In the past decades, our understanding of the central nervous system has evolved from one of an immune-privileged site, to one where inflammation is pathognomonic for some of the most prevalent neurodegenerative diseases, including Alzheimer’s dementia. Inflammation, whether in the brain or periphery, is almost always a secondary response to a primary pathogen. In Alzheimer’s dementia, inflammation is considered as a secondary response after impaired processing and precipitation of amyloid, which will ensue and likely cause additional neurone loss. In this chapter, visualization tools for these neuro-inflammatory processes, both structural and mainly functional, are critically reviewed and discussed. From the basic neuroinflammatory mechanisms and its biochemical characteristics, the role of its potential mediators playing a key role in neurodegenerative disorders has been explored, with Alzheimer’s disease as a prototype. Whereas structural imaging shows merely late anatomical consequences of an inflammatory response, functional imaging is a strong potential candidate to bridge this gap between in vitro and in vivo knowledge. A number of radioligands have been recently explored that allow the early in vivo visualization of inflammatory responses and, as such, open a promising window on both understanding as well as possible clinical management of inflammatory neurodegenerative disorders. Magnetic resonance imaging and 99mTc-ECD (ethylcysteinate dimer) single-photon emission tomography scans yielded conclusive results as to the exclusion of other pathologies and confirmation of diagnosis. 57Co single-photon emission tomography scanning did not reveal any regional raised uptake, ongoing tissue decay, or inflammation, irrespective of the type of dementia, the depth or extent of perfusion defects, the presence of atrophy on magnetic resonance imaging, or the results of neuropsychological tests. The use of PK11195 to detect cerebral inflammation was more positive. For instance, the mean (123I)iodo-PK11195 uptake was higher in Alzheimer’s dementia as compared with controls in many neocortical regions, particularly in the frontal and right mesotemporal regions. A significant correlation was found between regional increased (123I)iodo-PK11195 uptake and cognitive deficits. (123I)iodo-PK11195 and (11C)-PK-11195 are cellular disease activity markers that allow one to make an in vivo assessment of microglial inflammation in Alzheimer’s dementia inflammation.