Susanna Rosi, PhD

A B C D E F G H I J K L M N O P Q R S T U V W X Y Z
Susanna Rosi, PhD

Associate Professor, Director of Neurocognitive Research, Brain and Spinal Injury Center, BASIC

Susanna.Rosi@ucsf.edu

Phone: (415) 206-3708

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Cancer Center Membership

Program Member » Neurologic Oncology

Research Summary

My laboratory is located in the Brain and Spinal Injury Center (BASIC) at UCSF, and our research is focused on understanding how innate immune system activation and macrophages polarization affect information processing and cognition from a cellular and network perspective by using different animal models of brain injury. To examine the above effects, my laboratory employs three principle animal models: traumatic brain injury, therapeutic cranial γ-irradiation, and ionizing space radiation. Our ultimate goal is to understand the mechanisms responsible for the cognitive dysfunction observed after brain injury to identify diagnostic tools for treatment and prevention. Our published results demonstrate that neuroinflammation alters the coupling of neuronal activity with the transcription of genes that are implicated in long-term memory and synaptic plasticity (Rosi et al., Journal of Neuroscience, 2005). By modulating different aspects of neuroinflammation we reported that it is possible to restore synaptic plasticity and cognitive functions in different animal models of chronic neuroinflammatory conditions (Rosi et al., Brain 2009; Belarbi et al., Journal of Neuroinflammation, 2012; Twediee et al.; Journal of Neuroinflammation, 2012; Belarbi et al., Journal of Neuroinflammation, 2012; Belarbi et al., Cancer Research, 2013). More recently, we reported that peripheral monocytes infiltrate the brain after traumatic brain injury and drive the inflammatory response to TBI. Most importantly, targeting monocytes infiltration it is possible to modify macrophages polarization and prevent long-term loss of synaptic and cognitive function after injury (Morganti et al., Journal of Neuroscience, 2015).

Education

University of Florence, Italy, B.S., 06/1995, Science
University of Florence, Italy, Ph.D., 06/2000, Biological Sciences
University of Florence, Italy, Postdoctoral, 2000-2001, Pharmacology
University of Arizona, Tucson, Arizona, Postdoctoral Research Associate , 2002-2006, Psychology
 


Professional Experience

  • 2000-2001
    Postdoctoral Fellow, University of Florence, Italy
  • 2002-2006
    Postdoctoral Research Associate, University of Arizona, Tucson, AZ
  • 2006-2011
    Assistant Professor, Departments of Physical Therapy Rehabilitation Science and Neurological Surgery, University of California, San Francisco, San Francisco, CA
  • 2011-present
    Associate Professor (1 year Accelerated), Departments of Physical Therapy Rehabilitation Science and Neurological Surgery, University of California, San Francisco, San Francisco.
  • 2011-present
    Director of Neurocognitive Research, Brain and Spinal Injury Center, University of California, San Francisco, San Francisco, CA

Honors & Awards

  • 1996-2000
    Graduate Fellowship, University of Florence, Italy

  • 2000
    Graduated with Distinction, University of Florence, Italy

  • 2001
    Postdoctoral Fellowship Award, Department of Pharmacology, University of Florence, Italy

  • 2004
    Travel Award, Winter Conference on Brain Research

  • 2006
    Special Award for Research and Career, “Vel l’Etrusco”, Castiglion Fiorentino, Arezzo, Italy

  • 2007
    UCSF, Academic Senate Committee on Research - Individual Investigator Award: seed funding

  • 2007
    UCSF, Research Evaluation and Allocation Committee Award: seed funding

  • 2007
    Tuscany Special Award “Young Talents and Magnificent Excellences”, Arezzo, Italy

  • 2008
    New Investigator Research Grant, Alzheimer’s Association

  • 2012
    UCSF, Department of Radiology and Biomedical Imaging, Seed Grant

Selected Publications

  1. Effects of Proton and Combined Proton and (56)Fe Radiation on the Hippocampus. Radiat Res. 2016 Jan; 185(1):20-30.
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  2. CCR2 Antagonism Alters Brain Macrophage Polarization and Ameliorates Cognitive Dysfunction Induced by Traumatic Brain Injury. J Neurosci. 2015 Jan 14; 35(2):748-60.
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  3. Targeted overexpression of mitochondrial catalase prevents radiation-induced cognitive dysfunction. Antioxid Redox Signal. 2015 Jan 1; 22(1):78-91.
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  4. Delayed administration of alpha-difluoromethylornithine prevents hippocampus-dependent cognitive impairment after single and combined injury in mice. Radiat Res. 2014 Nov; 182(5):489-98.
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  5. Human neural stem cell transplantation provides long-term restoration of neuronal plasticity in the irradiated hippocampus. Cell Transplant. 2015; 24(4):691-702.
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  6. Cranial irradiation alters the brain's microenvironment and permits CCR2+ macrophage infiltration. PLoS One. 2014; 9(4):e93650.
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  7. (28)Silicon radiation-induced enhancement of synaptic plasticity in the hippocampus of naïve and cognitively tested mice. Radiat Res. 2014 Apr; 181(4):362-8.
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  8. Radiation exposure prior to traumatic brain injury induces responses that differ as a function of animal age. Int J Radiat Biol. 2014 Mar; 90(3):214-23.
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  9. Modulation of adult-born neurons in the inflamed hippocampus. Front Cell Neurosci. 2013; 7:145.
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  10. Effects of radiation combined injury on hippocampal function are modulated in mice deficient in chemokine receptor 2 (CCR2). Radiat Res. 2013 Jul; 180(1):78-88.
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  11. Effects of (56)Fe radiation on hippocampal function in mice deficient in chemokine receptor 2 (CCR2). Behav Brain Res. 2013 Jun 1; 246:69-75.
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  12. Effects of whole body (56)Fe radiation on contextual freezing and Arc-positive cells in the dentate gyrus. Behav Brain Res. 2013 Jun 1; 246:162-7.
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  13. Sustained transcription of the immediate early gene Arc in the dentate gyrus after spatial exploration. J Neurosci. 2013 Jan 23; 33(4):1631-9.
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  14. CCR2 deficiency prevents neuronal dysfunction and cognitive impairments induced by cranial irradiation. Cancer Res. 2013 Feb 1; 73(3):1201-10.
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  15. Cranial irradiation alters dendritic spine density and morphology in the hippocampus. PLoS One. 2012; 7(7):e40844.
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  16. Tumor necrosis factor-a synthesis inhibitor 3,6'-dithiothalidomide attenuates markers of inflammation, Alzheimer pathology and behavioral deficits in animal models of neuroinflammation and Alzheimer's disease. J Neuroinflammation. 2012; 9:106.
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  17. The polyamine inhibitor alpha-difluoromethylornithine modulates hippocampus-dependent function after single and combined injuries. PLoS One. 2012; 7(1):e31094.
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  18. TNF-a protein synthesis inhibitor restores neuronal function and reverses cognitive deficits induced by chronic neuroinflammation. J Neuroinflammation. 2012; 9:23.
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  19. Effects of 56Fe-particle cranial radiation on hippocampus-dependent cognition depend on the salience of the environmental stimuli. Radiat Res. 2011 Oct; 176(4):521-6.
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  20. Chronic neuroinflammation impacts the recruitment of adult-born neurons into behaviorally relevant hippocampal networks. Brain Behav Immun. 2012 Jan; 26(1):18-23.
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