Immunotherapy directed to reduce amyloid levels in the brains of patients with Alzheimer disease (AD) and provide clinical benefit has not definitely been successful using either passive immunizations with preformed antiamyloid (anti-Aβ42 as the toxic processed form of amyloid β protein), monoclonal antibodies (moabs), or active immunization with amyloid peptides. A recent press release by Biogen1 has indicated that their moab aducanumab has shown clinical benefit after reanalysis of larger data panels of a phase 3 clinical trial that ended in March 2019. This reanalysis has not been published or reproduced, but it is potentially an important finding and supportive of immunotherapy for AD. Thus, antiamyloid immunotherapy still holds promise for clinical benefit, as amyloid (Aβ) accumulation in the brain can be detected decades before the onset of symptoms and amyloid accumulation is a trigger for many downstream pathologies, such as loss of neuronal plasticity, tau hyperphosphorylation, and frank neuronal death. Targeting more than one pathology with a single therapy, as we have shown for the DNA Aβ42 trimer vaccine, might be the path forward in finding an option for AD prevention or delay of disease progression.2
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Rosenberg RN, Lambracht-Washington D. Active Immunotherapy to Prevent Alzheimer Disease—A DNA Amyloid β 1-42 Trimer Vaccine. JAMA Neurol. 2020;77(3):289–290. doi:10.1001/jamaneurol.2019.4182
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