Enhanced levels of mitochondrial enzyme 17beta-hydroxysteroid dehydrogenase type 10 in patients with Alzheimer disease and multiple sclerosis
Jazyk angličtina Země Anglie, Velká Británie Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
19756307
DOI
10.1039/b904799a
Knihovny.cz E-zdroje
- MeSH
- 17-hydroxysteroidní dehydrogenasy mozkomíšní mok metabolismus MeSH
- Alzheimerova nemoc mozkomíšní mok enzymologie MeSH
- amyloidní beta-protein mozkomíšní mok metabolismus MeSH
- biosenzitivní techniky MeSH
- dospělí MeSH
- ELISA MeSH
- lidé středního věku MeSH
- lidé MeSH
- mitochondrie enzymologie MeSH
- roztroušená skleróza mozkomíšní mok enzymologie MeSH
- senioři MeSH
- vazba proteinů MeSH
- Check Tag
- dospělí MeSH
- lidé středního věku MeSH
- lidé MeSH
- mužské pohlaví MeSH
- senioři MeSH
- ženské pohlaví MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- 17-hydroxysteroidní dehydrogenasy MeSH
- 3 (or 17)-beta-hydroxysteroid dehydrogenase MeSH Prohlížeč
- amyloidní beta-protein MeSH
The multifunctional mitochondrial enzyme 17beta-hydroxysteroid dehydrogenase type 10 might play a role in the development of Alzheimer disease via its high-affinity binding to amyloid beta peptides and its neuronal over-expression. It is suggested that the cerebrospinal fluid levels of the enzyme, free or bound to amyloid beta peptides, are a potential specific biomarker of Alzheimer disease. However, mitochondrial dysfunction seems to play a role in many neurological diseases including multiple sclerosis. In this study, the specificity of changes in relation to the enzyme over-expression was evaluated using enzyme-linked immunosorbent and surface plasmon resonance sensors. The data indicated pronounced increases in the enzyme levels, specifically to 179% in multiple sclerosis and to 573% in Alzheimer disease when compared to the age-matched controls. Although the differences between both diseases were statistically significant, enzyme levels do not appear to be a highly specific biomarker of Alzheimer disease. On the other hand, enhancement in levels of the enzyme bound to amyloid beta peptides was only observed in people with Alzheimer disease, which suggests that the complex should be further considered as a possible biomarker. In patients with multiple sclerosis, our results are the first to demonstrate significant changes in enzyme expression and to suggest possible alterations in amyloid beta peptides.
Alzheimer Disease Center Prague Psychiatric Centre Ustavní 91 181 03 Prague 8 Bohnice Czech Republic
Citace poskytuje Crossref.org
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