ライフサイエンスコーパス: TSPO

1 gands that bind to the translocator protein (TSPO).

2 and targets the 18-kDa translocator protein (TSPO).

3 DPH oxidase (NOX2) and translocator protein (TSPO).

4 gulation of the 18-kDa translocator protein (TSPO).

5 ly using PET is translocator protein 18 kDa (TSPO).

6 th the 36 kDa dimer of translocator protein (TSPO).

7 vestigate the phenotypes of cells expressing TSPO.

8 specially because of the basal expression of TSPO.

9 the regional variation of Kb and endothelial TSPO.

10 ease the expression of translocator protein (TSPO) 18 kDa, thereby making the TSPO expression a marke

11 (18)F-FDG (n = 43) and translocator protein (TSPO) ((18)F-GE180; n = 58) small-animal PET, with volum

12 e) binds to the 18-kDa translocator protein (TSPO), a biomarker of glia.

13 PET imaging of 18-kDa translocator protein (TSPO), a biomarker of neuroinflammation, most second-gen

14 d radioligands for the translocator protein (TSPO), a marker for glial activation, have yielded incon

15 To measure translocator protein 18 kDa (TSPO), a marker of activated glial cell response, in a c

16 xpression of the 18kDa translocator protein (TSPO), a marker of activated microglia/macrophages, in c

17 Brain levels of 18-kDa translocator protein (TSPO), a marker of microglial activation and neuroinflam

18 imaging of the 18-kDa translocator protein (TSPO), a marker of neuroinflammation.

19 imaging of the 18-kDa translocator protein (TSPO), a microglial biomarker, was conducted in 23 indiv

20 both TSPO wild type (WT) and the polymorphic TSPO A147T.

21 The progression of TSPO activation to 13 mo also showed a moderate associat

22 blood draws during PET scanning to determine TSPO affinity genotype and plasma nicotine levels.

23 Probes with relevant TSPO affinity, favorable spectroscopic properties, and i

24 The translocator protein (TSPO), an 18-kDa transmembrane protein primarily found i

25 pression of the 18 kDa translocator protein (TSPO), an activated glial marker expressed on mitochondr

26 is first PET investigation with longitudinal TSPO and amyloid PET together with terminal cognitive te

27 Methods: We compiled serial PET measures of TSPO and amyloid with terminal cognitive assessment (wat

28 Ex vivo immunofluorescent staining for TSPO and CD68 (macrophage marker) resulted in the same p

29 The correlation between TSPO and endothelial cell mRNA supports the relationship

30 ficant correlation was seen between mRNA for TSPO and genes specific to endothelial cells.

31 0-fold increase in cells double positive for TSPO and HLA-DR in active lesions and in the rim of chro

32 LPS further increased expression of TSPO and IL-6 in SNCA mice.

33 ves 4-10 with improved potencies toward both TSPO and MDM2.

34 ols, but showed lower relative expression of TSPO and microglia-associated genes TNFRSF14 and TSPOAP1

35 croglia/macrophages (GAM) were identified as TSPO and MMP sources.

36 tion and quantification of the expression of TSPO and MMP.

37 ble atomic structures of mouse and bacterial TSPO and propose a rationale for the development of new

38 e we have studied the cellular expression of TSPO and specific binding of two TSPO targeting radiolig

39 nd an upregulation of TSPO pathway proteins (TSPO and VDAC), both in terms of mRNA and protein levels

40 [(18)F]DPA-714 (TSPO) and [(18)F]BR-351 (MMP) matched with histology.

41 invasive imaging by PET with [(18)F]DPA-714 (TSPO) and [(18)F]BR-351 (MMP) was used for the assessmen

42 invasion, such as the translocator protein (TSPO) and matrix metalloproteinases (MMP), may serve as

43 toma multiforme (GBM), translocator protein (TSPO) and murine double minute (MDM)2/p53 complex repres

44 the radiotracer [(11)C]DAA1106 (a ligand for TSPO) and positron emission tomography (PET) to determin

45 he glial marker 18 kDa translocator protein (TSPO), and changes in functional connectivity.

46 icroglia (18-kD translocator protein ligand [TSPO]) and static 30- to 60-min recordings with (18)F-FD

47 Immunohistochemical analyses with TSPO antisera, methoxy-X04 staining for fibrillary beta-

48 ia with caution, especially when measures of TSPO are not complemented with other markers of inflamma

49 multiple centers and increases the power of TSPO as a biomarker for future therapeutic trials.

