M
Michael T. Heneka
Researcher at German Center for Neurodegenerative Diseases
Publications - 341
Citations - 35729
Michael T. Heneka is an academic researcher from German Center for Neurodegenerative Diseases. The author has contributed to research in topics: Microglia & Neuroinflammation. The author has an hindex of 83, co-authored 286 publications receiving 27372 citations. Previous affiliations of Michael T. Heneka include University of Bonn & University Hospital Bonn.
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Journal ArticleDOI
Neuroinflammation in Alzheimer's disease
Michael T. Heneka,Monica J. Carson,Joseph El Khoury,Gary E. Landreth,Frederic Brosseron,Douglas L. Feinstein,Andreas H. Jacobs,Tony Wyss-Coray,Tony Wyss-Coray,Javier Vitorica,Richard M. Ransohoff,Karl Herrup,Sally A. Frautschy,Bente Finsen,Guy C. Brown,Alexei Verkhratsky,Alexei Verkhratsky,Alexei Verkhratsky,Koji Yamanaka,Jari Koistinaho,Eicke Latz,Eicke Latz,Annett Halle,Gabor C. Petzold,Terrence Town,Dave Morgan,Mari L. Shinohara,V. Hugh Perry,Clive Holmes,Clive Holmes,Nicolas G. Bazan,David J. Brooks,Stéphane Hunot,Bertrand Joseph,Nikolaus Deigendesch,Olga Garaschuk,Erik Boddeke,Charles A. Dinarello,John C.S. Breitner,Greg M. Cole,Douglas T. Golenbock,Markus P. Kummer +41 more
TL;DR: Genome-wide analysis suggests that several genes that increase the risk for sporadic Alzheimer's disease encode factors that regulate glial clearance of misfolded proteins and the inflammatory reaction.
Journal ArticleDOI
NLRP3 is activated in Alzheimer´s disease and contributes to pathology in APP/PS1 mice
Michael T. Heneka,Markus P. Kummer,Andrea Stutz,Andrea Delekate,Stephanie Schwartz,Ana Vieira-Saecker,Angelika Griep,Daisy Axt,Anita Remus,Te-Chen Tzeng,Ellen Gelpi,Annett Halle,Martin Korte,Eicke Latz,Eicke Latz,Douglas T. Golenbock +15 more
TL;DR: The role of the NLRP3/caspase-1 axis in the pathogenesis of Alzheimer's disease was investigated in this article, which showed an important role for the inflammasome.
Journal ArticleDOI
Innate immune activation in neurodegenerative disease
TL;DR: How the activation of innate immune signalling pathways — in particular, the NOD-, LRR- and pyrin domain-containing 3 (NLRP3) inflammasome — by aberrant host proteins may be a common step in the development of diverse neurodegenerative disorders is discussed.
Journal ArticleDOI
Inflammatory processes in Alzheimer's disease.
TL;DR: While inflammation has been thought to arise secondary to degeneration, recent experiments demonstrated that inflammatory mediators may stimulate APP processing by upregulation of beta secretase 1 and therefore are able to establish a vicious cycle.
Journal ArticleDOI
NLRP3 inflammasome activation drives tau pathology
Christina Ising,Carmen Venegas,Shuangshuang Zhang,Hannah Scheiblich,Susanne V. Schmidt,Ana Vieira-Saecker,Stephanie Schwartz,Shadi Albasset,Róisín M. McManus,Dario Tejera,Angelika Griep,Francesco Santarelli,Frederic Brosseron,Sabine Opitz,James Stunden,Maximilian Merten,Rakez Kayed,Douglas T. Golenbock,David Blum,Eicke Latz,Eicke Latz,Eicke Latz,Luc Buée,Michael T. Heneka,Michael T. Heneka +24 more
TL;DR: An important role of microglia and NLRP3 inflammasome activation in the pathogenesis of tauopathies is identified and the amyloid-cascade hypothesis in Alzheimer’s disease is supported, demonstrating that neurofibrillary tangles develop downstream of amyloids-beta-induced microglial activation.