Protection from Alzheimer's-like disease in the mouse by genetic ablation of inducible nitric oxide synthase
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...
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| Published in | The Journal of experimental medicine Vol. 202; no. 9; pp. 1163 - 1169 |
|---|---|
| Main Authors | , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
The Rockefeller University Press
07.11.2005
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| Subjects | |
| Online Access | Get full text |
| ISSN | 0022-1007 1540-9538 1892-1007 |
| DOI | 10.1084/jem.20051529 |
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| Abstract | 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 β-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 β-amyloid levels, protein tyrosine nitration, astrocytosis, and microgliosis. Thus, iNOS seems to be a major instigator of β-amyloid deposition and disease progression. Inhibition of iNOS may be a therapeutic option in AD. |
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| AbstractList | 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.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. 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 β -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 β -amyloid levels, protein tyrosine nitration, astrocytosis, and microgliosis. Thus, iNOS seems to be a major instigator of β -amyloid deposition and disease progression. Inhibition of iNOS may be a therapeutic option in AD. 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 {szligbeta}-amyloid precursor protein (hAPP) and presenilin-1 (hPS1). We bred hAPP-, hPS1-double transgenic mice to be iNOS super(+/+) or iNOS super(-/-), and compared them with a congenic WT strain. Deficiency of iNOS substantially protected the AD-like mice from premature mortality, cerebral plaque formation, increased {szligbeta}-amyloid levels, protein tyrosine nitration, astrocytosis, and microgliosis. Thus, iNOS seems to be a major instigator of {szligbeta}-amyloid deposition and disease progression. Inhibition of iNOS may be a therapeutic option in AD. 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. 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 β-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 β-amyloid levels, protein tyrosine nitration, astrocytosis, and microgliosis. Thus, iNOS seems to be a major instigator of β-amyloid deposition and disease progression. Inhibition of iNOS may be a therapeutic option in AD. |
| Author | Vodovotz, Yoram Ehrt, Sabine Fuortes, Michele Calingasan, Noel La Perle, Krista Kipiani, Khatuna Ding, Aihao Nezezon, Jon Lin, Michael Kwon, Nyoun Soo Nathan, Carl Lucia, M. Scott Chen, Junyu Beal, M. Flint |
| AuthorAffiliation | 3 Department of Surgery, Weill Cornell Medical College, New York, NY 10021 2 Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, NY 10021 6 Center for Inflammation and Regenerative Modeling and Department of Surgery, University of Pittsburgh, Pittsburgh, PA 15260 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 1 Department of Microbiology and Immunology, Weill Cornell Medical College, New York, NY 10021 |
| AuthorAffiliation_xml | – name: 1 Department of Microbiology and Immunology, Weill Cornell Medical College, New York, NY 10021 – name: 3 Department of Surgery, Weill Cornell Medical College, New York, NY 10021 – name: 2 Department of Neurology and Neuroscience, Weill Cornell Medical College, New York, NY 10021 – name: 5 Department of Pathology, University of Colorado Health Sciences Center, Denver, CO 80262 – name: 6 Center for Inflammation and Regenerative Modeling and Department of Surgery, University of Pittsburgh, Pittsburgh, PA 15260 – name: 4 Research Animal Resource Center, Weill Cornell Medical College, New York, NY 10021 |
| Author_xml | – sequence: 1 givenname: Carl surname: Nathan fullname: Nathan, Carl – sequence: 2 givenname: Noel surname: Calingasan fullname: Calingasan, Noel – sequence: 3 givenname: Jon surname: Nezezon fullname: Nezezon, Jon – sequence: 4 givenname: Aihao surname: Ding fullname: Ding, Aihao – sequence: 5 givenname: M. Scott surname: Lucia fullname: Lucia, M. Scott – sequence: 6 givenname: Krista surname: La Perle fullname: La Perle, Krista – sequence: 7 givenname: Michele surname: Fuortes fullname: Fuortes, Michele – sequence: 8 givenname: Michael surname: Lin fullname: Lin, Michael – sequence: 9 givenname: Sabine surname: Ehrt fullname: Ehrt, Sabine – sequence: 10 givenname: Nyoun Soo surname: Kwon fullname: Kwon, Nyoun Soo – sequence: 11 givenname: Junyu surname: Chen fullname: Chen, Junyu – sequence: 12 givenname: Yoram surname: Vodovotz fullname: Vodovotz, Yoram – sequence: 13 givenname: Khatuna surname: Kipiani fullname: Kipiani, Khatuna – sequence: 14 givenname: M. Flint surname: Beal fullname: Beal, M. Flint |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/16260491$$D View this record in MEDLINE/PubMed |
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| Copyright | Copyright © 2005, The Rockefeller University Press |
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| Snippet | Brains from subjects who have Alzheimer's disease (AD) express inducible nitric oxide synthase (iNOS). We tested the hypothesis that iNOS contributes to AD... |
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| SubjectTerms | Alzheimer Disease - enzymology Alzheimer Disease - genetics Alzheimer Disease - mortality Alzheimer Disease - pathology Animals Brain - enzymology Brain - pathology Brief Definitive Report Crosses, Genetic Disease Models, Animal Gene Deletion Humans Inbreeding Mice Mice, Inbred C57BL Mice, Knockout Mice, Transgenic Nitric Oxide Synthase Type II - deficiency Nitric Oxide Synthase Type II - genetics |
| Title | Protection from Alzheimer's-like disease in the mouse by genetic ablation of inducible nitric oxide synthase |
| URI | https://www.ncbi.nlm.nih.gov/pubmed/16260491 https://www.proquest.com/docview/19443729 https://www.proquest.com/docview/68777739 https://pubmed.ncbi.nlm.nih.gov/PMC2213235 |
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