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Published online 31 October 2005 doi:10.1084/jem.20051529
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 202, Number 9, 1163-1169
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BRIEF DEFINITIVE REPORT

 Protection from Alzheimer's-like disease in the mouse by genetic ablation of inducible nitric oxide synthase

Carl Nathan1, Noel Calingasan2, Jon Nezezon1, Aihao Ding1, M. Scott Lucia5, Krista La Perle4, Michele Fuortes3, Michael Lin2, Sabine Ehrt1, Nyoun Soo Kwon1, Junyu Chen2, Yoram Vodovotz6, Khatuna Kipiani2, and M. Flint Beal2

1 Department of Microbiology and Immunology, Weill Cornell Medical College, New York, NY 10021
2 Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, NY 10021
3 Department of Surgery, Weill Cornell Medical College, New York, NY 10021
4 Research Animal Resource Center, Weill Cornell Medical College, New York, NY 10021
5 Department of Pathology, University of Colorado Health Sciences Center, Denver, CO 80262
6 Center for Inflammation and Regenerative Modeling and Department of Surgery, University of Pittsburgh, Pittsburgh, PA 15260

CORRESPONDENCE Carl Nathan: cnathan{at}med.cornell.edu

Brains from subjects who have Alzheimer's disease (AD) express inducible nitric oxide synthase (iNOS). We tested the hypothesis that iNOS contributes to AD pathogenesis. Immunoreactive iNOS was detected in brains of mice with AD-like disease resulting from transgenic expression of mutant human ß-amyloid precursor protein (hAPP) and presenilin-1 (hPS1). We bred hAPP-, hPS1-double transgenic mice to be iNOS+/+ or iNOS–/–, and compared them with a congenic WT strain. Deficiency of iNOS substantially protected the AD-like mice from premature mortality, cerebral plaque formation, increased ß-amyloid levels, protein tyrosine nitration, astrocytosis, and microgliosis. Thus, iNOS seems to be a major instigator of ß-amyloid deposition and disease progression. Inhibition of iNOS may be a therapeutic option in AD.


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