Abstract
The brain responds to the challenge of disease with marked changes in the functional state of its glial cells. One of the most rapid and obvious events is the activation of microglia, the brain’s resident tissue macrophages. Microglial activation is increasingly recognised as an important, early step in the pathophysiological response to traumatic, inflammatory and degenerative tissue changes and even to neoplastic transformation that may affect the nervous system. Microglia react rapidly and in a territorially highly confined way to subtle, acute as well as chronic pathological stimuli. Microglia have been aptly called a “sensor” of pathology in the CNS by Kreutzberg [1,2]. This unique behaviour, which may be due to a lack of gap junctions in these cells [3] is of great practical diagnostic use. Thus, detection of microglial activation provides useful information on formal parameters of disease, such as accurate spatial localisation of the disease process, rate of disease progression and insights into secondary neurodegenerative or adaptive alterations which may take place quite remote from the actual lesion site. Part of the remarkable structural and functional plasticity of microglia is the de novo expression of the “peripheral benzodiazepine binding site" (PBBS). PBBS is linked to important functions, such as immune modulation, steroid synthesis and mitochondrial activity. The PBBS is bound by the isoquinoline, PK11195, which labelled with carbon-11 can be used for positron emission tomography (PET). This opens up a unique window to study glial activity in the living human brain.