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Nat Rev Neurosci. 2015 Jun;16(6):358-72. doi: 10.1038/nrn3880.

Immune attack: the role of inflammation in Alzheimer disease.

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1] Department of Neuropathology, Charitéplatz 1, Charité - Universitätsmedizin Berlin, D-10117 Berlin, Germany. [2] Cluster of Excellence, NeuroCure, Charitéplatz 1, D-10117 Berlin, Germany.
Biogen, 225 Binney Street, Cambridge, Massachusetts 02142, USA.
Institute of Experimental Immunology, University of Zürich, Winterthurerstrasse 190, CH-8057 Zrich, Switzerland.


The past two decades of research into the pathogenesis of Alzheimer disease (AD) have been driven largely by the amyloid hypothesis; the neuroinflammation that is associated with AD has been assumed to be merely a response to pathophysiological events. However, new data from preclinical and clinical studies have established that immune system-mediated actions in fact contribute to and drive AD pathogenesis. These insights have suggested both novel and well-defined potential therapeutic targets for AD, including microglia and several cytokines. In addition, as inflammation in AD primarily concerns the innate immune system - unlike in 'typical' neuroinflammatory diseases such as multiple sclerosis and encephalitides - the concept of neuroinflammation in AD may need refinement.

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