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TSPO imaging in stroke: from animal models to human subjects

Boutin, Hervé; Pinborg, Lars H

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      <creatorName>Boutin, Hervé</creatorName>
      <affiliation>Wolfson Molecular Imaging Centre, Faculty of Medical and Human Sciences, University of Manchester, Manchester, M19 1GX, United Kingdom.</affiliation>
      <creatorName>Pinborg, Lars H</creatorName>
      <givenName>Lars H</givenName>
      <affiliation>Neurobiology Research Unit, Department of Neurology, Rigshospitalet, Copenhagen, Denmark</affiliation>
    <title>TSPO imaging in stroke: from animal models to human subjects</title>
    <subject>Translocator protein 18 kDa   </subject>
    <subject> Stroke</subject>
    <date dateType="Issued">2015-09-30</date>
  <resourceType resourceTypeGeneral="Text">Journal article</resourceType>
    <alternateIdentifier alternateIdentifierType="url"></alternateIdentifier>
    <relatedIdentifier relatedIdentifierType="DOI" relationType="IsIdenticalTo">10.1007/s40336-015-0146-7</relatedIdentifier>
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    <rights rightsURI="">Creative Commons Attribution 4.0 International</rights>
    <rights rightsURI="info:eu-repo/semantics/openAccess">Open Access</rights>
    <description descriptionType="Abstract">&lt;p&gt;Stroke is a major health problem in developed countries and neuroinflammation has emerged over the last 2 decades as major contributor to the pathophysiological processes of brain damage following stroke. PET imaging of the translocator 18&amp;nbsp;kDa protein (TSPO) provides a unique non-invasive point of access to neuroinflammatory processes and more specifically microglial and astrocytic reaction after stroke in both animal models and patients. Here, we are reviewing both the experimental and clinical literature about in vivo TSPO PET and SPECT imaging in stroke. The studies in animal models of stroke reviewed here highlight a slightly faster time-course for TSPO expression in permanent vs. temporary stroke and a stronger activation in the infarct core in temporary stroke vs. a stronger activation in peri-infarct areas in permanent stroke. Altogether these findings suggest that areas where neuroinflammatory events occur post-stroke are at higher risk of secondary damage. The time-course of TSPO expression is slower in humans versus animal models of stroke. In human studies, the TSPO expression in the peri-infarct areas peaks 3&amp;ndash;4&amp;nbsp;weeks after stroke and increased TSPO expression is demonstrated for months after the stroke in remote areas both ipsilesional to pyramidal tracts damage and in the contralesional hemisphere. Further clinical studies are warranted to address the role of TSPO and neuroinflammation in functional recovery and reorganization after stroke and the possible therapeutic implications. TSPO imaging appears to be a valid biomarker for demonstrating the dynamic process of neuroinflammation in stroke. But it is also clear that as the processes of microglial activation are increasingly complex, the need for new biomarkers and tracers targeting other aspect of glial reaction are needed to further investigate neuroinflammatory processes in patients.&lt;/p&gt;</description>
      <funderName>European Commission</funderName>
      <funderIdentifier funderIdentifierType="Crossref Funder ID">10.13039/501100000780</funderIdentifier>
      <awardNumber awardURI="info:eu-repo/grantAgreement/EC/FP7/278850/">278850</awardNumber>
      <awardTitle>Imaging of Neuroinflammation in Neurodegenerative Diseases</awardTitle>
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