R
Robert E. Mrak
Researcher at University of Toledo
Publications - 181
Citations - 17674
Robert E. Mrak is an academic researcher from University of Toledo. The author has contributed to research in topics: Alzheimer's disease & Senile plaques. The author has an hindex of 58, co-authored 180 publications receiving 16624 citations. Previous affiliations of Robert E. Mrak include John L. Scott & University of Arkansas for Medical Sciences.
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Journal ArticleDOI
Inflammation and Alzheimer's disease.
Haruhiko Akiyama,Steven W. Barger,Scott R. Barnum,B Bradt,Jürgen Bauer,Greg M. Cole,Neil R. Cooper,Piet Eikelenboom,Mark R. Emmerling,Bernd L. Fiebich,Caleb E. Finch,Sally A. Frautschy,W. S. T. Griffin,Harald Hampel,Michael Hüll,Gary E. Landreth,Lih-Fen Lue,Robert E. Mrak,Ian R. A. Mackenzie,Patrick L. McGeer,M K O'Banion,Joel S. Pachter,Giulio Maria Pasinetti,C Plata-Salaman,Joseph G. Rogers,Russell E. Rydel,Yueyang Shen,Wolfgang J. Streit,Ronald Strohmeyer,I Tooyoma,F L van Muiswinkel,R. Veerhuis,David G. Walker,Scott D. Webster,Beatrice Hauss–Wegrzyniak,Gary L. Wenk,Tony Wyss-Coray +36 more
TL;DR: By better understanding AD inflammatory and immunoregulatory processes, it should be possible to develop anti-inflammatory approaches that may not cure AD but will likely help slow the progression or delay the onset of this devastating disorder.
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Microglia and neuroinflammation: a pathological perspective
TL;DR: The role of microglia in central nervous system diseases, including infections, is discussed in terms of a participation in both acute and chronic neuroinflammatory responses.
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Glial‐Neuronal Interactions in Alzheimer's Disease: The Potential Role of a ‘Cytokine Cycle’ in Disease Progression
W. S. T. Griffin,J. G. Sheng,J. G. Sheng,M.C. Royston,S.M. Gentleman,J.E. McKenzie,David I. Graham,G.W. Roberts,Robert E. Mrak +8 more
TL;DR: The hypothesis that chronic activation of glial inflammatory processes, arising from genetic or environmental insults to neurons and accompanied by chronic elaboration of neuroactive glia‐derived cytokines and other proteins, sets in motion a cytokine cycle of cellular and molecular events with neurodegenerative consequences is advanced.
Journal ArticleDOI
Glia and their cytokines in progression of neurodegeneration
Robert E. Mrak,W. Sue T. Griffin +1 more
TL;DR: Normal age-related glial changes, likely a response to the normal wear and tear of the aging process, raise the threshold of glial activation and thus may explain the fact that even genetically determined Alzheimer's disease only shows the full manifestation of the disease decades after birth.
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Interleukin-1 Expression in Different Plaque Types in Alzheimer's Disease: Significance in Plaque Evolution
TL;DR: The results suggest an important immunological component in the evolution of amyloid-contining plaques in Alzheimer's disease and suggest that IL-1-expressing cells are necessary to intitiate dystrophic neurite formation in diffuse β-amyloid deposits.