Asymmetrical dimethylarginine is increased in plasma and decreased in cerebrospinal fluid of patients with Alzheimer's disease.

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Asymmetrical dimethylarginine is increased in plasma and decreased in cerebrospinal fluid of patients with Alzheimer's disease. / Arlt, Sönke; Schulze, Friedrich; Eichenlaub, Martin; Maas, Renke; Lehmbeck, Jan; Schwedhelm, Edzard; Jahn, Holger; Böger, Rainer.

in: DEMENT GERIATR COGN, Jahrgang 26, Nr. 1, 1, 2008, S. 58-64.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

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@article{0678d81d21ce4158ad2930d4fc96a64b,
title = "Asymmetrical dimethylarginine is increased in plasma and decreased in cerebrospinal fluid of patients with Alzheimer's disease.",
abstract = "BACKGROUND: Asymmetrical dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide (NO) synthase and may alter NO production during pathological conditions. Concerning Alzheimer's disease (AD), there are reports on altered cerebral NO metabolism, but only few studies on ADMA concentrations in plasma and cerebrospinal fluid (CSF). METHODS: We assessed plasma ADMA in 80 AD patients and 80 age- and gender-matched controls and CSF ADMA in a subgroup of 53 AD patients and 20 controls. RESULTS: ADMA plasma concentrations were increased, while CSF ADMA concentrations were decreased in AD patients. There was a significant association between decreasing CSF ADMA levels and the severity of cognitive impairment. CONCLUSION: Elevated ADMA in plasma might be a contributing factor for AD through alterations of NO metabolism, for example decreased cerebral microperfusion, while decreased levels of CSF ADMA might lead to a cerebral increase of NO, peroxynitrite production and oxidative protein damage. Our study reveals different mechanisms of plasma and CSF ADMA regulation, both potentially contributing to AD pathology.",
author = "S{\"o}nke Arlt and Friedrich Schulze and Martin Eichenlaub and Renke Maas and Jan Lehmbeck and Edzard Schwedhelm and Holger Jahn and Rainer B{\"o}ger",
year = "2008",
language = "Deutsch",
volume = "26",
pages = "58--64",
journal = "DEMENT GERIATR COGN",
issn = "1420-8008",
publisher = "S. Karger AG",
number = "1",

}

RIS

TY - JOUR

T1 - Asymmetrical dimethylarginine is increased in plasma and decreased in cerebrospinal fluid of patients with Alzheimer's disease.

AU - Arlt, Sönke

AU - Schulze, Friedrich

AU - Eichenlaub, Martin

AU - Maas, Renke

AU - Lehmbeck, Jan

AU - Schwedhelm, Edzard

AU - Jahn, Holger

AU - Böger, Rainer

PY - 2008

Y1 - 2008

N2 - BACKGROUND: Asymmetrical dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide (NO) synthase and may alter NO production during pathological conditions. Concerning Alzheimer's disease (AD), there are reports on altered cerebral NO metabolism, but only few studies on ADMA concentrations in plasma and cerebrospinal fluid (CSF). METHODS: We assessed plasma ADMA in 80 AD patients and 80 age- and gender-matched controls and CSF ADMA in a subgroup of 53 AD patients and 20 controls. RESULTS: ADMA plasma concentrations were increased, while CSF ADMA concentrations were decreased in AD patients. There was a significant association between decreasing CSF ADMA levels and the severity of cognitive impairment. CONCLUSION: Elevated ADMA in plasma might be a contributing factor for AD through alterations of NO metabolism, for example decreased cerebral microperfusion, while decreased levels of CSF ADMA might lead to a cerebral increase of NO, peroxynitrite production and oxidative protein damage. Our study reveals different mechanisms of plasma and CSF ADMA regulation, both potentially contributing to AD pathology.

AB - BACKGROUND: Asymmetrical dimethylarginine (ADMA) is an endogenous inhibitor of nitric oxide (NO) synthase and may alter NO production during pathological conditions. Concerning Alzheimer's disease (AD), there are reports on altered cerebral NO metabolism, but only few studies on ADMA concentrations in plasma and cerebrospinal fluid (CSF). METHODS: We assessed plasma ADMA in 80 AD patients and 80 age- and gender-matched controls and CSF ADMA in a subgroup of 53 AD patients and 20 controls. RESULTS: ADMA plasma concentrations were increased, while CSF ADMA concentrations were decreased in AD patients. There was a significant association between decreasing CSF ADMA levels and the severity of cognitive impairment. CONCLUSION: Elevated ADMA in plasma might be a contributing factor for AD through alterations of NO metabolism, for example decreased cerebral microperfusion, while decreased levels of CSF ADMA might lead to a cerebral increase of NO, peroxynitrite production and oxidative protein damage. Our study reveals different mechanisms of plasma and CSF ADMA regulation, both potentially contributing to AD pathology.

M3 - SCORING: Zeitschriftenaufsatz

VL - 26

SP - 58

EP - 64

JO - DEMENT GERIATR COGN

JF - DEMENT GERIATR COGN

SN - 1420-8008

IS - 1

M1 - 1

ER -