Meet The Hopp Lab
Microglia in Alzheimer's disease and other brain disorders
Microglia are the resident immune cells of the brain. Normally microglia support neurons and perform homeostatic functions in the central nervous system. However, during Alzheimer’s disease, microglia get overwhelmed, fail to perform their normal functions, and can promote a neurotoxicity. Microglia are also dysfunctional in many disorders. The goal of the Hopp Lab is to understand why microglia get overwhelmed and how to reverse their dysfunction during Alzheimer’s disease and other disorders. We use cell culture and mouse models to approach these problems.
Hopp Lab Team
The Hopp Lab is committed to STEM education and is excited to mentor trainees at all levels in the lab. Dr. Hopp is affiliated with UT Health San Antonio's Integrated Biomedical Sciences Ph.D. program's subdisciplines in Neuroscience, Physiology & Pharmacology, and Biology of Aging as well as the South Texas Medical Scientist Training Program and Research Connect for UTHSA MD students. Undergraduate students should feel free to reach out to Dr. Hopp for current openings in the lab or apply to the UT Health SURF or SPUR programs. Postdoctoral applicants should also contact Dr. Hopp directly for potential openings.
Associate Professor
Department of Pharmacology
Biggs Institute
Dr. Sarah Hopp, PhD
Sarah received her S.B. in Brain and Cognitive Sciences from MIT where they conducted undergraduate research at the Whitehead Institute and Novartis and post-bac research at EnVivo Pharmaceuticals. Sarah obtained a Ph.D. in Neuroscience from the Ohio State University under the mentorship of Dr. Gary Wenk and completed a postdoctoral fellowship in the lab of Dr. Brad Hyman at Massachusetts General Hospital / Harvard Medical School. In September of 2018 the Hopp Lab opened at the University of Texas Health Science Center at San Antonio. Dr. Hopp was promoted to Associate Professor with Tenure in 2025.
Outside of the lab, Sarah is a dedicated cat parent and also enjoys pottery, hiking, camping, and other outdoor activities.
Lab Manager
Sabrina Smith
Sabrina grew up in San Antonio, TX and received a B.S in Biology and B.A in Anthropology from the University of Texas San Antonio. Sabrina has worked for UT Health for 14+ years doing various forms of research. Outside of the lab, she enjoys outdoor activities and reading.
PhD Candidate in Neuroscience
Co-Mentored by Dr. Juan Pablo Palavicini
Eduardo Gutierrez Kuri
Eduardo is working on understanding the role of PLCG2 in microglia and other immune cells in the Hopp and Palavicini labs.
Postdoctoral Research Fellow
Dr. Celso Santos Gonçalves Catumbela, PhD
Celso is working on understanding how L-type calcium channel blocking drugs like amlodipine might protect the brain from Alzheimer's disease. He is also studying how sex and brain region alter microglia uptake of misfolded tau.
Postdoctoral Research Fellow
Dr. Lubov Ezerskiy, PhD
Luba is working on understanding the role of L-type calcium channels on astrocyte functions as they relate to tau pathobiology.
PhD Student in Biology of Aging
Brinda Palliyana
Brinda is working on understanding how Cav1.2 and Cav1.3 L-type calcium channels regulate microglia function.
MD/MS student in Clinical Investigation & Translational Science
Rachael Cundey
Rachael is working on understanding how knocking out Cav1.2 and Cav1.3 L-type calcium channels on microglia alter brain and behavior.
Lab Alumnus
PhD in Neuroscience,2024
Dr Kristian Falkon, PhD
Dissertation title: Endo/lysosomal Uptake and Degradation of Protein Aggregates in Tauopathy
Current position: Postdoctoral researcher at Johnson and Johnson
Lab Alumnus
PhD in Biology of Aging, 2025
Co-mentored by Dr. Kevin Bieniek
Dr. Caitlyn Fastenau, PhD
Dissertation title: The Dynamic Role of Sialylation on Microglia Activity in Alzheimer’s Disease.
Current position: Postdoctoral research fellow at the Buck Institute.
Lab Alumnus
PhD in Physiology and Pharmacology, 2023
Dr. Jessica Wickline, PhD
Dissertation title: Cav1.2 L-Type Calcium Channel Regulation of Microglia and Dystrophic Neurites in the Context of Alzheimer’s Disease
Current position: Faculty at University of Iowa
Lab Projects
What we're currently working on
Cav1 calcium channels in Alzheimer's disease and other brain disorders
Chronic neuroinflammation induces calcium dysregulation via a variety of mechanisms which is thought to contribute to memory deficits and neurotoxicity. Our work so far has found that this dysregulation is reversible by chronic treatment with L-type calcium channel blockers which can also reverse memory deficits, reduce microglia activation, and alter amyloid pathology. However, it is unclear what cells these drugs targeting.
We are currently investigating L-type calcium channels, specifically Cav1.2 and Cav1.3, and their role in calcium dysregulation during Alzheimer's disease and other brain disorders using genetic and pharmacological manipulation.
Microglia interaction with tau pathology
Microglia are found near tau tangle-bearing neurons in Alzheimer’s disease brains. It has long been assumed that microglia associate with these pathological aggregates to facilitate clearance of these deposits, although since the lesions persist there is clearly a failure in this process. Our work so far has found that microglia from tangle-bearing mouse and human brains contain tau aggregates and these aggregates are capable of inducing tau misfolding in recipient cells. Furthermore, microglia can engulf tau but only partially reduce its ability to transmit aggregates. Overall this work demonstrates a dual role for microglia in tau pathology: one of beneficial clearance and another of contribution to pathology.
Our work currently aims to determine the mechanism by which microglia uptake tau and to identify what mechanism is dysfunctional in microglia degradation of tau to identify manipulations that can improve microglia-mediated tau degradation.
Microglial sialylation in aging and Alzheimer's disease
Terminal sialic acid carbohydrate groups on glycosylated aggregate-associated and microglia-associated proteins and lipids also can regulate molecular machinery involved in recognition, degradation, and neurotoxicity of plaques, tangles, and other neurodegenerative protein aggregates.
Our preliminary data suggest that plaque-associated microglia display distinct enhancement of sialylation that has not been observed previously. We are currently working to characterize the localization and function of these sialic acid residues on microglia function in aging and Alzheimer's pathology.