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Gianturco 113, 80143, Naples, Italy" } ], "person_or_org": { "family_name": "Salvatore", "given_name": "M", "name": "Salvatore, M", "type": "personal" } }, { "affiliations": [ { "name": "Institute of Biostructure and Bioimaging, National Research Council, Via T. De Amicis 95, 80145, Naples, Italy" } ], "person_or_org": { "family_name": "Pappat\u00e0", "given_name": "S", "name": "Pappat\u00e0, S", "type": "personal" } } ], "description": "
PURPOSE: To evaluate the feasibility and sensitivity of 18F-DPA-714 for the study of microglial activation in the brain and spinal cord of transgenic SOD1G93A mice using high-resolution PET/CT and to evaluate the Iba1 and TSPO expression with immunohistochemistry.
\n\nMETHODS: Nine symptomatic SOD1G93A mice (aged 117 ± 12.7 days, clinical score range 1 - 4) and five WT SOD1 control mice (aged 108 ± 28.5 days) underwent 18F-DPA-714 PET/CT. SUV ratios were calculated by normalizing the cerebellar (rCRB), brainstem (rBS), motor cortex (rMCX) and cervical spinal cord (rCSC) activities to that of the frontal association cortex. Two WT SOD1 and six symptomatic SOD1G93A mice were studied by immunohistochemistry.
\n\nRESULTS: In the symptomatic SOD1G93A mice, rCRB, rBS and rCSC were increased as compared to the values in WT SOD1 mice, with a statistically significantly difference in rBS (2.340 ± 0.784 vs 1.576 ± 0.287, p = 0.014). Immunofluorescence studies showed that TSPO expression was increased in the trigeminal, facial, ambiguus and hypoglossal nuclei, as well as in the spinal cord, of symptomatic SOD1G93A mice and was colocalized with increased Iba1 staining.
\n\nCONCLUSION: Increased 18F-DPA-714 uptake can be detected with high-resolution PET/CT in the brainstem of transgenic SOD1G93A mice, a region known to be a site of degeneration and increased microglial activation in amyotrophic lateral sclerosis, in agreement with increased TSPO expression in the brainstem nuclei shown by immunostaining. Therefore, 18F-DPA-714 PET/CT might be a suitable tool to evaluate microglial activation in the SOD1G93A mouse model.
", "funding": [ { "award": { "acronym": "INMIND", "id": "00k4n6c32::278850", "identifiers": [ { "identifier": "https://cordis.europa.eu/projects/278850", "scheme": "url" } ], "number": "278850", "program": "FP7", "title": { "en": "Imaging of Neuroinflammation in Neurodegenerative Diseases" } }, "funder": { "id": "00k4n6c32", "name": "European Commission" } } ], "publication_date": "2016-01-27", "publisher": "Zenodo", "resource_type": { "id": "publication-article", "title": { "de": "Zeitschriftenartikel", "en": "Journal article" } }, "rights": [ { "description": { "en": "The Creative Commons Attribution license allows re-distribution and re-use of a licensed work on the condition that the creator is appropriately credited." }, "icon": "cc-by-icon", "id": "cc-by-4.0", "props": { "scheme": "spdx", "url": "https://creativecommons.org/licenses/by/4.0/legalcode" }, "title": { "en": "Creative Commons Attribution 4.0 International" } } ], "subjects": [ { "subject": "SOD1G93A" }, { "subject": "TSPO" }, { "subject": "PET/CT" }, { "subject": "18F-DPA-714" }, { "subject": "mice" } ], "title": "Imaging of brain TSPO expression in a mouse model of amyotrophic lateral sclerosis with 18F-DPA-714 and micro-PET/CT." }, "parent": { "access": { "owned_by": { "user": 1964 } }, "communities": { "default": "724cc757-0e37-4b01-a81f-b8aa5f1d7b44", "entries": [ { "access": { "member_policy": "open", "members_visibility": "public", "record_policy": "open", "review_policy": "open", "visibility": "public" }, "children": { "allow": false }, "created": "2014-01-06T13:42:25+00:00", "custom_fields": {}, "deletion_status": { "is_deleted": false, "status": "P" }, "id": "724cc757-0e37-4b01-a81f-b8aa5f1d7b44", "links": {}, "metadata": { "curation_policy": "all uploads acknowledging the INMiND project are accepted", "page": "The goal of the EC FP7 Collaborative Project INMiND (GA 278850) is to carry out collaborative research on molecular mechanisms that link neuroinflammation with neurodegeneration in order to identify novel biological targets for activated microglia, which may serve for both diagnostic and therapeutic purposes, and to translate this knowledge into clinical application and patient benefit.
