The article by Browne et al. under "Related Papers" (Browne et al., 2013) directly addresses why it may be beneficial not only reduce to amyloid-β with targeted antibodies, but also to promote an anti-inflammatory Th2 and T regulatory response towards Th1 cell-mediated inflammation. This could be important, because once activated by amyloid-β, it is likely that Th1 cell-mediated inflammation will continue and may require only residual amounts of amyloid to maintain the inflammatory response and promote progression of disease pathology. Passive vaccination with amyloid-β-reducing monoclonals won't address the cell-mediated inflammation, and a Th1-type response to an active vaccine could exacerbate the problem.

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