50 Therefore, we evaluated the validity of TSPO as a disease-relevant marker of inflammation using

51 TSPO+ astrocytes were increased up to 7-fold compared to

52 nd multi-cellular gene expression pattern of TSPO at basal conditions in the adult mouse hippocampus.

53 d that these probes specifically labeled the TSPO at the mitochondrial level in the U343 cell line.

54 /pharmacodynamics and efficacy assessment by TSPO autoradiography and CSF proteomics.

55 also associated with lower prefrontal-limbic TSPO availability and PTSD severity.

56 Correlations were investigated between TSPO availability and symptom severity.

57 In a post hoc analysis, we also compared TSPO availability between patients with and without suic

58 have used [(11)C](R)-PK11195 PET to compare TSPO availability in a predominantly antipsychotic-naive

59 We found no evidence for increased TSPO availability in antipsychotic-free patients compare

60 1195 positron emission tomography to compare TSPO availability in the anterior cingulate cortex (ACC)

61 This study aimed to measure TSPO availability in the largest patient group to date,

62 Prefrontal-limbic TSPO availability in the PTSD group was negatively assoc

63 In the patients, TSPO availability was also strongly correlated with nega

64 Regional TSPO availability was measured as a distribution volume

65 However, TSPO availability was significantly elevated in medicate

66 We confirm evidence for increased TSPO availability, suggestive of predominantly microglia

67 the development of high-affinity ligands for TSPO-based therapies or diagnostics.

68 ding signatures for lipid and protoporphyrin TSPO binders, molecular classes that likely interact wit

69 all correlation between (18)F-FDG uptake and TSPO binding (R = 0.69, P < 0.005).

70 er underscores the need to interpret altered TSPO binding in schizophrenia with caution, especially w

71 -713 revealed a strong trend towards reduced TSPO binding in the middle frontal gyrus of patients wit

72 Similarly, cortical TSPO binding increased to a maximum at 14.5 mo (+15%, P

73 that accounts for the effect of endothelial TSPO binding on the quantification of (18)F-DPA-714 PET

74 ly that the pathological meanings of altered TSPO binding or expression are disease-specific, and the

75 While altered TSPO binding or expression may indeed mirror ongoing neu

76 these ligands are still easily lodged in the TSPO binding site.

77 The observed decrease in TSPO binding suggests reduced numbers or altered functio

78 blems, including a polymorphism that affects TSPO binding.

79 tically stratified for translocator protein (TSPO) binding status, underwent PET scanning with TSPO r

80 d in vivo using 18-kDa translocator protein (TSPO)-binding radioligands and PET.

81 factor determining steroidogenic efficacy of TSPO-binding compounds.

82 It is a high-quality second-generation TSPO-binding PET radiotracer.

83 3 HABs underwent a repeated brain scan after TSPO blockade with XBD173 (N-benzyl-N-ethyl-2-(7-methyl-

84 ata suggest ageing is associated with higher TSPO but a diagnosis of schizophrenia is not.

85 We suggest that TSPO can be a good marker for early pathogenesis detecti

86 ng signal for both tracers and the number of TSPO+ cells across all of the tissues examined.

87 lesion subtypes and accounted for 25% of the TSPO+ cells in these lesions.

88 udies, for the first time, demonstrated that TSPO could serve as a potential imaging biomarker for BA

89 o expectations, our results demonstrate that TSPO deficiency does not adversely affect erythropoiesis

90 ion in brain and peripheral organs with high TSPO densities such as lung and spleen were greater in H

91 TSPO distribution volume (VT) is an index of TSPO density.

92 e activated during neuroinflammation and the TSPO distribution volume (VT) is an index of TSPO densit

93 n these findings, we conclude that mammalian TSPO does not have a critical physiological function rel

94 ET imaging with 18-kDa translocator protein (TSPO) enables longitudinal monitoring of microglial acti

95 rch has mostly accepted these denotations of TSPO, even if they may be inadequate and misleading unde

96 or protein (TSPO) 18 kDa, thereby making the TSPO expression a marker for neuroinflammation.

97 In summary, in multiple sclerosis, TSPO expression arises from microglia of different pheno

98 nsity in PS2APP mice was predicted by higher TSPO expression at 8 mo.

99 ed for neuropathological characterization of TSPO expression for the interpretation of TSPO PET in ot

100 voxelwise analysis confirmed lower regional TSPO expression in ASD at this later time point.

