期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 202, 期 9, 页码 1163-1169出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20051529
关键词
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资金
- NIA NIH HHS [R01 AG020729, R01 AG019520, AG19520, AG20729] Funding Source: Medline
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 beta-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 beta-amyloid levels, protein tyrosine nitration, astrocytosis, and microgliosis. Thus, iNOS seems to be a major instigator of beta-amyloid deposition and disease progression. Inhibition of iNOS may be a therapeutic option in AD.
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