학술논문
PET Imaging to Measure Neuroinflammation In Vivo.
Document Type
Academic Journal
Author
Malpetti M; Department of Clinical Neurosciences, University of Cambridge, Cambridge, UK.; Franzmeier N; Institute for Stroke and Dementia Research, LMU University Hospital, LMU Munich, Munich, Germany.; Munich Cluster for Systems Neurology (SyNergy), Munich, Germany.; Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, University of Gothenburg, Mölndal and Gothenburg, Sweden.; Brendel M; Munich Cluster for Systems Neurology (SyNergy), Munich, Germany. Matthias.brendel@med.uni-muenchen.de.; Department of Nuclear Medicine, LMU University Hospital, LMU Munich, Munich, Germany. Matthias.brendel@med.uni-muenchen.de.; German Center for Neurodegenerative Diseases (DZNE), Munich, Germany. Matthias.brendel@med.uni-muenchen.de.
Source
Publisher: Humana Press Country of Publication: United States NLM ID: 9214969 Publication Model: Print Cited Medium: Internet ISSN: 1940-6029 (Electronic) Linking ISSN: 10643745 NLM ISO Abbreviation: Methods Mol Biol Subsets: MEDLINE
Subject
Language
English
Abstract
This paper provides an overview of the role of neuroinflammation in Alzheimer's disease and other neurodegenerative diseases, highlighting the potential of anti-inflammatory treatments to slow or prevent decline. This research focuses on the use of positron emission tomography (PET) imaging to visualize and quantify molecular brain changes in patients, specifically microglial activation and reactive astrogliosis. We discuss the development and application of several PET radioligands, including first-generation ligands like PK11195 and Ro5-4864, as well as second- and third-generation ligands such as [11C]PBR28, [18F]DPA-714, [18F]GE-180, and [11C]ER176. These ligands target the 18-kDa translocator protein (TSPO), which is overexpressed in activated microglia and upregulated in astrocytes. We also address the limitations of these ligands, such as low brain uptake, poor penetration of the blood-brain barrier, short half-life, and variable kinetic behavior. Furthermore, we demonstrate the impact of genetic polymorphisms on ligand binding.
(© 2024. The Author(s), under exclusive license to Springer Science+Business Media, LLC, part of Springer Nature.)
(© 2024. The Author(s), under exclusive license to Springer Science+Business Media, LLC, part of Springer Nature.)