News Release

Antioxidants decrease disease in a Drosophila model of Alzheimer's disease

Peer-Reviewed Publication

JCI Journals

Alzheimer’s disease (AD) is one of a number of neurodegenerative disorders in which brain cells damaged by naturally occurring chemicals known as reactive oxygen species (ROS) have been observed. However, whether this oxidative damage causes neurodegeneration or is a consequence of it has not been previously determined. A study appearing online on December 14, in advance of publication in the January print issue of the Journal of Clinical Investigation, indicates that oxidative damage is a factor contributing to neurodegeneration in a Drosophila model of neurodegenerative disorders such as AD.

Mel Feany and colleagues from Brigham and Women’s Hospital and Harvard Medical School assessed neuron cell death in Drosophila expressing a neurodegenerative disease–associated form of the human protein tau. The number of dying neurons was increased if these insects were also genetically modified to have high levels of ROS. By contrast, if the insects were treated with the antioxidant vitamin E they had decreased numbers of dying neurons. This demonstration that oxidative stress contributes to neurodegeneration in this model of AD suggests that targeting antioxidant pathways might provide a new approach for treating individuals with AD and other related neurodegenerative disorders.

TITLE: Oxidative stress mediates tau-induced neurodegeneration in Drosophila.

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AUTHOR CONTACT:
Mel B. Feany
Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Phone: (617) 525-4405; Fax: (617) 525-4422; E-mail: mel_feany@hms.harvard.edu.

View the PDF of this article at: https://www.the-jci.org/article.php?id=28769


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