There is also a debate regarding the role of certain vitamins such as vitamin D and folic acid in the pathogenesis of AD. Clearly from all of this mounting evidence, multiple metabolic pathways may play a key role in AD��s progression. Recent studies of gene expression from brains of AD patients further point to the strong association between metabolic alterations and AD, already from the early stages of the disease. However, such gene expression analyses have been limited to transcriptional alterations and therefore cannot encompass the effects of putative post-transcriptional modifications that are known to play an important role in metabolism. Furthermore, they do not allow the identification of biomarkers and drug targets in any direct manner. Our aim here is to go beyond these gene expression results and to elucidate the metabolic changes in AD by employing the increasingly prevalent toolkit of Cyclopentyl Chloroformate analysis methods provided by the emerging field of Genome-Scale Metabolic Modeling. GSMMs have become trusted tools in the study of metabolic networks, and provide a platform for interpreting omics data in a biochemically meaningful manner. GSMM analysis mostly relies on constraint-based modeling, in which constraints are systematically imposed on the GSMM solution space, and the outcomes of the model are limited to physically realizable phenotypes. GSMMs have been extensively used for the study of metabolism in microorganisms and in humans both in health and disease, enabling the prediction of various metabolic phenotypes such as enzyme activities and metabolite uptake and secretion fluxes, as well as interpretation of various types of high throughput data, often yielding clinically relevant results. In a recent GSMM paper studying brain metabolism, three different neuronal sub-types were reconstructed in a GSMM of brain energy metabolism. Focused on the core of cerebral energy metabolism, this reconstruction has suggested that glutamate Cloxiquine decarboxylase provides a neuroprotective effect which is correlated with the brain regional specificity of AD.