Research Update #2

I spent third week of June developing a baseline PLAS model of inflammation in PD for the systems. All the reactions in the cell model were tagged before writing flux equations and systems equations. After sorting out all the species into dependent and independent variables, I started to write flux equations and systems equations for each reaction. There were some minor changes in the cell model.

I also added a model to the cell model describing the role of modulation of brain hemichannels and gap junction channels by pro-inflammatory agents in Parkinson’s disease. Dysfunctional gap junction channels and activated hemichannels by cytokines released from microglia are known to induce apoptosis of dopaminergic neurons. Dysfunctional gap junction prevents normal functioninig of buffering of neurotoxic substrates in astrocytes which seems to be associated with neuronal death.

I hope to finish writing the baseline PLAS model and start developing a model of diseased state next week.