Angelika Griep

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Alzheimer's disease is the world's most common dementing illness. Deposition of amyloid-β peptide drives cerebral neuroinflammation by activating microglia. Indeed, amyloid-β activation of the NLRP3 inflammasome in microglia is fundamental for interleukin-1β maturation and subsequent inflammatory events. However, it remains unknown whether NLRP3 activation(More)
Alzheimer's disease (AD) is characterized by the extracellular deposition of amyloid-β (Aβ), neurofibrillary tangle formation, and a microglial-driven inflammatory response. Chronic inflammatory activation compromises microglial clearance functions. Because peroxisome proliferator-activated receptor γ (PPARγ) agonists suppress inflammatory gene expression,(More)
Neuroinflammation plays a fundamental role in the pathogenesis of Alzheimer's disease (AD), resulting in the extensive activation of microglial and astroglial cells. Here we describe the role of myeloid-related protein Mrp14, a recently described amplifier of inflammation, in Alzheimer's disease and in the related amyloid precursor protein/presenilin1(More)
Markus P. Kummer,1 Thomas Vogl,2 Daisy Axt,1 Angelika Griep,1 Ana Vieira-Saecker,1 Frank Jessen,3,4 Ellen Gelpi,5 Johannes Roth,2 and Michael T. Heneka1,4 1Clinical Neurosciences Unit, Department of Neurology, University of Bonn, 53105 Bonn, Germany, 2Institute of Immunology, University of Münster, 48129 Münster, Germany, 3Department of Psychiatry,(More)
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