\r\n\r\n\r\n\r\n
The general objectives of INMiND are:
\r\n\r\n(i) to identify novel mechanisms of regulation and function of microglia under various conditions (inflammatory stimuli; neurodegenerative and -regenerative model systems);
\r\n\r\n(ii) to identify and implement new targets for activated microglia, which may serve for diagnostic (imaging) and therapeutic purposes;
\r\n\r\n(iii) to design new molecular probes (tracers) for these novel targets and to implement and validate them in in vivo innovative model systems and in patients;
\r\n\r\n(iv) to image and quantify modulated microglia activity in patients undergoing immune therapy for cognitive impairment, and to relate the findings to clinical outcome.
\r\n\r\nThe INMiND projects brings together a group of excellent basic scientists and clinicians with a proven background in efficiently accomplishing common scientific goals (FP6 DiMI, www.dimi.eu), who belong to highly complementary fields of research (from genome-oriented to imaging scientists and clinicians), and who are dedicated to formulate novel image-guided therapeutic strategies for neuroinflammation-related neurodegenerative diseases.
\r\n\r\nThe strength of the project is that, across Europe, it coordinates research and training activities related to neuroinflammation, neurodegeneration, neuroregeneration, and imaging with special emphasis on translating basic mechanisms into clinical applications that shall provide health benefits for our aging population.
\r\n\r\nWith its intellectual excellence and its crucial mass the INMiND consortium is playing a major role in the European Research Area and will gain European leadership in the creation of new image-guided diagnosis and therapy paradigms in patients with neurodegenerative diseases.
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", "description": "Open repository for EU-funded research outputs from Horizon Europe, Euratom and earlier Framework Programmes.", "organizations": [ { "id": "00k4n6c32" } ], "page": "The EU Open Research Repository is a Zenodo-community dedicated to fostering open science and enhancing the visibility and accessibility of research outputs funded by the European Union. The community is managed by CERN on behalf of the European Commission.
\nThe mission of the repository is to support the implementation of the EU's open science policy, providing a trusted and comprehensive space for researchers to share their research outputs such as data, software, reports, presentations, posters and more. The EU Open Research Repository simplifies the process of complying with open science requirements, ensuring that research outputs from Horizon Europe, Euratom, and earlier Framework Programmes are freely accessible, thereby accelerating scientific discovery and innovation.
\nThe EU Open Research Repository serves as a complementary platform to the Open Research Europe (ORE) publishing platform. Open Research Europe focuses on providing a publishing venue for peer-reviewed articles, ensuring that research meets rigorous academic standards. The EU Open Research Repository provides a space for all the other research outputs including data sets, software, posters, and presentations that are out of scope for ORE. This holistic approach enables researchers to not only publish their findings but also share the underlying data and materials that support their work, fostering transparency and reproducibility in the scientific process.
\nCurrently in its pilot phase and set to be fully operational during autumn 2024, the EU Open Research Repository is constantly evolving. Efforts are committed to integrating cutting-edge features, including automated curation checks and FAIR (Findable, Accessible, Interoperable, and Reusable) assistance, to further support the research community. The goal is to provide researchers with a simple goto solution for making their publicly funded research open and as FAIR as possible.
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