Alamar Biosciences, Inc.
Blood biomarkers associated with amyloid clearance differ from those associated with cognitive decline in patients receiving lecanemab
FREMONT, Calif., Sept. 24, 2026 (GLOBE NEWSWIRE) -- Alamar Biosciences, Inc. (Nasdaq: ALMR), a leader in precision proteomics dedicated to enabling the earliest detection of disease, today announced the publication in The Lancet Neurology of the first longitudinal cohort study to evaluate a broad panel of plasma biomarkers in patients receiving anti-amyloid antibody therapy in real-world clinical practice. The study shows that patients with early symptomatic Alzheimer's disease exhibit markedly different biological responses during treatment with lecanemab.
Led by investigators at Washington University School of Medicine in St. Louis, the study used Alamar's NULISAseq™ CNS 120 panel to measure 130 plasma proteins spanning amyloid and tau pathology, inflammation, neurodegeneration and synaptic function. Researchers profiled 2,385 samples from 1,967 participants using just 25 microliters of plasma per sample, including patients receiving lecanemab as part of standard clinical care at the Washington University Memory Diagnostic Center and untreated comparison groups from the Knight Alzheimer Disease Research Center.
"Anti-amyloid therapies are now part of routine care, but until now we have had a very narrow window into what is actually happening biologically in the patients receiving them," said Carlos Cruchaga, PhD, Professor of Psychiatry and director of the NeuroGenomics and Informatics Center at Washington University School of Medicine, and co-senior author of the study. "Our findings show that Alzheimer's disease and neurodegeneration biomarkers have unique trajectories that capture specific biological process associated with treatment response."
The proteins associated with amyloid clearance were largely different from those associated with subsequent cognitive decline. The findings show that amyloid clearance and cognitive response reflect different biological processes, helping explain why clearing amyloid does not produce the same degree of clinical benefit in every patient, a pattern observed both in this cohort and across anti-amyloid trials.
Additionally, among 197 patients treated with lecanemab, 34 of the 130 biomarkers measured significantly changed with the number of infusions received, and they did not all move in the same direction. Among the proteins that most strongly distinguished these patients from controls, the brain-derived forms of tau consistently outperformed the same proteins circulating in the periphery, accounting for four of the top five both before treatment and at the last infusion stage. Separating tau that originates in the brain from its systemic counterpart requires both high specificity for the brain-derived form and the sensitivity to detect it at very low concentrations. Measuring these variants alongside more than 100 additional proteins in a single sample is what allowed the investigators to track pathology and treatment response in one assay.