Journal of Clinical and Cellular Immunology
Open Access

Henrietta M. Nielsen

Publications

• Research Article
  Increased IRAK-4 Kinase Activity in Alzheimer’s Disease; IRAK-1/4 Inhibitor I Prevents Pro-inflammatory Cytokine Secretion but not the Uptake of Amyloid Beta by Primary Human Glia
  Author(s): Jeroen J.M. Hoozemans, Elise S. van Haastert, Sandra D. Mulder, Henrietta M. Nielsen, Robert Veerhuis, Rob Ruijtenbeek, Annemieke J.M. Rozemuller, Riet Hilhorst, and Saskia M. van der ViesJeroen J.M. Hoozemans, Elise S. van Haastert, Sandra D. Mulder, Henrietta M. Nielsen, Robert Veerhuis, Rob Ruijtenbeek, Annemieke J.M. Rozemuller, Riet Hilhorst, and Saskia M. van der Vies
  
  Alzheimer’s disease (AD) is characterized by the deposition of amyloid-β (Aβ), which is associated with a neuroinflammatory response involving microglia and astrocytes. This neuroinflammatory response has detrimental effects on disease progression but also has a beneficial function on removal of excess Aβ. Microglia and astrocytes are involved in the clearance of Aβ from the brain, but neuroinflammation also promotes neurodegeneration. In order to identify signal transduction pathways critically involved in AD we analysed human brain tissue using protein kinase activity profiling. We identified increased activity of the Interleukin 1 Receptor Associated Kinase 4 (IRAK-4) in AD compared to control brain tissue. IRAK-4 is a component of the signal transduction pathway that functions downstream of the Toll-like receptors and the interleukin-1 receptor. Immunohis.. View More»
  DOI: 10.4172/2155-9899.1000243

  Abstract PDF

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