Co-Localization of Alzheimer's Risk Factors and Immune System Initiator in Plasma HDL
Apolipoproteins play a role in neuroinflammation and the progression of Alzheimer's disease (AD). Apolipoprotein J (apoJ) regulates the terminal cascade of the complement immune response and the aggregation of proteins in AD patients. Another type of apolipoprotein, apolipoprotein E (apoE), functions in modulating the initiation of the complement cascade and is shown to have correlations with AD pathology as well. In both cases, the regulation of the complement cascade, in turn, regulates inflammatory response. Given apoE and apoJ are localized in similar areas of the brain in AD patients, this project aims to explore the relationship between apoJ with apoE and C1q, an activator of our immune response, within the plasma as an extension of the brain tissue studies. Here we show the co-localization of C1q and apoJ in the plasma HDL of AD patients. While the co-localization between apoE and C1q has been shown previously in the brain, C1q and apoJ has not been demonstrated before. This study can be used as the basis of exploring the interactions between apolipoproteins and the immune system, particularly with regulating neuroinflammation. This information can be used to improve medical treatments of AD through drug therapies that combat the excessive inflammation seen in AD pathology.