Erzsebet Maria Szatmari, PhD
The Szatmari laboratory at ECU studies early-onset synaptic alterations and dysfunction associated with Alzheimer disease (AD), using advanced imaging, cell biology, biochemistry and behavioral techniques, transgenic mice and mouse models of AD. We are particularly interested in identifying signaling pathways that provide resilience against AD or protect against disease progression.
Project 1 focuses on the small GTPase, Rab 10, as chronic reduction in the level and activity of this protein reduces the risk of AD development even in individuals that carry the ApoE epsilon allele. Using AD model mice (J20 and 5xFAD) on Rab10 +/- background, we attempt to identify the signaling pathways that underly Rab10-dependent resilience against AD.
Project 2 focuses on the role of a brain specific protein, called ADAP1 (Centaurin alpha-1) in development of AD. Our studies strongly suggest that ADAP1 is a negative regulator of synaptic plasticity and dendritic spine density and that reduction in ADAP1 level protects neurons from dendritic spine elimination by toxic amyloid. We are currently using mice KO for ADAP1 to dissect the role of ADAP1 in the brain and in age related brain disorders.
About Dr. Erzsebet Maria Szatmari
Dr. Szatmari started her research program at ECU in 2018 as an assistant professor in the Department of Physical Therapy, focusing on signaling pathways involved in early-onset Alzheimer’s disease. Prior to this appointment, she worked as a research scientist II at Max Planck Florida Institute for Neuroscience (2012-2018).
Dr. Szatmari’s early postgraduate training was in neuroprotection against excitotoxicity at the Kentucky Spinal Cord Injury Research Center (2003-2006), where she identified the role of GSK-3β in excitotoxicity and the neuroprotective role of the brain-specific scaffolding protein, called KSR-1. In 2007, Dr. Szatmari joined the laboratory of Dr. Ryohei Yasuda at Duke University Medical Center as a postdoctoral research associate. While at Duke University, Dr. Szatmari identified the role of the brain-specific protein, ADAP1 (Centaurin alpha-1) in synaptic dysfunction associated with early-stage Alzheimer’s disease. Her work at Duke University was supported by a Ruth K. Broad Award and an individual NRSA (F32) fellowship.
Dr. Szatmari received her PhD in Cell Biology from Babes-Bolyai University, Cluj, Romania and Biological Research Center, Szeged, Hungary in 2003 for her work on signaling mechanisms regulating permeability of the blood-brain barrier.
In her free time, Erzsebet Szatmari likes to read history and philosophy, spend time in kitchen cooking for her friends and family and explore the absolutely beautiful outdoors of eastern North Carolina.
Chang JY, Parra-Bueno P, Laviv T, Szatmari EM, Lee SR, Yasuda R (2017) CaMKII Autophosphorylation Is Necessary for Optimal Integration of Ca2+ Signals during LTP Induction, but Not Maintenance. Neuron 94:800-808 e804.
Murakoshi H, Shin ME, Parra-Bueno P, Szatmari EM, Shibata AC, Yasuda R (2017) Kinetics of Endogenous CaMKII Required for Synaptic Plasticity Revealed by Optogenetic Kinase Inhibitor. Neuron 94:37-47 e35.
Szatmari EM, Oliveira O, Johnson E, Yasuda R (2013) Centaurin-α1-Ras-Elk1 Signaling At Mitochondria Mediates β-Amyloid-Induced Synaptic Dysfunction. J Neurosci. 33(12):5367-74.
Patterson MA, Szatmari EM, Yasuda R (2010) AMPA receptors are exocytosed in stimulated spines and adjacent dendrites in a Ras-ERK-dependent manner during long-term potentiation. PNAS 107(36):15951-6
Lee SJ, Escobedo-Lozoya Y, Szatmari EM, Yasuda R (2009) Activation of CaMKII in single dendritic spines during long-term potentiation. Nature 458:299-304. (Evaluated by Faculty of 1000)
Vishwanath Vasudev Prabhu, PhD
Wyatt Bunner, MSc
Rachel Dodson, BSc
Graduate Research Assistant
Erzsebet Maria Szatmari, PhD
Department of Physical Therapy
College of Allied Health Sciences
Ross Hall 4254