ライフサイエンスコーパス: neuroinflammation

1 f CD33 reduced amyloid beta accumulation and neuroinflammation.

2 icant additional interest in both cancer and neuroinflammation.

3 throughout infection, and it associated with neuroinflammation.

4 myelitis from murine betacoronavirus-induced neuroinflammation.

5 l migration, extracellular matrix injury and neuroinflammation.

6 proach to model neurodegeneration-associated neuroinflammation.

7 ased NOX2- and NLRP3 inflammasome-associated neuroinflammation.

8 s in the spinal cord and exaggerates ongoing neuroinflammation.

9 croptosis to promote cerebral hemorrhage and neuroinflammation.

10 olecule for regulating neurodegeneration and neuroinflammation.

11 opiate abuse is associated with more severe neuroinflammation.

12 els is associated with neurodegeneration and neuroinflammation.

13 bitor ameliorated disability in experimental neuroinflammation.

14 cal conditions, in particular during chronic neuroinflammation.

15 us, immune-mediated disease that can include neuroinflammation.

16 n, we investigated the NAS mode of action in neuroinflammation.

17 roperties in numerous experimental models of neuroinflammation.

18 Activation of astrocytes is a hallmark of neuroinflammation.

19 y when combined with standard CSF indices of neuroinflammation.

20 essible link between the circadian clock and neuroinflammation.

21 liosis, viral CNS infections, and autoimmune neuroinflammation.

22 eased reactive oxygen species, and excessive neuroinflammation.

23 play their remedial potential by controlling neuroinflammation.

24 ndent pathogenic functions of B cells during neuroinflammation.

25 tracellular Abeta plaques and suppression of neuroinflammation.

26 way from neurons and towards glial cells and neuroinflammation.

27 o effect of its own on sickness behavior and neuroinflammation.

28 rotein NLRP3 inflammasome complex to promote neuroinflammation.

29 nonhuman primate lipopolysaccharide model of neuroinflammation.

30 y curtailing the deleterious consequences of neuroinflammation.

31 etabolite of tryptophan that plays a role in neuroinflammation.

32 7 receptor (P2X7R) is a promising target for neuroinflammation.

33 ficant improvement of synaptic pathology and neuroinflammation.

34 gnition that PGN could contribute to chronic neuroinflammation.

35 filtration of immunoglobulin, and attenuated neuroinflammation.

36 in neurons contributes to the regulation of neuroinflammation.

37 on degeneration/neuronal death and sustained neuroinflammation.

38 tic value of HuR for treatment of autoimmune neuroinflammation.

39 cule 1) markers was performed to investigate neuroinflammation.

40 nfection, indicating enhanced post-traumatic neuroinflammation.

41 ations but enhanced neurogenesis and reduced neuroinflammation.

42 tly reduced hippocampal oxidative stress and neuroinflammation.

43 s for microglial immunometabolism in shaping neuroinflammation.

44 thus highlighting the importance of Kv1.3 in neuroinflammation.

45 ent in the CNS during the inception of acute neuroinflammation.

46 and have been well-documented as inducers of neuroinflammation.

47 nt and in the context of ischemic injury and neuroinflammation.

48 tivation in pain-comorbid NA, identifying in neuroinflammation a potential therapeutic target for thi

49 oring the in vivo spatiotemporal dynamics of neuroinflammation across applications.

50 portant population to study the evolution of neuroinflammation across the Alzheimer's continuum.

51 Development of neuroinflammation agents targeting the translocator prot

52 uld inhibit microglial activation, attenuate neuroinflammation, alter selective gut microbial communi

53 croglia of AD mice, leading to resolution of neuroinflammation, an increase in microglial phagocytosi

54 We report in vivo patterns of neuroinflammation and abnormal protein aggregation in se

55 with cirrhosis results in higher degrees of neuroinflammation and activation of GABAergic and neuron

56 nscriptome profiles of genes associated with neuroinflammation and AD in the hippocampus.

57 , was sufficient to repress aging-associated neuroinflammation and alleviate aging-associated cogniti

58 r cerebral insulin resistance contributes to neuroinflammation and Alzheimer's disease (AD) pathogene

59 meningeal lymphatic drainage could decrease neuroinflammation and ameliorate HE.