101 Lower TSPO expression in ASD could reflect abnormalities in ne

102 Positive correlation between high TSPO expression in cancer cells and susceptibility to ph

103 ndividuals with ASD exhibited lower regional TSPO expression in several brain regions, including the

104 No brain region exhibited higher regional TSPO expression in the ASD group compared with the contr

105 the cellular neuropathology associated with TSPO expression is of clear importance for understanding

106 TSPO expression levels in cancer cells do not correlate

107 hallenge the general assumption that altered TSPO expression or binding unequivocally mirrors ongoing

108 on in schizophrenia is mirrored by increased TSPO expression or ligand binding.

109 terval of 3.6 months, and we determined that TSPO expression over this period of time was stable and

110 Finally, in aged RPE cells, TSPO expression was reduced and cholesterol efflux impai

111 ith the exception of cortical lesions, where TSPO expression was similar, (11) C-PBR28 uptake across

112 displayed a specific uptake consistent with TSPO expression, a slow metabolism in blood (69% of pare

113 in resident microglia using Cx3cr1(CreERT2):TSPO(fl/fl) mice or targeting the protein with the synth

114 We generated a TSPO floxed mouse, and then crossed this mouse with a Cr

115 ed to search for a new translocator protein (TSPO) fluorescent probe endowed with improved affinity a

116 n the presence of light, and in vertebrates, TSPO function has been linked to porphyrin transport and

117 gical mechanisms of translocator protein 18 (TSPO) function but also indicate that translocator prote

118 t) approaches led to consistent increases in TSPO gene and protein levels in neurons, but not in micr

119 ng to generate a cellular landscape of basal TSPO gene expression in the hippocampus of adult (12 wee

120 analyses were performed controlling for both TSPO genotype, which is known to affect [(11)C]PBR28 bin

121 In mammals, TSPO has been described as a key member of a multiprotei

122 used to detect discrete neurotoxic damages, TSPO has generally turned into a biomarker of 'neuroinfl

123 Although imaging TSPO has yielded valuable clinical data linking neuroinf

124 ers that target translocator protein 18 kDa (TSPO) has become a popular approach to assess putative n

125 lective for the 18 kDa translocator protein (TSPO) has become the most widely used technique to asses

126 n agents targeting the translocator protein (TSPO) has been hindered by a common single nucleotide po

127 The 18-kDa translocator protein (TSPO) has been used in PET as an inflammatory biomarker.

128 imaging of the 18 kDa translocator protein (TSPO) has been used to investigate whether microglial ac

129 s targeting the translocator protein 18 kDa (TSPO) have been limited by high nonspecific binding of t

130 s targeting the 18-kDa translocator protein (TSPO) have been used as in vivo markers of neuroinflamma

131 Ten healthy controls, 6 TSPO high-affinity binders, and 4 mixed-affinity binders

132 e, we evaluated various ratio approaches for TSPO imaging and compared them with standard kinetic mod

133 In this review, the developments in TSPO imaging are discussed, and current limitations and

134 It remains unclear, however, whether TSPO imaging can accurately capture low-grade inflammato

135 Although TSPO imaging demonstrates great promise, its signal exhi

136 recently showed microglia involvement using TSPO imaging.

137 By comparing TSPO in 15 young adult males with ASD with 18 age- and s

138 While the majority of cells expressing TSPO in active lesions or chronic active rims are microg

139 (11)C-PBR28 images showed overexpression of TSPO in brain regions known to be affected in the HSE ra

140 Here, we investigate the function of TSPO in cholesterol efflux from the RPE cells.

141 rent tumor cell lines to examine the role of TSPO in erythropoiesis, heme levels, PPIX biosynthesis,

142 we sought to determine the specific role of TSPO in experimental autoimmune encephalomyelitis (EAE),

143 unctions and cellular expression patterns of TSPO in health and disease.

144 quantitative framework for interpretation of TSPO in multiple sclerosis and highlight the need for ne

145 s of variance indicated significantly higher TSPO in patients compared with control subjects (p = .00

146 at tamoxifen-induced conditional deletion of TSPO in resident microglia using Cx3cr1(CreERT2):TSPO(fl

147 These data define a distinct role for TSPO in retinal phagocyte reactivity and highlight the p

148 SPO specific ligands or by overexpression of TSPO in RPE cells.

149 g, indicating an in vivo functional role for TSPO in suppressing EAE.

