Abstract
Nitric oxide (NO) may play a role in the pathophysiology of Alzheimer's disease (AD). Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of NO synthase, is involved in regulation of NO production. Recently it has been reported that dimethylarginine dimethylaminohydrolase, an enzyme that hydrolyses ADMA into citrulline and dimethylamine, is specifically elevated in neurons displaying cytoskeletal abnormalities and oxidative stress in AD. We hypothesized that this could lead to altered CSF concentrations of ADMA in AD. Measurement of ADMA and dimethylamine in CSF revealed no significant differences between AD patients (n = 20) and age-matched control subjects (n = 20). Our results suggest that in early stages of AD overall regulation of NO production by ADMA is not aberrant.
MeSH terms
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Aged
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Alzheimer Disease / cerebrospinal fluid*
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Alzheimer Disease / enzymology
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Alzheimer Disease / physiopathology
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Amyloid beta-Peptides / cerebrospinal fluid
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Arginine / analogs & derivatives*
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Arginine / cerebrospinal fluid*
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Brain / enzymology*
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Brain / pathology
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Brain / physiopathology
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Cytoskeleton / enzymology
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Cytoskeleton / pathology
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Dimethylamines / cerebrospinal fluid
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Female
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Humans
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Male
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Middle Aged
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Neurons / enzymology*
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Neurons / pathology
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Nitric Oxide / biosynthesis*
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Nitric Oxide Synthase / metabolism*
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Oxidative Stress / physiology
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Peptide Fragments / cerebrospinal fluid
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tau Proteins / cerebrospinal fluid
Substances
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Amyloid beta-Peptides
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Dimethylamines
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Peptide Fragments
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amyloid beta-protein (1-42)
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tau Proteins
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Nitric Oxide
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N,N-dimethylarginine
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Arginine
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Nitric Oxide Synthase