60 ecreased microglia activation (P < .001) and neuroinflammation and ameliorated motor dysfunction (P =

61 w, we discuss the interrelationships between neuroinflammation and amyloid and tau pathologies as wel

62 perfusion, and BBB function; and ameliorated neuroinflammation and amyloid deposition in AD mice.

63 for late stage AD cases and show changes in neuroinflammation and amyloid pathologic processes.

64 ing CSF1R inhibitors markedly reduce chronic neuroinflammation and associated neurodegeneration, as w

65 sruption and hemorrhage decreasing cytotoxic neuroinflammation and attenuating the chronic loss of ol

66 zes the most recent advances in the field of neuroinflammation and autonomic control in HF.

67 translation of systemic therapies targeting neuroinflammation and brain tumors.

68 , helped to clear viruses, it also increased neuroinflammation and caused immunopathology in the mous

69 ave been implicated in microglial-associated neuroinflammation and chronic neurodegeneration.

70 uppresses the formation of amyloid deposits, neuroinflammation and cognitive deficits in the AD mouse

71 orced expression of this protein exacerbates neuroinflammation and cognitive dysfunction in an AD mou

72 observing protection against obesity-induced neuroinflammation and cognitive impairment in NLRP3-KO m

73 Using a viral model of neuroinflammation and demyelination, we demonstrate that

74 cally focus on microglia as major players in neuroinflammation and discuss the spatial and temporal v

75 of genes associated with cell proliferation, neuroinflammation and disruption of the blood spinal cor

76 Given the critical role of neuroinflammation and ECM microenvironments in neuroinhi

77 ion or binding unequivocally mirrors ongoing neuroinflammation and emphasize the need to consider non

78 ognitive disorder (HAND) is characterized by neuroinflammation and glial activation that, together wi

79 PET is well suited to quantify neuroinflammation and has the potential to discriminate

80 tors with neurotrophic support or exacerbate neuroinflammation and hasten neuronal cell death.

81 sting a possible causal relationship between neuroinflammation and Ia axon removal.

82 f auto-aggressive T helper (Th) cells during neuroinflammation and identified the signature and patho

83 duces pain associated with EAE by decreasing neuroinflammation and increasing myelination independent

84 ndependently of motor symptoms by decreasing neuroinflammation and increasing myelination.SIGNIFICANC

85 od-brain barrier dysfunction, and markers of neuroinflammation and injury in the cerebrospinal fluid

86 y axis is a potential therapeutic target for neuroinflammation and ischemic stroke.

87 lecular and cellular mechanisms that lead to neuroinflammation and its effect on HF progression remai

88 rmalized, and the neurodegeneration, chronic neuroinflammation and loss of Purkinje cell dendrites ob

89 glia are multifunctional cells that regulate neuroinflammation and maintain homeostasis within the br

90 cute systemic inflammation is able to induce neuroinflammation and may negatively affect neuronal mor

91 MT material colonization was associated with neuroinflammation and microglial activation and dysbiosi

92 Neuroinflammation and necroptosis are major contributors

93 ic dysfunction before TBI leads to increased neuroinflammation and negative cognitive outcomes.

94 and other cells in the CNS in the context of neuroinflammation and neurodegeneration and discuss how

95 ins, improved behavioral deficits, decreased neuroinflammation and neurodegeneration, and increased s

96 nhibition of IFN-beta reduces post-traumatic neuroinflammation and neurodegeneration, resulting in im

97 on the remarkable suppression of LPS-induced neuroinflammation and neurodegeneration-associated mitoc

98 en under ART, are believed to occur, causing neuroinflammation and neurological disorders in HIV-infe

99 irs remains detectable, which contributes to neuroinflammation and neurological disorders in HIV-infe

100 tivation in CNS reservoirs, thereby reducing neuroinflammation and neurological disorders in HIV-infe

101 Rise in both neuroinflammation and neuronal injury markers can be rev

102 neuroinjury and a potential drug target for neuroinflammation and other disorders.

103 proteasome and autophagy-lysosomal systems), neuroinflammation and oxidative stress.

104 can release the alarmin IL-1alpha, promoting neuroinflammation and parasite control.

