Professor, Department of Neurosurgery
Dr. Elkabes graduated from Bogazici University in Istanbul, Turkey with a Bachelor of Science degree in Chemistry. She received her M.S. and Ph.D. degrees in Neuroendocrinology from the Weizmann Institute of Science in Rehovot, Israel where she was awarded the Feinberg Graduate School Award for Excellence. Dr. Elkabes pursued her post-doctoral training in neurobiology at the National Institute of Health and Cornell University Medical College. She was a visiting scientist in the Department of Pharmacology, University of Milan, Italy. She held a faculty appointment in the Department of Neuroscience and Cell Biology, Robert W. Johnson Medical School, University of Medicine and Dentistry of New Jersey, before joining the faculty at New Jersey Medical School, Rutgers.
Dr. Elkabes’ research focuses on innate immunity in the central nervous system, neuro-immune interactions, the crosstalk between neurons and glia and mechanisms underlying neuronal and axonal protection, neural regeneration, and neuropathic pain in animal models of spinal cord injury and multiple sclerosis. Her research has been funded by various agencies including the National Institute of Health and New Jersey Commission on Spinal Cord Research. Dr. Elkabes has been a reviewer in NIH study sections since 2008. She has served as a reviewer in national and international funding agencies including The Israel Science Foundation; The Marsden Fund Council, New Zealand; The Medical Research Council, United Kingdom, and The Department of Defense. Dr. Elkabes has served as an ad hoc reviewer in numerous scientific journals.
Dr. Elkabes is a full member of the School of Graduate Studies (SGS) at Rutgers. She received the Golden Axon Award for excellence in neuroscience teaching at NJMS. She has served as an acting co-director, executive committee member, admission committee member, and incoming student advisor of the Integrative Neuroscience Graduate Program, NJMS-Rutgers University joined the graduate program in Newark, NJ. She is currently a member of the Cell Biology, Neuroscience, and Physiology (CBNP) and Infection, Immunity and Inflammation (I3) tracks in the SGS at NJMS-Rutgers.
Research Interests:
- Discovery of novel targets for therapeutic interventions in acute and chronic SCI and MS.
- Development of new therapeutic strategies to reduce neuropathic pain.
- Unraveling the role of innate immunity in the CNS.
- Role of toll-like receptors in CNS development, disorders and injury.
- Contribution of neuronal calcium pumps to neuroprotection and neurodegeneration.
- Axonal protection and regeneration.
- Astrocyte function in injury and disease.
Publication Highlights:
- Acioglu C, Elkabes S (2025) Innate immune sensors and regulators at the blood brain barrier: focus on toll-like receptors and inflammasomes as mediators of neuro-immune crosstalk and inflammation. Neuroinflammation, 22:39 DOI: 10.1186/s12974-025-03360-3
- Acioglu C, Elkabes S (2024) Immune Sensors, Regulators, and Effectors of Brain Health. In: Gendelman, H.E., Ikezu, T. (eds) Neuroimmune Pharmacology and Therapeutics. Springer, Cham. https://doi.org/10.1007/978-3-031-68237-7_3
- Acioglu C, Heary RF, Elkabes S (2022) Roles of neuronal toll-like receptors in neuropathic pain and central nervous system injuries and diseases. Brain Behav. Immun. 102:163-178. DOI: 10.1016/j.bbi.2022.02.016
- Li L, Acioglu C, Heary RF, Elkabes S (2021) Role of astroglial toll-like receptors (TLRs) in central nervous system infections, injury and neurodegenerative diseases. Brain Behav. Immun. 91:740-755. DOI: 10.1016/j.bbi.2020.10.007
- Li L, Ni L, Heary RF, Elkabes S. (2020) Astroglial TLR9 antagonism promotes chemotaxis and alternative activation of macrophages via modulation of astrocyte-derived signals: implications for spinal cord injury. J Neuroinflammation. 17:73. DOI: 10.1186/s12974-020-01748-x
- Li L, Ni L, Eugenin EA, Heary RF, Elkabes S (2019) Toll-like Receptor 9 Antagonism Modulates Astrocyte Function and Preserves Proximal Axons following Spinal Cord Injury. Brain Behav Immun. 80:328-343. DOI: 10.1016/j.bbi.2019.04.010
- Mirabelli E, Ni L, Li L, Acioglu C, Heary RF, Elkabes S (2019) Pathological pain processing in mouse models of multiple sclerosis and spinal cord injury: contribution of plasma membrane calcium ATPase 2 (PMCA2). J Neuroinflammation. 16:207. DOI: 10.1186/s12974-019-1585-2
Complete list of published work: http://www.ncbi.nlm.nih.gov/pubmed/?term=Elkabes+S
Related Projects:
Spinal Cord Injury
Our research focuses on the contribution of innate immunity to spinal cord injury. More specifically, our studies investigate the contribution of toll-like receptors (TLRs) to functional outcomes and secondary injury following spinal cord trauma. The investigations utilize mouse models of spinal cord contusion injury, genetically modified mice, spinal cord neuronal and glial cultures and co-cultures, molecular and cellular approaches and behavioral assays to study neuroimmune interactions, the crosstalk between neurons and glia, mechanisms of neuronal protection and degeneration, axonal protection, functional recovery and alleviation of co-morbidities including neuropathic pain.
Projects include:
- Effects of TLR9 agonists and antagonists on functional recovery following SCI.
- TLR9 as a therapeutic target to prevent neuropathic pain associated with SCI.
- The modulation of astrocyte function by TLR9 at the glial scar and in vitro.
- The role of TLR9 in astrocyte-macrophage interactions.
- The contribution of TLR9 to the polarization of macrophages into beneficial or detrimental phenotypes in the injured spinal cord.
- Role of neuronal TLR9 in cell survival and astrocyte-neuron interactions.
Multiple Sclerosis
The goal of our investigations is to delineate the molecular mechanisms underlying neuronal dysfunction and axonal damage in experimental autoimmune encephalomyelitis (EAE), a well-established animal model that mimics features of multiple sclerosis. The contribution of neuroinflammation to neuronal /axonal damage is also studied.
The investigations address:
- the role of plasma membrane calcium ATPase 2 (PMCA2), a neuronal calcium pump, in neuronal dysfunction and death in EAE.
- the identification of the inflammatory signals that modulate PMCA2 expression and function in EAE and in vitro.
- the contribution of astrocytes and microglia to the modulation of PMCA2-mediated neuronal dysfunction and death.
- the involvement of PMCA2 in mechanisms underlying neuropathic pain in EAE.