contributes to bone disease. And interestingly, in mild cognitive impairment, we see a totally different set of bone proteins that are expressed. VISP1, which is a bone formation protein, is seen to be altered in the plasma of MCI patients compared to controls and also OLN protein. And since the last few years, my focus was on senescence. And then I truly believe that during aging, many of these diseases exist together. And senescence is a key hallmark of age-associated pathophysiologies, not just Alzheimer’s disease, but even osteoarthritis, osteoporosis, and many others. So we were interested to look if there is also senescence biomarkers upregulated in AD versus MCI patients. And we found that PAI-1 and then [inaudible] were also altered in the plasma of MCI and AD patients when compared to the controls. So this is the first step where we showed that there’s some senescent proteins that are altered in the bone, in the plasma as even bone markers. So next step is once we receive more funding, we want to kind of establish the timeline of changes of these bone and senescent proteins in these patients. And we also, even in cognitively normal individuals, they’re amyloid positive and amyloid negative. And we want to measure the bone turnover markers in those. And in addition, we want to perform some HR-pQCT studies and bone mineral density in these patients and see if they’re correlating with the bone outcomes that we see in the plasma. And once we do all that, then we are kind of ready to kind of see it in the clinic and be able to detect bone changes early on and then even prevent cognitive decline. Because what is known in the literature is that people with Alzheimer’s disease have a higher risk of falls and fractures. And even the other way is true, like people with falls and fractures have a higher risk for cognitive decline. And we found for the first time in our preclinical models that even before onset of amyloid pathology, we see changes in the bone as early as one month. So that’s what prompted us to see if we detect these bone changes in the humans. And as the first step, we did the plasma biomarkers. And as the next step, we would be doing BMD and HR-pQCT to look at the detailed bone microarchitecture and see how they would correlate with the Alzheimer’s pathology. And then probably if we can improve bone health, there is a higher chance that we can prevent cognitive decline by improving that.
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