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Browse 5,093 clinical trials for multiple sclerosis. Find studies that match your criteria and connect with research centers.
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NCT06280742
The Service Hospitalier Frédéric-Joliot (SHFJ) and Paris Brain Institute (ICM) groups have identified \[18F\]-DPA-714 as a promising second-generation TSPO tracer, a macromolecule overexpressed in neuroinflammatory conditions, for PET imaging. They have also developed a non-invasive quantification methodology, enabling the generation of individual neuroinflammation maps in MS patients. Recent findings from \[18F\]-DPA-714 PET imaging in MS patients revealed that most of the white matter lesions contained a smoldering component, even when considered inactive on MRI, and that their neuroinflammatory profiles were associated with longitudinal disability worsening. The Inflanet project aims to leverage a unique consortium comprising French radiochemists, radiopharmacists, nuclear medicine/neuroimaging experts, and MS neurologists to establish the first national network dedicated to \[18F\]-DPA-714 PET imaging in MS, so far limited to monocentric studies. The objectives of the INFLANET project are (1) to conduct the first multicenter study assessing neuroinflammation in patients with active MS using \[18F\]DPA-714 PET tracer, and (2) to establish a methodology suitable for the quantification of multicenter PET data obtained with \[18F\]DPA-714. The INFLANET initiative aims to disseminate TSPO PET within the French MS research community, thereby opening the unique perspective of future large-scale, multicenter studies. These endeavors are expected to enhance our capacity to predict diseases, stratify patients, and assess new therapeutic interventions.
NCT00339287
Human phagocytic cells such as polymorphonuclear leukocytes (PMNs) are readily mobilized to sites of infection and ingest microorganisms by a process known as phagocytosis. The combined effects of reactive oxygen species (ROS) and proteolytic peptides and enzymes released into forming bacterial phagosomes kill most ingested bacteria. However, many human bacterial pathogens have devised means to subvert normal phagocyte responses and the innate immune response and cause severe disease. The overall objective of this study is to elucidate specific features of pathogen-phagocyte interactions that underlie evasion of the innate immune response or contribute to the pathophysiology of disease or inflammatory disorders. Therefore, specific projects will: 1. Identify and characterize specific mechanisms used by pathogenic microorganisms to evade or subvert normal phagocyte responses and therefore cause disease. 2. Investigate phagocyte response mechanisms to specific pathogenic microorganisms. 3. Identify specific bacterial structures and/or (gene) products that dictate differences in phagocyte responses among a range of pathogens so that generalized statements can be made about the pathophysiology of disease states. The studies will be performed using multiple techniques including state-of-the-art equipment for genomics and proteomics strategies to identify target bacterial genes/proteins of interest or those up-regulated in phagocytes. Phagocyte-pathogen interactions will be examined using fluorescence-based real-time assays and video microscopy, confocal and electron microscopy in combination with enzymatic assays for ROS production, routine biochemistry, immunology and cell biology. Implementing these studies will require isolation of phagocytic leukocytes from venous blood of healthy human volunteers. The study population will be all-inclusive except in certain instances where individuals possess genetic defects that impair phagocyte function (e.g., myeloperoxidase-deficiency) or have altered phagocyte function due to outside influences such as recent bacterial or viral infection. The proposed studies will likely provide new information pertinent to understanding host cell-pathogen interactions and the pathophysiology of inflammatory conditions.