Figure 1
From: Tracking neuroinflammation in Alzheimer’s disease: the role of positron emission tomography imaging
PET biological targets for measuring neuroinflammation in AD. Amyloid-beta (Aβ)1–42 and neurofibrillary tangles (NFTs) - the classic hallmarks of Alzheimer’s disease (AD) - can trigger neuroinflammatory changes, which induces the release of complement factors, cytokines and others inflammatory factors. Positron emission tomography (PET) uses biological surrogates for measuring neuroinflammation. Microglial activation is estimated by the expression of the 18-kDa translocator protein (TSPO), which is mainly found on the outer mitochondrial membrane of the microglial cells under inflammatory conditions. Monoamine oxidase-B (MAO-B), an enzyme usually located on the outer mitochondrial membrane of astrocytes, is proposed as an index of reactive astrocytosis. Radiolabeled arachidonic acid (AA), a phospholipid present in the cell membrane and cleaved by phospholipase A2 (PLA2), can estimate the AA metabolism. AA is the precursor of eicosanoids - prostaglandins and leukotrienes - which are potent mediators of the inflammatory response.