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Specificity of mechanisms for plaque removal after Aβ immunotherapy for Alzheimer disease

Nature Medicine volume 10, pages 117–118 (2004)Cite this article

To the editor:

Nicoll et al. recently reported autopsy findings from an Alzheimer disease patient vaccinated with AN-1792, the amyloid-β (Aβ) protein preparation made by Elan Pharmaceuticals1. A clinical trial with this agent was halted because of central nervous system complications in several of the patients receiving the vaccine. The main autopsy findings were widespread encephalitis, infiltration of the brain by macrophages and a reduction of senile plaques in extensive areas of the neocortex1. We report here a similar reduction of senile plaques in a cortical area affected by incomplete ischemia in a typical case of Alzheimer disease. We interpret this finding as being the result of microglia and macrophage invasion of the affected area. We suggest that such a nonspecific effect might have influenced the results observed in the autopsy case described by Nicoll et al. and that encephalitis resulting from any cause might also lead to phagocytosis of senile plaques.

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Figure 1: Temporal cortex of an early Alzheimer disease case with an incidental, incomplete ischemic lesion.

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Acknowledgements

We thank M. Kato of Soga Hospital for providing the brain sample. This research was supported by grants to P.L.M. from the Jack Brown and Family AD Research Fund and the Alzheimer Society of Canada/CIHR/AstraZeneca. This study was approved by the ethical committee of the Tokyo Institute of Psychiatry.

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Authors and Affiliations

  1. Tokyo Institute of Psychiatry, Tokyo, 156-8585, Japan

    Haruhiko Akiyama

  2. Kinsmen Laboratory of Neurological Research, University of British Columbia, Vancouver, V6T 1Z3, British Columbia, Canada

    Patrick L McGeer

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  2. Patrick L McGeer
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Akiyama, H., McGeer, P. Specificity of mechanisms for plaque removal after Aβ immunotherapy for Alzheimer disease. Nat Med 10, 117–118 (2004). https://doi.org/10.1038/nm0204-117

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