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JCI table of contents, 17 May 2004

rmation and hippocampal defects in an Alzheimer disease mouse model

AUTHOR CONTACT:
Falk Fahrenholz
University of Mainz, Mainz, Germany.
Phone: 49-6131-392-5833; Fax: 49-6131-392-5348; E-mail: bio.chemie@uni-mainz.de

View the PDF of this article at: https://www.the-jci.org/press/20864.pdf

ACCOMPANYING COMMENTARY: Amyloid at the cutting edge: activation of alpha-secretase prevents amyloidogenesis in an Alzheimer disease mouse model

AUTHOR CONTACT:
Christian Haass
Ludwig-Maximilians-Universitat, Munich, Germany.
Phone: 49-89-5996-471; Fax: 49- 5996-415; E-mail: chaass@pbm.med.uni-muenchen.de

View the PDF of this commentary at: https://www.the-jci.org/press/21746.pdf

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Toll-free Road from Sepsis

Immune system failure to limit the spread of a bacterial infection results in sepsis: a loss of control on the normal inflammatory response, leading to tissue damage, increased vascular permeability, and finally multi-organ failure and shock. The death rate for sepsis patients is in the range of 70%, and the health-care sticker price for such runaway infections is around $15 billion annually in the US alone. Strategies for treating septic shock are aimed at limiting the inflammatory response, as treatments to directly reduce the bacterial infection, such as the use of antibiotics, can result in furthering the already out-of-control inflammatory response. Now, Cartson Kirschning and colleagues, from the Technical University of Munich, have tested a new therapeutic possibility by creating antibodies directed against the receptor to which bacteria bind in order to infect the cell. The strategy here, therefore, is to interrupt
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Contact: Laurie Goodman
press_releases@the-jci.org
212-342-4159
Journal of Clinical Investigation
17-May-2004


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