150 The loss of TSPO in the CNS did not result in overt developmental de

151 Accounting for endothelial TSPO in the kinetic model improved the fit of PET data.

152 MS WM lesions showed relatively modest TSPO increases.

153 t NADPH oxidase-deficient mice, we show that TSPO is a key regulator of NOX1-dependent neurotoxic ROS

154 e the downstream p53 signaling is intact and TSPO is overexpressed.

155 TSPO is upregulated in glial cells and used as a measure

156 The translocator protein (TSPO) is a commonly used imaging target to investigate n

157 The translocator protein (18 kDa) (TSPO) is described as a biomarker for reactive gliosis,

158 The 18 kDa translocator protein (TSPO) is increasingly used to study brain and spinal cor

159 In AD, the translocator protein 18 kDa (TSPO) is overexpressed in the activated microglia that s

160 mitochondrial protein, translocator protein (TSPO), is a widely used biomarker of neuroinflammation,

161 The 18 kDa translocator protein, TSPO, is a cholesterol-binding protein implicated in mit

162 regulating mitochondrial function and since TSPO itself impairs cellular mitophagy, we also investig

163 In this study, we used TSPO knock-out (Tspo(-/-)) mice, primary cells, and diff

164 A conditional TSPO knockout mouse was generated by utilizing the Cre-L

165 nctions of TSPO, we first developed a viable TSPO knockout mouse.

166 enesis and vascular leakage are prevented by TSPO knockout or XBD173 treatment.

167 tant mouse was a neural linage line specific TSPO knockout.

168 This work compared brain TSPO levels in 20 tobacco smokers (abstinent for at leas

169 ndence (P=0.034), corresponding to 10% lower TSPO levels in alcohol-dependent subjects.

170 Rather, subnormal TSPO levels in drug-free recent-onset patients may imply

171 Quantification of TSPO levels in MS could prove to be a sensitive tool for

172 euronal activity has the potential to modify TSPO levels in the adult central nervous system.

173 estigated whether neuronal activity modifies TSPO levels in the adult central nervous system.

174 that nonsmokers and smokers have comparable TSPO levels in the brain.

175 ory analyses found a negative association of TSPO levels in the hippocampus and striatum with alcohol

176 In both models, the changes in TSPO levels were not restricted to microglia but emerged

177 ation between mitophagy-related proteins and TSPO levels, while VDAC correlated negatively with p62/S

178 ssion are associated with reduced prefrontal TSPO levels.

179 (MRI) brain scan with the second-generation TSPO ligand [(11)C]PBR28.

180 A TSPO ligand attenuates brain injury after intracerebral

181 These results indicate that the TSPO ligand etifoxine attenuates brain injury and inflam

182 g pathway for different poses of PK-11195, a TSPO ligand used in neuroimaging.

183 In this study, we determined the impact of a TSPO ligand, etifoxine, on brain injury and inflammation

184 identity for a previously unknown endogenous TSPO ligand.

185 n to ligand binding, specific binding of the TSPO ligands 3H-PK11195 and 3H-PBR28 was determined in t

186 gle nucleotide polymorphism (A147T) at which TSPO ligands commonly lose affinity.

187 TSPO ligands have shown anti-inflammatory and neuroprote

188 st in simulations of (un)binding pathways of TSPO ligands, which could reveal the molecular interacti

189 ns for the design of new long-residence-time TSPO ligands.

190 high binding affinity and nondiscriminating TSPO ligands.

191 TSPO may be a viable therapeutic target that requires fu

192 In this study, we used TSPO knock-out (Tspo(-/-)) mice, primary cells, and different tumor cell

193 ron emission tomography (PET) imaging of the TSPO microglial marker and found increased neuroinflamma

194 We provide a review of TSPO monomeric and oligomeric states and their conformat

195 The TSPO-/- mouse showed a decrease in GFAP expression, corr

196 We then quantified TSPO mRNA and protein levels after stimulating neuronal

197 y correlated with all 3 probes extracted for TSPO mRNA expression (r = 0.80, r = 0.79, and r = 0.90),

198 othelial cells were correlated with regional TSPO mRNA expression.

199 en the volume of distribution and one of the TSPO mRNA probes (r = 0.65).

