• Corpus ID: 104191840

Neuronal nitric oxide synthase : a biomarker for Alzheimers disease : interaction of neuronal nitric oxide synthase with beta-amyloid peptides in the brain

@inproceedings{Padayachee2011NeuronalNO,
  title={Neuronal nitric oxide synthase : a biomarker for Alzheimers disease : interaction of neuronal nitric oxide synthase with beta-amyloid peptides in the brain},
  author={Eden Rebecca Padayachee},
  year={2011}
}
Make your own notes. NEVER undel"line or write in a hook. High levels of the amino acid arginine and low levels of the product citrulline in the cerebrospinal fluid of Alzheimer' s patients could mean that there is a decrease in the enzymes that metabolize this amino acid. One such enzyme is neuronal nitric oxide synthase (nNOS). In this study, neuronal nitric oxide synthase (nNOS), sourced from bovine brain was extracted and concentrated using two methods of precipitation: poly (ethylene… 

References

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TLDR
Nitric oxide has only recently been appreciated as a normal biologic substance with a role in signal transduction and appears to account for a major portion of neural damage following vascular stroke.
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TLDR
A new series of 1-[(Aryloxy)alkyl]-1H-imidazoles in which a longer methylene chain is present between the imidazole and the phenol part of molecule is reported, found to be more potent nNOS inhibitors than the parent ethylenic compounds, although this increase in potency resulted in a partial loss of selectivity.
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TLDR
Treatment with BN 80933 significantly reduced infarct volume and enhanced behavioral recovery in rats subjected to transient cerebral artery occlusion and 48-h or 7-day reperfusion, indicating that BN80933 represents a class of potentially useful therapeutic agents for the treatment of stroke or trauma and possibly neurodegenerative disorders that involve both NO and ROS.
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  • Biology, Chemistry
    FASEB journal : official publication of the Federation of American Societies for Experimental Biology
  • 2002
TLDR
The results represent the first evidence that amyloid fragments impair constitutive NOS activity in cell‐free and cellular systems, providing a possible molecular mechanism for the onset and/or maintenance of Alzheimer's disease.
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TLDR
It is shown that substrate amounts of rat cerebellar nitric oxide synthase, in the absence of added NADPH, catalyze the conversion of arginine to N-hydroxyarginine as the dominant product, indicating that brain nitricoxide synthase contains an endogenous reductant that can support oxygenation ofArginine but not of N-Hydroxyarg inine.
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TLDR
There is an insoluble nitric oxide synthase in rat cerebellum that has similar characteristics to the soluble type and exhibited an absolute requirement for FAD, in addition to NADPH and Ca2+/calmodulin.
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