作者: Guo‐Jun Liu , Ryan J. Middleton , Claire R. Hatty , Winnie Wai‐Ying Kam , Ronald Chan
DOI: 10.1111/BPA.12196
关键词: Knockout mouse 、 Neuroscience 、 Microglia 、 Biology 、 Receptor 、 Translocator protein 、 Mutation 、 Phenotype 、 Biomarker (cell) 、 Neuroinflammation
摘要: The 18 kDa translocator protein (TSPO), previously known as the peripheral benzodiazepine receptor, is expressed in injured brain. It has become an imaging marker of “neuroinflammation” indicating active disease, and best interpreted a nondiagnostic biomarker disease staging tool that refers to histopathology rather than etiology. therapeutic potential TSPO drug target mostly based on understanding it outer mitochondrial membrane required for translocation cholesterol, which thus regulates rate steroid synthesis. This pivotal role together with evolutionary conservation underpinned belief any loss or mutation should be associated significant physiological deficits outright incompatible life. However, against prediction, full Tspo knockout mice are viable across their lifespan do not show phenotype expected if cholesterol transport synthesis were significantly impaired. Thus, “translocation” function remains better substantiated. Here, we discuss literature before after introduction new nomenclature review some newer findings. In light controversy surrounding TSPO, emphasize continued importance identifying compounds confirmed selectivity suggest expression analyzed within specific contexts merely equated reified concept “neuroinflammation.”