Liu B, Frost JL, Sun J, Fu H, Grimes S, Blackburn P, Lemere CA. MER5101, a novel Aβ1-15:DT conjugate vaccine, generates a robust anti-Aβ antibody response and attenuates Aβ pathology and cognitive deficits in APPswe/PS1ΔE9 transgenic mice. J Neurosci. 2013 Apr 17;33(16):7027-37. PubMed.
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Ann Romney Center for Neurologic Diseases, Brigham and Women's Hospital and Harvard Medical School
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.
References:
Browne TC, McQuillan K, McManus RM, O'Reilly JA, Mills KH, Lynch MA. IFN-γ Production by amyloid β-specific Th1 cells promotes microglial activation and increases plaque burden in a mouse model of Alzheimer's disease. J Immunol. 2013 Mar 1;190(5):2241-51. PubMed.
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