 Sophie ChuStaff Research Associate shuhuic@uci.edu I am investigating the role of complement activation and subsequent inflammation in Alzheimer’s Disease by using in vivo models, such as triple transgenic and Tg2576 mouse models. I utilize sectioning of brain tissues, immunostaining of sections, and data analysis to study the pathology of transgenic mice. Also I participate in animal husbandry, breeding, and mouse colony maintanence and genotype transgenic mice by PCR and QPCR for breeding. |
Tiffany Petrisko Ph.D.
Postdoctoral Researcher tiffany.petrisko@uci.edu My research interests focus on understanding the role of neural-immune communication in the development, progression, and exacerbation of neurological disorders. The complement system is not only a critical part of the innate immune system but is also required for proper neurodevelopment. However, aberrant activation of the complement system in neurological diseases, such as Alzheimer’s disease, can increase neuroinflammation and further promote disease pathology as well as excessive synaptic pruning, enhancing cognitive decline. Currently, my work in the Tenner lab aims at delineating the role of the complement initiator protein, C1q, to determine if it may exert protective effects in the early stages of Alzheimer’s disease. Additionally, I am also interested in the bi-directional communication between the brain and immune system. To this end, I also explore the effect of complement deletion on the microbiome, and if these changes in the microbiome may influence cognition. Additionally, I am examining the effect of complement inhibition or deletion on perineruonal nets (PNNs) in multiple AD mouse models to further refine both the role of complement in the nervous system, as well as the relationship between PNNs, microglia, neuroinflammation, and cognitive function. |