200 The high correlation between Kb and TSPO mRNA suggests that the 2TC-1K model reveals more bi

201 mage expression of the translocator protein (TSPO) on activated microglia in the brain, has been used

202 e than (R)-(11)C-PK11195 in the detection of TSPO overexpression in the HSE rat model, because more b

203 , p62/SQSTM1 and LC3A and an upregulation of TSPO pathway proteins (TSPO and VDAC), both in terms of

204 PET imaging of translocator protein 18 kDa (TSPO) permits longitudinal, noninvasive visualization of

205 Abeta PET were analyzed in correlation with TSPO PET AIs.

206 gnificant correlations were observed between TSPO PET and activated astrocytes (glial fibrillary acid

207 Analysis and interpretation of TSPO PET are challenging, especially because of the basa

208 is across these 2 tracers enables pooling of TSPO PET data across multiple centers and increases the

209 rative diseases, considerable limitations of TSPO PET have prompted identification of other more cell

210 Hence, the increasing popularity of TSPO PET imaging has paradoxically introduced substantia

211 cellular and pathological processes on which TSPO PET imaging is reporting.

212 s unlikely to be achieved by the sole use of TSPO PET imaging.

213 ant correlation between AIs of Abeta PET and TSPO PET in 4 investigated Abeta mouse models (APP/PS1:

214 of TSPO expression for the interpretation of TSPO PET in other neurodegenerative disorders.

215 tic properties of the novel third-generation TSPO PET ligand (18)F-GE180 in humans: 2TCM4k is the opt

216 esent study uses the novel second-generation TSPO PET radioligand [(18)F]FEPPA to evaluate whether mi

217 The enhanced TSPO PET signal that arises during disease is widely con

218 ND) Conclusion: Our findings suggest that in TSPO PET studies, nondisplaceable binding can differ bet

219 ed for head-to-head comparisons of promising TSPO PET tracers across different disease states.

220 gether with 136 18-kDa translocator protein (TSPO) PET scans for microglial activation.

221 Since 18-kDa translocator protein (TSPO) plays an important role in regulating mitochondria

222 The translocator protein (TSPO), previously known as the peripheral benzodiazepine

223 ction of the mammalian translocator protein (TSPO; previously known as the peripheral benzodiazepine

224 To relate TSPO protein expression to ligand binding, specific bind

225 confocal laser scanning microscopy to verify TSPO protein in neuronal and non-neuronal cell populatio

226 cal laser scanning microscopy confirmed that TSPO protein is present in neuronal and non-neuronal (as

227 imaging of the 18-kDa translocator protein (TSPO) provides a biomarker for microglia, the primary im

228 remitting MS patients were studied using the TSPO radioligand (11)C-(R)-PK11195.

229 ts and 16 healthy controls using PET and the TSPO radioligand [(11)C]PBR28.

230 TSPO radioligand binding was increased up to seven times

231 TSPO radioligand uptake was increased in the brains of M

232 binding status, underwent PET scanning with TSPO radioligands ((11)C-PBR28 or (18)F-PBR111).

233 ynamic biomarker for ALS multicenter trials, TSPO radioligands have some challenges to overcome.

234 an be visualized using translocator protein (TSPO) radioligands.

235 uman PET imaging using the second-generation TSPO radiotracer [(11)C]DPA-713 revealed a strong trend

236 (MR-PET) scanner with the second-generation TSPO radiotracer [(11)C]PBR28.

237 inform previous PET studies reporting lower TSPO radiotracer concentrations in the brain (measured a

238 his study were to screen novel, fluorinated, TSPO radiotracers for susceptibility to the rs6971 genet

239 , the application of these second-generation TSPO radiotracers has revealed additional problems, incl

240 patients relative to healthy controls with 2 TSPO radiotracers.

241 agy, we also investigated the changes in the TSPO-related pathway.

242 en NLRP3-related inflammasome activation and TSPO-related proteins.

243 o)lipoprotein and human serum, while loss of TSPO resulted in impaired cholesterol efflux.

244 TSPO-/- RPE cells also had significantly increased produ

245 and accumulation were markedly increased in TSPO-/- RPE cells.

246 All analyses were corrected for TSPO rs6971 polymorphism (which is implicated in differe

247 development of any improved radioligand for TSPO should consider the possibility that in vitro prope

248 firm these findings and to determine whether TSPO signal and white matter changes in young NFL athlet

249 brain injury and repair, indicated by higher TSPO signal and white matter changes, may be associated

250 The ambiguity of conceiving TSPO simply as a biomarker of 'neuroinflammation' or 'mi

251 d immunohistochemical analyses confirmed the TSPO small-animal PET findings.

