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JCI table of contents, January 20 2005

ology, Beth Israel Deaconess Medical Center, Boston, Massachusetts, USA.
Phone: 617-667-2816; Fax: 617-975-5531; E-mail: rbates@caregroup.harvard.edu.

View the PDF of this article at: https://www.the-jci.org/press/23183.pdf

From 5:00PM USA EST Thursday January 20, 2005 a PDF of this article will be available at: http://www.jci.org/papbyrecent.shtml


Antibody treatment partially reverses nerve damage in Alzheimer disease

Researchers from Washington University School of Medicine have shown that an antibody treatment administered to the brain surface in mice with Alzheimer disease is capable of rapidly reversing disease-related structural nerve damage. The study will appear online on January 20 in advance of print publication in the February 1 issue of the Journal of Clinical Investigation.

One of the many hallmarks of Alzheimer disease is the presence of deposits or "plaques" made up of amyloid-beta peptide (Abeta) in areas of the brain responsible for memory and cognition. While several approaches to decreasing Abeta production or increasing its clearance from the brain are being studied as potential treatments for Alzheimer disease, it is not known whether, upon clearance of Abeta, if significant structural damage to nerves is reversed, remains, or continues.

Using a mouse model of Alzheimer disease in which a subset of neurons and Abeta in the mouse brain express colored fluorescent proteins that can be visualized in the living animal under a microscope, David Holtzman and colleagues administered an anti- Abeta antibody treatment and monitored the structural changes to nerves within the mouse brains. They observed that following treatment of the brain surface, there was a significant decrease in the amo
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Contact: Brooke Grindlinger
press_releases@the-jci.org
212-342-9006
Journal of Clinical Investigation
20-Jan-2005


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