Eisai (ESAIY) and Biogen (BIIB) “announced that the latest data confirming the pharmacological effect of lecanemab, an anti-Abeta protofibril antibody, on Abeta protofibrils in cerebrospinal fluid was presented at the 18th Clinical Trials on Alzheimer’s Disease Conference. The findings represent the results from a large-scale clinical study demonstrating, for the first time, that binding of lecanemab to PF can be measured in CSF, enabling further understanding of how lecanemab slows Alzheimer’s disease progression. The increase in total CSF PF with lecanemab treatment suggests that lecanemab binds to PF (target engagement) and facilitates its mobilization from the vicinity of Abeta plaques within the brain parenchyma into the CSF (pharmacodynamic effect). This suggests that lecanemab is having the desired effect of mitigating the toxic effects of PF by mobilizing it outside of the brain parenchyma. In the placebo group, a statistically significant correlation was observed between changes in CSF PF and changes in neurodegeneration biomarkers (total tau, neurogranin) as well as tau pathology biomarkers at baseline. This correlation disappeared with lecanemab treatment, suggesting that lecanemab reduces neurotoxicity by binding to PF. These findings reinforce lecanemab as the only AD treatment that targets neurotoxic PF and Abeta plaques, resulting in slower tau tangle accumulation on PET imaging.”
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