Autor: |
Broderick, Patricia A., Rahni, David N., Kolodny, Edwin H., Volicer, Ladislav, Wrona, Monika Z., Matson, Wayne, Dryhurst, Glenn |
Zdroj: |
Bioimaging in Neurodegeneration; 2005, p85-93, 9p |
Abstrakt: |
Excessive generation of reactive oxygen species and reactive nitrogen species in the Alzheimer's disease (AD) brain and the presence of serotonin in the brain regions that are damaged in this disorder may lead to oxidation of serotonin to tryptamine-4,5-dione, which may possess neurotoxic properties. Efforts to detect this dione in brain tissue or cerebrospinal fluid of AD patients have been so far unsuccessful. However, it may be of relevance that the expression of NAD(P)H:quinone oxidoreductase 1 (NQO1), an enzyme that acts to protect against oxidative stress caused by xenobiotic quinones, is localized not only to neurofibrillary tangles in the AD brain but also to the cytoplasm of hippocampal neurons. In contrast, very little NQO1 is present in the same neuronal populations in age-matched controls. The expression of NQO1 in the AD brain not only provides additional support for excessive production of oxygen free radicals but also, possibly, for a role of a quinone such as tryptamine-4,5-dione. [ABSTRACT FROM AUTHOR] |
Databáze: |
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