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JCI table of contents: May 22, 2008
Date:5/22/2008

ony Wyss-Coray and colleagues, at Stanford University, have indicated that decreased autophagy in nerve cells can increase neurodegeneration in a mouse model of AD.

In the study, mice lacking one of their Becn1 genes, which carry the information required to make the key autophagy protein beclin 1, were found to exhibit decreased nerve cell autophagy and this was associated with increased neurodegeneration. When a mouse model of AD was similarly engineered to lack one Becn1 gene, an increased amount of neurodegeneration and protein accumulation in the brain was observed. Conversely, if the mouse model of AD was engineered to express increased amounts of beclin 1, decreased protein accumulation in the brain was observed. The authors therefore suggest that increasing levels of beclin 1 might be of benefit to individuals with AD.

In an accompanying commentary, Jin-A Lee and Fen-Biao Gao, at the University of California at San Francisco, note that although modulating beclin 1 levels might be an attractive approach for treating individuals with AD, further studies in other animal models are required to verify the viability of this strategy.

TITLE: The autophagy-related protein beclin 1 shows reduced expression in early Alzheimer disease and regulates amyloid-beta accumulation in mice

AUTHOR CONTACT:
Tony Wyss-Coray
Stanford University, Stanford, California, USA.
Phone: (650) 852-3220; Fax: (650) 849-0434; E-mail: twc@stanford.edu.

View the PDF of this article at: https://www.the-jci.org/article.php?id=33585

ACCOMPANYING COMMENTARY
TITLE: Regulation of A-beta pathology by beclin 1: a protective role for autophagy?

AUTHOR CONTACT:
Fen-Biao Gao
University of California at San Francisco, San Francisco, California, USA.
Phone: (415) 734-2514; Fax: (415) 355-0824; E-mail:

Contact: Karen Honey
press_releases@thje-jci.org
215-573-1850
Journal of Clinical Investigation
Source:Eurekalert

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