[en] Alzheimer's disease (AD) is the world's most common dementing illness, affecting over 150 million patients. Classically AD has been viewed as a neurodegenerative disease of the elderly, characterized by the extracellular deposition of misfolded amyloid-β (Aβ) peptide and the intracellular formation of neurofibrillary tangles. Only recently has neuroinflammation emerged as an important component of AD pathology. Experimental, genetic and epidemiological data now indicate a crucial role for activation of the innate immune system as a disease-promoting factor. The sustained formation and deposition of Aβ aggregates causes chronic activation of the immune system and disturbance of microglial clearance functions. Here we review advances in the molecular understanding of the inflammatory response in AD that point to novel therapeutic approaches for the treatment of this devastating disease.
Disciplines :
Neurology
Author, co-author :
HENEKA, Michael ; 1] Clinical Neuroscience, Department of Neurology, University of Bonn, Bonn, Germany. [2] Department of Medicine, Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, Massachusetts, USA. [3] German Center for Neurodegenerative Diseases, Bonn, Germany
Golenbock, Douglas T; Department of Medicine, Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, Massachusetts, USA
Latz, Eicke; 1] Department of Medicine, Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, Massachusetts, USA. [2] German Center for Neurodegenerative Diseases, Bonn, Germany. [3] Institute of Innate Immunology, University of Bonn, Bonn, Germany
Supported by the Deutsche Forschungsgemeinschaft (Excellence Cluster ImmunoSensation and KFO177 to E.L. and M.T.H.) and by the US National Institutes of Health (1R01HL112661 to E.L.).
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