The 18 kDa translocator protein, microglia and neuroinflammation

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dc.contributor.authorLiu, GJen_AU
dc.contributor.authorMiddleton, RJen_AU
dc.contributor.authorHatty, CRen_AU
dc.contributor.authorKam, WWYen_AU
dc.contributor.authorChan, RHYen_AU
dc.contributor.authorPham, TQen_AU
dc.contributor.authorHarrison-Brown, Men_AU
dc.contributor.authorDodson, Een_AU
dc.contributor.authorVeale, Ken_AU
dc.contributor.authorBanati, RBen_AU
dc.date.accessioned2020-03-17T01:23:27Zen_AU
dc.date.available2020-03-17T01:23:27Zen_AU
dc.date.issued2014-10-26en_AU
dc.date.statistics2020-03-11en_AU
dc.description© 2014 The Authors. Brain Pathology published by John Wiley & Sons Ltd on behalf of International Society of Neuropathology. This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.en_AU
dc.description.abstractThe 18 kDa translocator protein (TSPO), previously known as the peripheral benzodiazepine receptor, is expressed in the injured brain. It has become known as an imaging marker of “neuroinflammation” indicating active disease, and is best interpreted as a nondiagnostic biomarker and disease staging tool that refers to histopathology rather than disease etiology. The therapeutic potential of TSPO as a drug target is mostly based on the understanding that it is an outer mitochondrial membrane protein required for the translocation of cholesterol, which thus regulates the rate of steroid synthesis. This pivotal role together with the evolutionary conservation of TSPO has underpinned the belief that any loss or mutation of TSPO should be associated with significant physiological deficits or be outright incompatible with life. However, against prediction, full Tspo knockout mice are viable and across their lifespan do not show the phenotype expected if cholesterol transport and steroid synthesis were significantly impaired. Thus, the “translocation” function of TSPO remains to be better substantiated. Here, we discuss the literature before and after the introduction of the new nomenclature for TSPO and review some of the newer findings. In light of the controversy surrounding the function of TSPO, we emphasize the continued importance of identifying compounds with confirmed selectivity and suggest that TSPO expression is analyzed within specific disease contexts rather than merely equated with the reified concept of “neuroinflammation.” © 2014 The Authorsen_AU
dc.identifier.citationLiu, G. J., Middleton, R. J., Hatty, C. R., Kam, W. W. Y., Chan, R., Pham, T. Harrison-Brown, M, Dodson, E., Veale, K., & Banati, R. B. (2014). The 18 kDa translocator protein, microglia and neuroinflammation. Brain Pathology, 24(6), 631-653. doi:10.1111/bpa.12196en_AU
dc.identifier.govdoc8804en_AU
dc.identifier.issn1750-3639en_AU
dc.identifier.issue6en_AU
dc.identifier.journaltitleBrain Pathologyen_AU
dc.identifier.pagination631-653en_AU
dc.identifier.urihttp://dx.doi.org/10.1111/bpa.12196en_AU
dc.identifier.urihttp://apo.ansto.gov.au/dspace/handle/10238/9163en_AU
dc.identifier.volume24en_AU
dc.language.isoenen_AU
dc.publisherWileyen_AU
dc.subjectProteinsen_AU
dc.subjectReceptorsen_AU
dc.subjectBrainen_AU
dc.subjectInjuriesen_AU
dc.subjectDiseasesen_AU
dc.subjectMitochondriaen_AU
dc.subjectMembranesen_AU
dc.subjectMiceen_AU
dc.subjectCholesterolen_AU
dc.subjectSteroidsen_AU
dc.subjectInflammationen_AU
dc.titleThe 18 kDa translocator protein, microglia and neuroinflammationen_AU
dc.typeJournal Articleen_AU
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