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Cerebrospinal fluid, serum and plasma protein oxidation in Alzheimer’s disease
Author(s) -
Korolainen M. A.,
Pirttilä T.
Publication year - 2009
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1111/j.1600-0404.2008.01057.x
Subject(s) - cerebrospinal fluid , protein carbonylation , nitrotyrosine , alzheimer's disease , oxidative stress , chemistry , pathogenesis , blood proteins , nitration , immunoassay , oxidative phosphorylation , medicine , endocrinology , pathology , immunology , antibody , disease , biochemistry , enzyme , nitric oxide synthase , oxidative damage , organic chemistry
Objectives – Many studies have shown differences in carbonylation and nitration of individual proteins in brain and body fluids of Alzheimer’s disease (AD) patients. Therefore, we wanted to examine whether total levels of these oxidative stress markers of proteins were altered in AD. Patients and methods – Total levels of carbonyls and nitrotyrosine in cerebrospinal fluid, serum and plasma were measured in 22 AD patients and 18 age‐matched controls using commercially available enzyme immunoassay kits. Results – Protein carbonylation in cerebrospinal fluid did not differ between AD patients and controls but was decreased in APOE ɛ4 carriers as compared with non‐carriers. Serum but not plasma levels of carbonyls tended to be decreased in AD patients as compared with aged controls. Nitrotyrosine concentrations did not differ between the groups. Surrogate cerebrospinal fluid markers for AD, beta‐amyloid (1–42) and tau, correlated with blood carbonyl and nitrotyrosine levels. Conclusions – According to these preliminary data, changes in oxidative metabolism related to the pathogenesis of AD cannot be detected as increased cerebrospinal fluid, serum or plasma protein carbonylation or nitration.