New Alzheimer’s Therapy Shows Promise in Reducing Amyloid Plaques in Brain

New Alzheimer’s Therapy Shows Promise in Reducing Amyloid Plaques in Brain
An investigational treatment for Alzheimer's disease (AD) could be on the horizon, according to a study from researchers at Biogen and the University of Zurich. Aducanumab, a human monoclonal antibody, shows evidence of reducing Alzheimer's amyloid plaques -- the culprit behind AD-induced brain cell death. The treatment candidate is potentially the first of its kind, since current medications for Alzheimer's slightly delay symptoms and do not prevent the disease from progressing. The research report, "The antibody aducanumab reduces Abeta plaques in Alzheimer's disease," was recently published in the journal Nature. Previous studies in mouse models of AD showed reductions in the sticky brain amyloid plaques with injections of aducanumab. In this trial, humans with mild Alzheimer's disease received intravenous aducanumab for one year. A total of 165 patients participated in the study and received treatment from October 2012 to January 2014 at 33 clinical sites in the U.S. Participants in the study received monthly intravenous infusions of a placebo or aducanumab at four different increasing doses. As the dose increased, so did improvements in clinical measurements of cognition and memory, known as Clinical Dementia Rating—Sum of Boxes and Mini-Mental State Examination scores. Even more remarkably, brain amyloid plaques decreased, and were almost completely gone in the group that received the highest dose of medication. "The results of this clinical study make us optimistic that we can potentially make a great step forward in treating Alzheimer's disease ... ," Prof. R
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  1. Dante J Marciani says:

    Apparently plaque has also a protective role by sequestering the neurotoxic amyloid beta oligomers; indeed, mentally functional individuals may have plaque as shown by postmortem examination. Yet, few mention that aducanumab recognizes that conformational epitope characteristic of neurotoxic Abeta oligomers only, quite possible interfering with their cytotoxic activity, regardless of plaque reduction. After all, most of the failing active and passive AD immunotherapy tested products were quite good in reducing plaque, but they failed in reversing or slowing down the loss of cognitive functions. That is the big difference between aducanumab and other agents. Of relevance is that this antibody is a natural one, i.e. it is produced by the body, a fact that strongly support the vaccine concept, assuming that such a vaccine is designed properly to mimic natural immune protection, and not to induce some odd immune response that would be most likely damaging.

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