Dimethylarginines, homocysteine metabolism, and cerebrospinal fluid markers for Alzheimer's disease.
Details
Request a copy Under indefinite embargo.
UNIL restricted access
State: Public
Version: author
UNIL restricted access
State: Public
Version: author
Serval ID
serval:BIB_F82C79E379FF
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Dimethylarginines, homocysteine metabolism, and cerebrospinal fluid markers for Alzheimer's disease.
Journal
Journal of Alzheimer's Disease : Jad
ISSN
1875-8908 (Electronic)
ISSN-L
1387-2877
Publication state
Published
Issued date
2012
Peer-reviewed
Oui
Volume
31
Number
4
Pages
751-758
Language
english
Notes
Publication types: Journal ArticlePublication Status: ppublish
Abstract
Dimethylarginine and homocysteine metabolism are closely linked and alterations of both were observed in plasma and cerebrospinal fluid (CSF) of patients with Alzheimer's disease (AD). CSF parameters of homocysteine metabolism have recently been found to be associated with the CSF level of the AD biomarker phosphorylated tau (ptau) in AD patients. To investigate possible relationships between homocysteine and dimethylarginine metabolism and the AD CSF biomarkers ptau181 and amyloid-β 1-42 (Aβ42), we assessed parameters of homocysteine metabolism (CSF homocysteine, S-adenosylmethionine (SAM), S-adenosylhomocysteine (SAH), 5-methyltetrahydrofolate (5-MTHF)) and dimethylarginine metabolism (plasma and CSF asymmetric dimethylarginine (ADMA), symmetric dimethylarginine, L-arginine) as well as CSF Aβ42 and ptau181 in 98 controls and 51 AD patients. Multivariate linear regression analyses were performed to assess associations between the considered parameters. SAH concentrations show significant associations to CSF ADMA levels, and CSF ADMA and L-arginine to ptau181, but not to Aβ42 concentrations in AD patients. When including concentrations of homocysteine, 5-MTHF, SAM, and SAH into the analysis, CSF ADMA concentrations independently predicted ptau181 levels in AD patients but homocysteine-related metabolites were associated with ptau181 only when ADMA was removed from the analysis model. These results suggest that CSF ADMA may interact with CNS homocysteine metabolism and may contribute to neurodegeneration and accumulation of phosphorylated tau in AD. Functional and interventional studies are needed to further proof this hypothesis.
Pubmed
Web of science
Create date
22/06/2012 15:21
Last modification date
20/08/2019 16:24