252 timulating cellular cholesterol removal with TSPO specific ligands or by overexpression of TSPO in RP

253 We demonstrate in RPE cells that TSPO specific ligands promoted cholesterol efflux to acc

254 eat deal of work into the development of new TSPO-specific PET radiotracers.

255 arker for BAT imaging using [(18)F]-F-DPA, a TSPO-specific PET tracer.

256 Participants underwent a PET scan using the TSPO-specific radioligand [(11)C](R)-PK11195.

257 vivo using positron emission tomography and TSPO-specific radioligands.

258 pression of TSPO and specific binding of two TSPO targeting radioligands (3H-PK11195 and 3H-PBR28) in

259 ic information about the regional density of TSPO than the 2TC.

260 27 were independent of translocator protein (TSPO), the reported target for this small molecule, and

261 In clinical studies of TSPO, the ligand total distribution volume, V(T), is fre

262 The analyses also reveal the role of TSPO, TP53, and many other immune or cell cycle related

263 med in vivo findings demonstrating increased TSPO tracer uptake in infarcted versus contralateral bra

264 with Pittsburgh compound B ((11)C-PIB) and a TSPO tracer, flutriciclamide ((18)F-GE-180), in the APP2

265 is a second-generation translocator protein (TSPO) tracer with characteristics supposedly superior to

266 hether multicenter data pooling of different TSPO tracers ((11)C-PBR28 and (18)F-DPA714) is feasible,

267 Many TSPO tracers have been developed, however, it is unclear

268 rectly compare 2 promising second-generation TSPO tracers, (11)C-DPA-713 and (18)F-GE-180, for the fi

269 ter than that reported for commonly used PET TSPO tracers.

270 o reduce the complexity of blood analyses of TSPO tracers.

271 ter than that reported for commonly used PET TSPO tracers.

272 ission tomography-based regional measures of TSPO using [11C]DPA-713, diffusion tensor imaging measur

273 rameter sigmoidal model in which PFC and ACC TSPO V(T) accounted for 84% and 92% of the variance, res

274 e primary objective was to determine whether TSPO V(T) in the prefrontal cortex (PFC) and anterior ci

275 ration in the presence of gliosis labeled by TSPO V(T) is associated with greater reduction of sympto

276 Given the predictiveness of TSPO V(T) on symptom reduction, this personalized medici

277 here was no reduction in HDRS scores, but as TSPO V(T) values increased, there was a reduction in HDR

278 At low TSPO V(T) values, there was no reduction in HDRS scores,

279 nslocator protein total distribution volume (TSPO V(T)), measured with positron emission tomography,

280 of treatment was plotted against PFC and ACC TSPO V(T), showing a significant nonlinear relationship.

281 ssion tomography scan to measure PFC and ACC TSPO V(T).

282 The data reported here suggest that TSPO-VDAC complex upregulation in BD patients, the simul

283 issue (BAT) and translocator protein 18 kDa (TSPO) via a combination of disulfiram, an FDA approved d

284 Slightly lower elevations in TSPO VT (22%-29%) were present in other gray matter regi

285 The regional distribution of elevated TSPO VT argues that the autoimmune/neuroinflammatory the

286 sive behaviors significantly correlated with TSPO VT in the orbitofrontal cortex (uncorrected Pearson

287 To determine whether TSPO VT is elevated in the dorsal caudate, orbitofrontal

288 The TSPO VT was measured in the dorsal caudate, orbitofronta

289 In OCD, TSPO VT was significantly elevated in these brain region

290 In bacteria, TSPO was identified to regulate tetrapyrrole metabolism

291 On the other hand, TSPO was markedly upregulated in a mouse model of acute

292 TSPO was not elevated in patients without suicidal think

293 Results: LW223 binding to TSPO was not susceptible to the rs6971 genetic polymorph

294 TSPO was uniformly expressed across myeloid cells irresp

295 TSPO was up-regulated in Iba1(+) cells from brains of pa

296 To fundamentally elucidate the functions of TSPO, we first developed a viable TSPO knockout mouse.

297 Translocator protein (TSPO), which is upregulated in activated glia (predomina

298 imaging of the 18 kDa translocator protein (TSPO), which is upregulated in activated microglia, is a

299 AT contrast was due to (64)Cu-Dis binding to TSPO, which was further confirmed as a specific biomarke

300 quirements for high-affinity binding to both TSPO wild type (WT) and the polymorphic TSPO A147T.