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

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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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