105 indings indicate a close association between neuroinflammation and protein aggregation in frontotempo

106 n in pEVs contributes to the perpetuation of neuroinflammation and relapses in disease.

107 ary tumor resection attenuates tumor-induced neuroinflammation and sickness behavior following an imm

108 ifests the infiltration of T cells to induce neuroinflammation and subsequently white matter injury.

109 rodegenerative disease mechanisms, including neuroinflammation and synaptic dysfunction, and to demon

110 We tested the hypothesis that neuroinflammation and tau protein aggregation colocalize

111 l link between LMP2/Y and microglia-mediated neuroinflammation and that inhibition of these subunits

112 We hypothesised that neuroinflammation and the microglial TLR2-system may act

113 is significantly lower, while the associated neuroinflammation and the neurologic deficits are dramat

114 he effect of revascularization on poststroke neuroinflammation and the role of anti-inflammatory stra

115 recovery in association with hyperglycemia, neuroinflammation, and atrophy of PV(+) interneurons.

116 cubation period, prion protein accumulation, neuroinflammation, and changes in macroautophagy.

117 e blood-brain barrier, astrocyte activation, neuroinflammation, and cognitive and behavioral alterati

118 of RT-induced complement cascade activation, neuroinflammation, and cognitive dysfunction, we used a

119 uced the infiltration of T cells, attenuated neuroinflammation, and decreased alpha-synucleinopathy i

120 t with increased prion protein accumulation, neuroinflammation, and decreased autophagy.

121 lls is essential for leukocyte infiltration, neuroinflammation, and demyelination in experimental aut

122 lating proinflammatory cytokines, monocytes, neuroinflammation, and depressive and anxiety-like behav

123 nd cognition, attenuating neuropathology and neuroinflammation, and enhancing resistance to defined p

124 n of spines in the prefrontal cortex, induce neuroinflammation, and increase AD biomarkers in the cer

125 Tau pathology, neuroinflammation, and neurodegeneration are key aspects

126 antly more seizures, higher clinical scores, neuroinflammation, and neuronal damage (mainly in the CA

127 G signaling in aging, neurodegeneration, and neuroinflammation, and on therapeutic implications.

128 genes associated with astrocyte activation, neuroinflammation, and oxidative stress in FBN-ARO-KO mi

129 act of metabolic reprogramming on microglia, neuroinflammation, and subsequently on brain function is

130 a relationship between disease time course, neuroinflammation, and the autophagic stress response, a

131 of activated microglia and a proxy index of neuroinflammation; and (ii) 18F-AV-1451, a radioligand w

132 differences in subcortical tau pathology and neuroinflammation are linked to clinical severity.

133 Neuronal mitochondria dysfunction and neuroinflammation are two prominent pathological feature

134 l outcomes were also associated with reduced neuroinflammation as measured by a reduction in activate

135 f the cortex (P < .001) as well as increased neuroinflammation, as indicated by significant increases

136 barrier integrity, reduced astrogliosis and neuroinflammation, as well as improved cognition and beh

137 otor symptoms, and contribute to the chronic neuroinflammation associated with PD pathology.

138 ng of Mfn2 may present a novel treatment for neuroinflammation-associated diseases.

139 present a model system to study drug-induced neuroinflammation at single-cell resolution.

140 thway analyses implicate LXR/RXR activation, neuroinflammation, atherosclerosis signaling, and amyloi

141 on of IFN-beta signaling resulted in reduced neuroinflammation, attenuated neurobehavioral deficits,

142 s that attribute to diseases such as chronic neuroinflammation, autoimmunity, CNS injury, and more.

143 es in lesion size, fibrotic scar, gliosis or neuroinflammation between groups.

144 n, quantification, and tracking of different neuroinflammation biomarkers in living subjects longitud

145 ntribute to delirium pathogenesis, including neuroinflammation, brain vascular dysfunction, altered b

146 ive astrocytic Glia Limitans not only during neuroinflammation but also when BBB integrity is comprom

147 s dispensable with regard to contributing to neuroinflammation, but its deletion enhances remyelinati

148 rotein (TSPO), is a widely used biomarker of neuroinflammation, but its non-selective cellular expres

149 and cell Ca(2+) dysregulation participate in neuroinflammation, but their impact on neuron function i

150 The suppressed neuroinflammation by maternal LB supplementation was ass

151 obstacles to the reliable quantification of neuroinflammation by PET imaging.

