Enhanced levels of mitochondrial enzyme 17beta-hydroxysteroid dehydrogenase type 10 in patients with Alzheimer disease and multiple sclerosis
Language English Country England, Great Britain Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
19756307
DOI
10.1039/b904799a
Knihovny.cz E-resources
- MeSH
- 17-Hydroxysteroid Dehydrogenases cerebrospinal fluid metabolism MeSH
- Alzheimer Disease cerebrospinal fluid enzymology MeSH
- Amyloid beta-Peptides cerebrospinal fluid metabolism MeSH
- Biosensing Techniques MeSH
- Adult MeSH
- Enzyme-Linked Immunosorbent Assay MeSH
- Middle Aged MeSH
- Humans MeSH
- Mitochondria enzymology MeSH
- Multiple Sclerosis cerebrospinal fluid enzymology MeSH
- Aged MeSH
- Protein Binding MeSH
- Check Tag
- Adult MeSH
- Middle Aged MeSH
- Humans MeSH
- Male MeSH
- Aged MeSH
- Female MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- 17-Hydroxysteroid Dehydrogenases MeSH
- 3 (or 17)-beta-hydroxysteroid dehydrogenase MeSH Browser
- Amyloid beta-Peptides 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
References provided by Crossref.org
Interactions of 17β-Hydroxysteroid Dehydrogenase Type 10 and Cyclophilin D in Alzheimer's Disease
Protein τ-mediated effects on rat hippocampal choline transporters CHT1 and τ-amyloid β interactions