Bruno Stankoff, MD, PhD, is professor of neurology at the University Pierre et Marie Curie (UPMC), Paris, France. He was trained in the fields of clinical neurology and neurobiology.
During his PhD (Inserm, Pitié-Salpêtrière), he investigated molecular and pharmacological mechanisms of myelin formation in the central nervous system (CNS), and identified several pathways of interest for putative remyelinating therapies. He further performed a post-doctoral fellowship in CEA (French government-funded technological research organization), where he initiated a molecular imaging project using positron emission tomography (PET) for the evaluation of remyelination in multiple sclerosis (MS).
Dr Stankoff was also assistant to the head of the clinical investigation center of Pitié- Salpêtrière for 2 years. Currently, Dr Stankoff is responsible for the MS center in Saint-Antoine Hospital in Paris, and is co-head of the research team entitled “Myelination and remyelination in the CNS: mechanisms, imaging and therapy” in the ICM (Institut du Cerveau et de la Moelle Epiniere, INSERM UMR1127). He drives several projects aimed at imaging remyelination, neurodegeneration, and microglial inflammation in MS.
PET with [18F] Flumazenil as an index of neurodegeneration in MS: Sensitivity at an
early disease stage and pathophysiological meaning
This study aims to develop and assess a new imaging biomarker that has the potential to be used as an index of neurodegeneration in multiple sclerosis (MS). Positron emission tomography (PET) and the isotypically radiofluorinated form of Flumazenil (FMZ), [18F]FMZ, will be used to assess neuronal damage at the early phase of either relapsing or primary progressive MS.
The study will investigate the pathophysiological correlates of this neuronal damage by combining PET with [18F]FMZ with magnetic resonance imaging (MRI) at 7T and 3T.
The main objective will be to quantify and map [18F]FMZ binding changes in the gray matter of patients with MS compared to healthy controls, both at the group and individual level. Secondary objectives will investigate the relationship between Flumazenil binding changes and cortical demyelinating lesions, cortical dendritic arborization, brain atrophy, brain connectivity, and clinical metrics.
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