152 results suggest that IL-9 reduces autoimmune neuroinflammation by suppressing GM-CSF production by CD

153 titutively a Nox2 enzyme that is involved in neuroinflammation by the generation of reactive oxygen s

154 Reduction in neuroinflammation by using samples from post-FMT patient

155 Neuroinflammation can be caused by various insults to th

156 if chronic and evolving microglial-mediated neuroinflammation can be inhibited or regulated in a pre

157 herapeutically targetable mechanism by which neuroinflammation can stimulate axon loss in neurodegene

158 glia, though important for the initiation of neuroinflammation, cannot establish a protective host im

159 Further, during chronic neuroinflammation CNS-infiltrating macrophages and not p

160 We show that tau pathology and neuroinflammation colocalize in PSP, and that individual

161 and age-related neurological diseases, where neuroinflammation contributes to disease progression.

162 This work thus demonstrates that poststroke neuroinflammation contributes to hemorrhagic transformat

163 Furthermore, although PET imaging of neuroinflammation does not have an established clinical

164 We studied how complement-dependent neuroinflammation drives the pathophysiology behind thes

165 s/encephalitis, neuroborreliosis, autoimmune neuroinflammation (due to anti-N-methyl-D-aspartate rece

166 r of these symptoms, yet cellular sources of neuroinflammation during malignancy are unknown.

167 The mechanism of initiation of neuroinflammation during SAE, which ultimately leads to

168 glial cells in initiating and driving acute neuroinflammation during SAE.

169 our data suggest that miR-124 could inhibit neuroinflammation during the development of PD by target

170 ondary injury processes including persistent neuroinflammation evolve over time and can contribute to

171 ivation of inflammatory cells and subsequent neuroinflammation following traumatic brain injury (TBI)

172 ychosine-induced demyelination and secondary neuroinflammation from galactosylceramide storage in mac

173 ncurable neurodegenerative disorder in which neuroinflammation has a critical function(1).

174 ed with innate immune functions suggest that neuroinflammation has a prominent role in the pathogenes

175 Neuroinflammation has been implicated in amyotrophic lat

176 ed cognitive impairments, synaptic loss, and neuroinflammation, highlighting the potential for C1q as

177 Virus infection of the brain triggers neuroinflammation; however, the role of neuroinflammatio

178 ions correlated strongly with CSF markers of neuroinflammation (ie, leukocyte count, lactate concentr

179 cal interaction between oxidative stress and neuroinflammation, impacting on PVI/PNN integrity.

180 reservoirs, thereby reducing HIV-associated neuroinflammation.IMPORTANCE Brain-resident microglia an

181 o contributes to immunopathology by inducing neuroinflammation.IMPORTANCE Developing targeted treatme

182 n ("survivors") in mice affects behavior and neuroinflammation in a nyctohemeral (day versus night)-d

183 k function as AD progresses, and whether the neuroinflammation in AD is reversible, as the basis of i

184 brain may contribute to Abeta deposition and neuroinflammation in AD.

185 s are viewed as triggers of cytotoxicity and neuroinflammation in Alzheimer disease (AD).

186 glial density, mitochondrial energetics, or neuroinflammation in ASD, alongside widespread starkly a

187 ration of hNSC-derived EV abrogates RICD and neuroinflammation in cranially irradiated wild-type rode

188 o support the strategy for targeting tau and neuroinflammation in disease-modifying therapy against A

189 vides further support for genetic control of neuroinflammation in disease.

190 the relative expression of tau pathology or neuroinflammation in distinct groups of brain regions.

191 lity of hippocampal circuits associated with neuroinflammation in epilepsy and other neurologic disor

192 tin dynamics and branching, protects against neuroinflammation in experimental autoimmune encephalomy

193 cuses on cellular and molecular mediators of neuroinflammation in HF and in particular on brain regio

194 enzyme heme oxygenase-1 (HO-1) and increased neuroinflammation in individuals with cognitive impairme

195 complement inhibition to suppress poststroke neuroinflammation in mice with or without concurrent rep

196 ignificantly inhibited neurodegeneration and neuroinflammation in multiple animal models of PD.

