Roberta Brambilla, Ph.D.
Assistant Professor, Department of Neurological Surgery
Modulation of the immune response in neurologic disease
For over 10 years the main focus of my research has been understanding the role of neuroinflammation in the pathophysiology of neurodegenerative disorders (e.g., multiple sclerosis, spinal cord injury, neuropathic pain), with a specific interest in the contribution of glial cells. I have been pursuing these investigations using both in vitro and in vivo models. In collaboration with Dr. John Bethea, I participated in developing and characterizing a novel transgenic mouse (GFAP-IkBa-dominant negative mice) where the transcription factor NF-kB, a master regulator of inflammation, is inactivated specifically in astrocytes. With this model we produced the first in vivo evidence that selective inhibition of the astrocyte-driven inflammatory response leads to significant functional recovery after spinal cord injury, experimental autoimmune encephalomyelitis (a model of multiples sclerosis), and neuropathic pain.
Currently, my lab is focused on two specific areas of interest:
1) Investigating the role of tumor necrosis factor (TNF), both membrane-bound and soluble forms, in the processes of neuroinflammation, demyelination and remyelination in experimental autoimmune encephalomyelitis and spinal cord injury. We are especially interested in TNF signaling via TNFR2, the receptor that has been associated with neuroprotective and anti-inflammatory properties in the central nervous system. We have been studying TNFR2 function in vivo using pharmacological and genetic approaches, including cell-specific TNFR2 conditional knockout mice with ablation of TNFR2 in various central nervous system ad immune-cell populations that we developed in the lab.
2) Investigating whether mitochondrial dysfunction in oligodendrocytes plays a role in the pathophysiology of multiple sclerosis. Despite the general consensus on the autoimmune component of multiple sclerosis, its etiology remains unknown. Our hypothesis is that, at least in some forms of multiple sclerosis, a primary dysfunction of the central nervous system is the initial trigger of the disease, then followed by the destructive autoimmune response. Using a mouse model generated in our lab where we can induce timed mitochondrial DNA deletions specifically in myelinating oligodendrocytes to study whether primary oligodendropathy may represent the insult initiating the cascade of pathological events in MS.
Roberta Brambilla, Ph.D.
- The Miami Project to Cure Paralysis
1095 NW 14th Terrace (R-48)
Miami, FL 33136
- (305) 243-7131
- (305) 243-3914
International Society for Neuroimmunology
Society for Neuroscience
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