Serum chemical elements and oxidative status in Alzheimer's disease, Parkinson disease and multiple sclerosis

The role of some chemical elements in neurodegeneration was suggested by various authors. To obtain a profile of chemical elements and oxidative status in complex neurological diseases, an unbiased “omics” approach, i.e., quantification of 26 elements and oxidative stress parameters (serum oxidative...

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Published inNeurotoxicology (Park Forest South) Vol. 28; no. 3; pp. 450 - 456
Main Authors Alimonti, Alessandro, Ristori, Giovanni, Giubilei, Franco, Stazi, Maria Antonia, Pino, Anna, Visconti, Andrea, Brescianini, Sonia, Monti, Micaela Sepe, Forte, Giovanni, Stanzione, Paolo, Bocca, Beatrice, Bomboi, Giuseppe, D’Ippolito, Cristina, Annibali, Viviana, Salvetti, Marco, Sancesario, Giuseppe
Format Journal Article
LanguageEnglish
Published Orlando, FL Elsevier B.V 01.05.2007
Elsevier
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Summary:The role of some chemical elements in neurodegeneration was suggested by various authors. To obtain a profile of chemical elements and oxidative status in complex neurological diseases, an unbiased “omics” approach, i.e., quantification of 26 elements and oxidative stress parameters (serum oxidative status (SOS) and serum anti-oxidant capacity (SAC)), combined with multivariate statistical procedures (forward discriminant analysis, FDA) to analyse the vast amount of data, was applied to four groups of subjects (53 patients with Alzheimer's disease (AD), 71 with Parkinson disease (PD), 60 with multiple sclerosis (MS) and 124 healthy individuals). Descriptive statistics revealed numerous differences between each disease and healthy status. A concordant imbalance (reduction in Fe, Zn and SAC, and increase in SOS) was shared by AD, PD and MS. The FDA yielded three significant discriminant functions based on age, SOS, Ca, Fe, Si, Sn, V, Zn and Zr, and identified disease-specific profiles of element imbalances, thus showing the appropriateness of the “omics” approach. It may help assess the contribution of chemical elements and oxidative stress to disease causation and may provide complex predictors of disease evolution or treatment response.
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ISSN:0161-813X
1872-9711
DOI:10.1016/j.neuro.2006.12.001