A mathematical model of redox/methylation metabolism in human neuronal cells
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- Tez No: 401055
- Danışmanlar: PROF. MIKHAIL MALIOUTOV, PROF. RICHARD DETH
- Tez Türü: Doktora
- Konular: Matematik, Mathematics
- Anahtar Kelimeler: Belirtilmemiş.
- Yıl: 2013
- Dil: İngilizce
- Üniversite: Northwestern University
- Enstitü: Yurtdışı Enstitü
- Ana Bilim Dalı: Belirtilmemiş.
- Bilim Dalı: Belirtilmemiş.
- Sayfa Sayısı: 119
Özet
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Özet (Çeviri)
It is vital for cells to control their state of reduction and oxidation (redox), and the metabolic pathways providing this crucial function intersect with pathways control- ling hundreds of methylation reactions. It has been hypothesized that abnormal redox and methylation status contributes to a number of brain disorders, including autism or Alzheimers disease (AD) [8, 30]. Following in the footsteps of Reed et al.[35], who created a mathematical model of these pathways in liver cells, I built a mathematical model of redox and methylation metabolism for human neuronal cells, in order to explore the pre- dictions of this hypothesis and to see if further insights can be gained based on this model. While redox and methylation metabolism exists in all human cells, in many regards the brain compartment provides a unique environment for its many aspects of regulation. Among other ndings, simulations with this neuronal model support the hypothesis that inhibition of selenoenzymes by mercury can alter the redox status of the cell to a signi cant extent, which can ultimately contribute to autism or AD, depending on age. In addition, inhibition of these enzymes could be essentially irreversible, in the sense that, no other treatment could restore the levels of key metabolites back to normal homeostatic levels. We further use the model to explore the behavior of neuronal cells under di erent metabolic circumstances.
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