Antibody treatment partially reverses nerve damage in Alzheimer disease

Main Category: Alzheimer's / Dementia
Article Date: 21 Jan 2005 - 4:00 PDT

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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 amount of structural nerve damage after only 3 days. The study suggests that Abeta deposition leads to ongoing nerve damage and that upon reducing buildup of Abeta in the brain, this structural damage is rapidly reversible.

The imaging technique used will also be a valuable tool for the study of the progression of Abeta deposition in the brain during experimental models of Alzheimer disease and to also assess the effectiveness of treatments including the anti-Abeta antibody treatment described here.

TITLE: Anti-Abeta antibody treatment promotes the rapid recovery of amyloid-associated neuritic dystrophy in PDAPP transgenic mice.

AUTHOR CONTACT: David M. Holtzman
Department of Neurology, Washington University, St. Louis, Missouri, USA.
Phone: 314-362-9872; Fax: 314-362-2826; E-mail: Holtzman@neuro.wustl.edu.

View the PDF of this article at: https://www.the-jci.org/press/23269.pdf

From 5:00PM USA EST Thursday January 20, 2005 a PDF of this article will be available at:
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Brooke Grindlinger
press_releases@the-jci.org
Journal of Clinical Investigation

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