Aducanumab Continues to Show Potential as Treatment for Mild Alzheimer’s in Long-term Extension of PRIME Trial

Aducanumab Continues to Show Potential as Treatment for Mild Alzheimer’s in Long-term Extension of PRIME Trial
Latest results from the long-term extension of a Phase 1b study assessing increasing and fixed doses of aducanumab continue to show its potential as a therapy for early or mild Alzheimer’s disease. Similar to previous interim analyses, data collected for up to 48 months reveal that the investigative treatment can effectively reduce the burden of amyloid plaques — a hallmark of the disease – and prevent cognitive decline in Alzheimer’s patients. Aducanumab, formerly known as BIIB037, is a monoclonal antibody being developed by Biogen in collaboration with Eisai. Prior preclinical and clinical data suggest that aducanumab’s therapeutic potential resides in its ability to target disease-causing amyloid protein clusters. The ongoing PRIME trial (NCT01677572) is evaluating the safety, tolerability, and overall reactivity of aducanumab in patients with prodromal (early) or mild Alzheimer’s disease dementia. A total of 196 participants, ages 50 to 90, were enrolled across some 30 research centers in the United States. They were randomized to receive either a fixed dose of aducanumab or placebo — 1, 3, 6, or 10 mg/kg — or to undergo a titration regimen in which they received a gradually increasing dose of the antibody or place
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    The more Aducanumab succeeds, the stronger the evidence of a natural protective immunity; i.e. we should remember that this monoclonal antibody is a replica of an antibody isolated from elderly but cognitively competent older individuals. Also, it shows that a preventive vaccine is doable, if rationally designed, which apparently has not been the case so far. Hence, by ignoring the facts leading to past failures, an obvious preventive approach is being rejected.


    I should add that reduction in amyloid plaque is irrelevant to determine if an antibody is effective. All anti-amyloid antibodies, good and bad, remove plaque in an unspecific manner. If removal of plaque was a significant factor in deciding the success of a product to treat/prevent Alzheimer’s disease, we should have by know a surplus of effective products. Indeed, it has been shown that amyloid oligomers released by antibodies are toxic, unless the antibody also neutralizes their cytotoxicity. Hence, the main parameter should be improvement or delay in the decline of cognitive functions, while considering plaque a symptom rather than the cause.

    • Alice Melão says:

      Dear Alice,
      mab is short for monoclonal antibody, which indicates that the antibody only binds to a specific protein sequence, or epitope. In the case of Aducanumab it only binds to an epitope present in the beta-amyloid aggregates.

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