Evaluating Human Plasma Biomakers for Alzheimer's Disease; Phosphorylated-tau 217, Phosphorylated-tau 181, and Glial Fibrillary Acidic Protein

Alzheimer’s Disease (AD) is a progressive neurodegenerative disease that is primarily identifiable by amyloid-beta (Aβ) neuronal plaques, neurofibrillary tangles (NFT) that form as aggregates of hyperphosphorylated tau (ptau) proteins clump together, and the presence of neuroinflammation; all of which are otherwise known as the hallmarks of AD pathology. Recent emerging research has discovered striking similarities between AD and diabetes mellitus pathology, illustrating how insulin deficiency and insulin resistance–both of which result in the chronic hyperglycemic state seen in the diabetic–are involved in an increase in the phosphorylation of tau. This leads to and intensifies the formation of intracellular NFTs serving to disrupt microtubule assembly and the intracellular trafficking of proteins. The focus of this study surrounds the analysis of ptau-217, a blood biomarker that has been found in our previous research to be indicative of progressing cognitive decline. The data has been collected using diagnostic tools such as the Lumipulse G1200, positron emission tomography (PET), and magnetic resonance imaging (MRI). Ptau-217 protein concentrations were monitored between disease states of AD in order to gain insight into the causality of brain amyloid status and were then compared to levels observed in diabetic subjects. The trends analyzed through this methodology were obtained with the intention of bridging the gap between what is known of AD and diabetes mellitus pathology as well as to further strengthen our understanding in the role the promising blood biomarker ptau-217 has in these varying disease states.