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AD/PD 2026 | Why are underrepresented minorities less likely to be eligible for amyloid-targeting treatments?

Casey Vanderlip, MD, PhD(c), University of California, Irvine, CA, explores disparities in eligibility for amyloid-targeting therapies in Alzheimer’s disease (AD). While current data suggest amyloid positivity thresholds may be broadly applicable across populations, he highlights the need to better understand biological and clinical differences driving inequities in diagnosis and treatment access. This interview took place at the AD/PD™ 2026 International Conference on Alzheimer’s and Parkinson’s Diseases in Copenhagen, Denmark.

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Transcript

Important area of research is better identifying why underrepresented minorities are less likely to be eligible for amyloid-lowering treatments. We know these individuals are less likely to be amyloid-positive despite having clinical symptoms. And this is a critical area of research. So the thresholds we use for amyloid positivity have been derived from small studies that have been focused on non-Hispanic white individuals...

Important area of research is better identifying why underrepresented minorities are less likely to be eligible for amyloid-lowering treatments. We know these individuals are less likely to be amyloid-positive despite having clinical symptoms. And this is a critical area of research. So the thresholds we use for amyloid positivity have been derived from small studies that have been focused on non-Hispanic white individuals. An important question is should these thresholds differ by groups? These thresholds are critical regulatory gatekeepers for who should go on to get treatment. So we’ve looked in a large diverse data set, the HABS-HD data set. We’ve also looked in the A4 clinical trial to investigate where these thresholds should differ by groups. We did not find strong evidence that these thresholds should truly differ, meaning that the same threshold can work across populations. This means that we need much more work to understand why there are differences, understanding comorbidities and copathologies that could account for these differences between groups. We really need to do a much more detailed investigation on how these changes can drive impairment, understanding that amyloid deposition by itself may not be the sole answer.

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