Lab Members

Sophie Chu
Staff 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 maintenence 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. I am also interested in the bi-directional communication between the nervous system and peripheral 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. I am also exploring the effects of an antiviral response on the healthy, gaining, and AD brain and the role of the complement system in initiating, maintaining, and ending a cerebral immune response. Other studies focus on the role of the of the peripheral antiviral immune response to the progression of AD and the role of the complement system in modulating both peripheral and cerebral immune responses. 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. 
 
Angela Gomez Arboledas Ph.D.
Postdoctoral Researcher/ Model-AD Project Scientist 
agomezar@uci.edu
There is strong evidence that neuroinflammation and the complement system are key components in the development of Alzheimer’s disease (AD). This, together with the excessive synaptic loss that has been described during the pathogenesis of AD, made me focused on exploring the relationship between glial cells and complement system in this devastating disease. To this end, I am studying the effect of C5a-C5aR1 signaling on excessive synaptic pruning mediated by microglial cells in a mouse model of Alzheimer’s disease. In addition, I am also studying the effect of a C5aR1 antagonist not only in the pathogenesis of AD, but specifically, in the activation of astroglial and microglial cells, with the latest objective of trying to better understand the role of these glial cells in Alzheimer’s disease and identify therapeutic targets for the human disorder.