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JCI table of contents: Oct. 19, 2009

EDITOR'S PICK: The protein APC slows Lou Gehrig's disease in mice

Amyotrophic lateral sclerosis (ALS), also known as Lou Gehrig's disease, is a neurodegenerative disease that causes progressive weakness, disability, and death. Treatments are largely palliative. Using mice carrying the mutated form of the human SOD1 gene that causes inherited forms of ALS, however, Berislav Zlokovic and colleagues, at the University of Rochester Medical Center, Rochester, have now found that administration of the protein APC slows disease progression and extends survival. The authors therefore suggest that strategies designed to activate APC might be of benefit to patients with inherited, and possibly sporadic, ALS. However, in an accompanying commentary, Charles Esmon and Jonathan Glass warn that such an approach would not be without risks.

In the study, administration of both APC, whose main function is to prevent blood clotting, and APC analogs with a reduced ability to prevent blood clotting slowed disease progression in the mutant SOD1expressing mice and extended their survival, even when the compounds were administered after disease onset. Further analysis indicated that these compounds were able to access the brain and that once there, they worked by decreasing expression of the mutant SOD1 in several cell types in the brain, including the nerve cells destroyed in individuals with ALS. This study therefore indicates that APC can have a neuroprotective effect in mouse models of inherited ALS.

TITLE: Activated protein C therapy slows ALS-like disease in mice by transcriptionally inhibiting SOD1 in motor neurons and microglia cells

Berislav V. Zlokovic
University of Rochester Medical Center, Rochester, New York, USA.
Phone: (585) 273-3132; Fax: (585) 273-3133; E-mail:

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TITLE: The APCs of neuroprotection

Charles T. Esmon
Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, USA.
Phone: (405) 271-6474; Fax: (405) 271-2872; E-mail:

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VASCULAR BIOLOGY: Too much of the protein building block homocysteine inhibits blood vessel formation

TITLE: Homocysteine inhibits neoangiogenesis in mice through blockade of annexin A2dependent fibrinolysis

Katherine A. Hajjar
Weill Cornell Medical College, New York, New York, USA.
Phone: (212) 746-2034; Fax: (212) 746-8809; E-mail:

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TITLE: Homocysteine-mediated thrombosis and angiostasis in vascular pathobiology

Joseph Loscalzo
Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA.
Phone: (617) 732-6340; Fax: (617) 732-6439; E-mail:

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ONCOLOGY: Loss of the protein Smad4 associated with head and neck cancer

TITLE: Smad4 loss in mice causes spontaneous head and neck cancer with increased genomic instability and inflammation

Shi-Long Lu
University of Colorado Denver, Aurora, Colorado, USA.
Phone: (303) 724-0784; Fax: (303) 724-4553; E-mail:

Xiao-Jing Wang
University of Colorado Denver, Aurora, Colorado, USA.
Phone: (303) 724-3001; Fax: (303) 724-4730; E-mail:

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TITLE: Smad4: gatekeeper gene in head and neck squamous cell carcinoma

Murray Korc
Dartmouth-Hitchcock Medical Center, Lebanon, New Hampshire, USA.
Phone: (603) 650-7936; Fax: (603) 650-6122; E-mail:

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NEPHROLOGY: ARH: another link in the molecular chain regulating potassium levels

TITLE: The ARH adaptor protein regulates endocytosis of the ROMK potassium secretory channel in mouse kidney

Paul A. Welling
University of Maryland School of Medicine, Baltimore, Maryland, USA.
Phone: (410) 706-3851; Fax: (410) 706-8341; E-mail:

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Contact: Karen Honey
Journal of Clinical Investigation

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