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    Home»Neurology»Aducanumab for the treatment of Alzheimer’s disease
    Neurology

    Aducanumab for the treatment of Alzheimer’s disease

    brainwealthy_vws1exBy brainwealthy_vws1exFebruary 2, 2023No Comments2 Mins Read
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    Marwan Sabag, M.D.: So I’m going to talk with Dr. Atri about aducanumab, our first approved monoclonal antibody. Can you talk about aducanumab from an approval perspective, how did you get to other monoclonals? Could you start with that?

    Alireza Atli, MD, PhD: Aducanumab received accelerated approval for the first time based on its biomarker effect of lowering amyloid plaques, as Dr. McDade said, rather than based on demonstrating definitive clinical efficacy. There is a link that this may lead to clinical efficacy. In which patients, for how long, and when the course of the disease is needed to lower amyloid and, potentially, clinical benefit before temporary delays occur. As for the clinical benefit, it is important to make sure my colleagues understand that clinically we are not talking about putting the clock back five years. We’re not talking about cures, but about meaningful things that can slow the progression of the disease, and by doing so, could potentially affect some individuals as well. There is. Dismissed.

    Unfortunately for aducanumab, the study was stopped early after an interim analysis did not go as planned.So there was always an asterisk next to these studies in one way or another, one was beneficial and the other was clearly negative. monoclonal, and lecanemab, a relative 20% to 40% deceleration over 18 months in global severity, approximately like CDR, if amyloid is sufficiently reduced in one group [Clinical Dementia Rating], for the measurement of cognition or function. That’s where we are now. We’re there, but even in those studies, after all, not everyone is amyloid-negative, it’s possible that only half the individuals or he I have.

    Also promising was the consistent effect on several downstream biomarkers, which not only influence the disease biology of the amyloid moieties, but also the pathology of p-tau and tangles. It has been suggested that it also influences Neurodegeneration and clinical benefits. In addition to that, there are always safety signals. These are manageable in the context of clinical trials, often associated with amyloid-related imaging abnormalities, which require not only careful patient population selection but also monitoring during trials.

    Edited transcript for clarity



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