Jose F Abisambra,
Associate Professor Of Neuroscience And CTRND, Deputy Director BRAIN Center, Assistant Dean For Health Care Excellence, Community And Belonging
About Jose F Abisambra
Dr. Abisambra is an Associate Professor of Neuroscience and Assistant Dean of Diversity & Health Equity at the University of Florida College of Medicine. He received his PhD in Medical Sciences/Molecular Medicine in 2010 from the University of South Florida and went on to complete a Postdoctoral Fellowship (2010-2012) at his alma mater. The overarching goal of his research program is to investigate the molecular mechanisms linking tau and ER dysfunction with neurodegeneration. This focus creates an opportunity to investigate the integration of essential cellular functions for development, aging, and disease by targeting one organelle. Ultimately, this work can aid in the identification of therapeutic targets for more than 30 million people currently suffering from tauopathies worldwide.
Dr. Abisambra’s research pertains to investigating fundamental biological processes critical to neuronal function that converge with endoplasmic reticulum (ER) proteins. His lab’s currently supported projects focus on the impact of the Unfolded Protein Response on neurodegenerative processes in Alzheimer’s and related proteinopathies. His work explores protein synthesis (Meier et al., 2016), trafficking (mitochondria, Golgi apparatus, plasma membrane, etc.) (Jinwal et al., 2010), folding (Abisambra et al., 2012; Abisambra et al., 2013a), and clearance (proteasome and autophagy) (Abisambra et al., 2013b) as fundamental processes during brain development, aging, and stress. He further investigates the impact of the ER on calcium homeostasis and lipid/carbohydrate metabolism (Abisambra et al., 2010) in the context of whole neuronal function. Alterations to these processes are linked to the pathogenesis of 25 known neurodegenerative disorders that share a common pathological hallmark: intracellular aggregation of tau. These tauopathies include Alzheimer’s disease (AD), chronic traumatic encephalopathy/traumatic brain injury (CTE/TBI; reviewed in (Abisambra and Scheff, 2014), and fronto-temporal degeneration with tau inclusions (FTD-tau).