Jose F. Abisambra (United States of America)
University of Florida
Department of Neuroscience
Dr. Abisambra is Associate Professor of Neuroscience in the CTRND, Vice-Chair of Strategic Operations in the Department of Neuroscience, Deputy Director of the BRAIN Injury Center, and Assistant Dean of Diversity & Health Equity at the University of Florida College of Medicine. The overarching goal of his research program is to investigate the molecular mechanisms linking tau and RNA translation with neurodegeneration. This focus creates the opportunity to investigate the integration of essential cellular functions for development, aging, and disease by targeting one protein. Tauopathies such as Alzheimer's disease, fronto-temporal dementia, and chronic traumatic encephalopathy are central to his research. Ultimately, this work can aid in the identification of biomarkers and therapeutic targets for more than 30 million people currently suffering from tauopathies worldwide.

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 Conference Calendar

REPETITIVE MILD TRAUMATIC BRAIN INJURY IMPAIRS RESTING STATE FMRI CONNECTIVITY AND ALTERS PROTEIN PROFILES IN SIGNALING NETWORKS

Session Name
4320 - SYMPOSIUM: THE VULNERABLE BRAIN AND DEGENERATIVE MECHANISMS IN AD, PD AND TRAUMATIC BRAIN INJURY (ID 116)
Session Type
SYMPOSIUM
Date
Sat, 01.04.2023
Session Time
08:40 - 10:40
Room
ONSITE - HALL F4+F5
Presenter
Lecture Time
09:40 - 09:55

Abstract

Aims

Repetitive mild traumatic brain injury (rmTBI) substantially increases risk for development of Alzheimer’s disease later in life. A major challenge in developing diagnostics and treatments for rmTBI before the onset of chronic neurodegenerative disorders, are the fundamental knowledge gaps that explain how they promote brain dysfunction. It is critical and urgent to understand the neuropathological and functional consequences of rmTBI to develop effective therapeutic strategies. In this study, we sought to define the extent of altered brain functional connectivity (FC) and levels of neuropathological markers after rmTBI.

Methods

We performed two impacts 24h apart in C57BL/6J (~2.5-3mo) mice using the closed head injury model of engineered rotational acceleration (CHIMERA). At 5-6 days post-injury (dpi), we measured changes in brain volume and FC using T2-weighted images, resting-state functional MRI (rsfMRI), and graph theory analyses; diffusion tensor imaging (DTI) assessed white matter integrity. At 7dpi, we measured levels of disease-associated protein markers in different brain regions using NanoString-GeoMx digital spatial protein profiling (DSP).

Results

The rsfMRI data revealed aberrant FC in areas that process somatosensory inputs; DTI revealed significant alterations in the optic tract and hippocampus. DSP showed significant changes in the levels of numerous proteins in distinct brain regions: phospho-tau species and glial proteins in the optic tract, the neuroinflammatory protein GPNMB and cell proliferation marker Ki-67 in the thalamus, and myelin basic protein in the somatosensory area.

Conclusions

Our data suggest that rmTBI alters brain connectivity and protein profiles in specific brain areas, thereby highlighting the underlying complexity of rmTBI mechanisms.

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