Jacobs, Andreas H.; Tavitian, Bertrand: Noninvasive molecular imaging of Neuroinflammation
Inhalt
- Figure 1 Components of the neurovascular unit (NVU), the ’Vicious Cycle’ of neuroinflammation, and the ’Ying and Yang’ of microglia.
- Molecular targets for imaging neuroinflammation
- Damage-Associated Molecular PatternssolPathogen-Associated Molecular Patterns
- Toll-Like Receptors, Receptor for Advanced Glycation End Products, Adhesion Molecules, Cytokines, and Chemokines
- Microglia Cells
- Infiltrating Neutrophils, Macrophages, and T Lymphocytes
- Alterations of and Within the Blood-Brain Barrier
- Astrocytes and Monoamine Oxidase Type B
- Imaging neuroinflammation in neurologic diseases
- Figure 2 Time course of microglia activation after experimental ischemia as determined by [18F]DPA-714 and muPET.
- Figure 3 Location and extent of microglia activation after focal subcortical ischemia as determined by [11C](R)-PK11195 and HRRT-PET in conjunction with diffusion tensor imaging (DTI) MRI.
- Figure 4 Cross-sectional patterns of lesion enhancement in patients with multiple sclerosis (MS) as detected by magnetic resonance imaging (MRI).
- Figure 5 Immune infiltrates in demyelinating lesions as depicted by two-photon laser scanning microscopy (TPLSM) are highly dynamic and show different motility patterns in distinct disease stages.
- Figure 6 Early detection of amyloid-beta as damage-associated molecular pattern (DAMP) and microglia activation in patients with mild cognitive impairment by positron-emission tomography (PET).
- Conclusion
- Disclosure
- References
- Principle investigators of the INMiND consortium: