Previous Lab Members

Angela Gomez Arboledas Ph.D.
Postdoctoral Researcher
agomezar@uci.edu
In the Tenner lab, Angela studied the effect of C5a-C5aR1 signaling on excessive synaptic pruning mediated by microglial cells in a mouse model of Alzheimer’s disease. She also studie the effects 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. Angela is now a Project Scientist with Model AD.

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Undergraduate Research Assistant (2021-2023)

I was a Human Biology major at UCI. I am proud to be a first-generation student for my family, along with my older brother. Karina will be taking a gap year while applying to medical school.

I am a 1st generation college student majoring in Neurobiology. Some of my goals after graduating this Spring 2023 quarter is to take a gap year and study for the MCAT in hopes to apply and attend Medical School. I have aspirations in pursuing a career as a neurosurgeon and I am willing to dedicate and commit another 10 years of education and learning to achieve my dream career. Outside of academics, I love playing sports in particular basketball and volleyball. I also like listening to music, going for walks, playing video games, and assembling legos!

Using a combination of pharmacologic and genetic approaches, Nicole’s research focused on elucidating the role of C5a-C5aR1 signaling in the progression of Alzheimer’s disease to identify its neuroprotective mechanisms. Nicole identified that C5a-C5aR1 signaling in the Arctic AD mouse model results in enhancement of microglial activation pathways resulting in accelerated disease progression and that inhibition of C5a-C5aR1 signaling prevents enhanced microglial activation. Nicole is continuing her work in AD as a postdoctoral scholar at University of Arkansas for Medical Sciences.

Marisa Fonseca Ph.D.
Research Associate Specialist (2022)
Marisa studied the role of complement and inflammation in the pathogenesis of Alzheimer’s Disease (AD). Using a mouse model of AD that is deficient in complement C1q, she have demonstrated a detrimental effect of complement activation on the neuropathology of the disease. She also demonstrated cell specific deletion of C1q, that  microglia are the main source of C1q synthesis in mouse brain. Marisa also studied the role of C1q, C5a and other complement proteins in synapse pruning that is exacerbated in AD models and other neurodegenerative diseases.

Michael Hernandez Ph.D.
Graduate Student- Pathology and Laboratory Medicine (2017)
Michael investigated the role of distinct activation states of microglia in the progression of Alzheimer’s Disease in mouse models like Tg2576, 3XTg, and Arctic. He also investigated the influence of complement on microglial activation states in ageing murine brain and AD mouse models. Michael is currently a technical sales specialist at Thermo Fisher Scientific.

Elizabeth Clarke Ph.D.
Graduate Student- Mol. Bio. & Biochemistry (2014)
 Elizabeth studied the immuno-regulatory role of complement protein C1q on inflammatory signaling and gene expression during the phagocytosis and degradation of dying cells and how these C1q-mediated changes in macrophage polarization may modulate T-cell activation under these conditions. Since the C1q-polarized state appears similar to that in tumor associated macrophages (TAM), she also investigated the potential for reversal/inhibition of these pathways that may be useful in reprogramming TAM to provide more anti-tumor activity. Elizabeth is now a medical writer at Aroga Biosciences.

Marie Benoit Ph.D.
Postdoctoral Researcher (2012)
Marie investigated the role of C1q in the activation profile of phagocytic cells upon ingestion of apoptotic cells. She used whole genome microarray to study gene expression and thus identify molecular pathways and signaling cascade stimulated by C1q in monocytes, macrophages and dendritic cells. She also studied the role of complement and inflammation in the pathogenesis of Alzheimer’s Disease (AD). We showed that C1q enhances neuronal survival and prevents neuronal cell death induced by amyloid-beta, a pathologic peptide that accumulates in the brain during AD. She used microarray approach to identify the C1q neuroprotective pathways and investigating the role of C1q-modulated genes that are associated with survival in rat and mouse neurons. Marie is now associate director at PPD Laboratories.