197 etween neuronal mitochondria dysfunction and neuroinflammation in neurodegeneration.SIGNIFICANCE STAT

198 volved in both mitochondrial dysfunction and neuroinflammation in neurodegenerative diseases.

199 -mediated signaling mechanism that amplifies neuroinflammation in PD.

200 igh saturated fat diets increase gliosis and neuroinflammation in reward-related brain regions, which

201 We examined neuroinflammation in the auditory cortex following noise

202 ng pathway via regulating microglia-mediated neuroinflammation in the brain.

203 ally, we will comment on what is known about neuroinflammation in the context of preserved vs. reduce

204 ed microglial genes, but this was not due to neuroinflammation in the Mef2c-Het cortex.

205 ent work has highlighted a potential role of neuroinflammation in the NAcc in animal models of diet-i

206 Necroptosis promotes further cell death and neuroinflammation in the pathogenesis of several neurode

207 gers neuroinflammation; however, the role of neuroinflammation in the pathogenesis of viral encephali

208 The data demonstrated that PD increases neuroinflammation in WT mice and disrupts the neuroinfla

209 Potential drivers of such neuroinflammation include toll-like receptors (TLRs).

210 rain cell death at 48 h, despite evidence of neuroinflammation, including the greatest increases in m

211 gulation of long genes, signs of DNA damage, neuroinflammation, increased poly(ADP-ribose) polymerase

212 Here, we focused on the effects of chronic neuroinflammation induced by lipopolysaccharides on hipp

213 t from cytokine changes in response to acute neuroinflammation induced by lipopolysaccharides.

214 MS), a progressive disorder characterized by neuroinflammation-induced demyelination in the central n

215 rm plate can contribute to the management of neuroinflammation-induced fluid accumulation and immune

216 Neuroinflammation is a key contributor to the pathology

217 Neuroinflammation is a key pathologic hallmark of numero

218 Numerous studies demonstrate that neuroinflammation is a key player in the progression of

219 Neuroinflammation is an important contributor to neurona

220 Because neuroinflammation is common to many neurodegenerative di

221 nt stem cell (hiPSC)-based in vitro model of neuroinflammation is demonstrated.

222 Noise-induced neuroinflammation is implicated in auditory processing d

223 Neuroinflammation is important in amyotrophic lateral sc

224 Microglial-mediated neuroinflammation is induced after severe TBI and contri

225 Neuroinflammation is involved in the pathogenesis of sev

226 Neuroinflammation is known to accelerate disease progres

227 titial motility patterns of Treg cells limit neuroinflammation is not well understood.

228 Although neuroinflammation is often depicted as detrimental, ther

229 Neuroinflammation is one of the hallmarks of Parkinson's

230 Though the exact mechanism of BD is unknown, neuroinflammation is one of the numerous investigated et

231 This case series suggests that neuroinflammation is part of the pathophysiology of fami

232 solute statement cannot be concluded whether neuroinflammation is present in BD due to the large numb

233 neurologic disorders.SIGNIFICANCE STATEMENT Neuroinflammation is thought to have a pathogenetic role

234 Prenatal stress-induced fetal neuroinflammation is thought to underlie aberrant neurod

235 to microglia influences pathological retinal neuroinflammation is unclear.

236 Cyclooxygenase-1 (COX-1), a biomarker for neuroinflammation, is implicated in the progression and

237 key pathophysiological processes, including neuroinflammation, lysosomal function and synaptic healt

238 (E60) alone caused the greatest increase in neuroinflammation, mainly in the ipsilateral striatum an

239 f neuronal mitochondria in the regulation of neuroinflammation, male and female transgenic mice with

240 Neuroinflammation manifested in PD mice warranted target

241 gically heterogeneous, but processes such as neuroinflammation may be common across the disease spect

242 to proinflammatory cytokines released during neuroinflammation may be deleterious and contribute to n

243 Because neuroinflammation may promote the onset and progression

244 the crosstalk between neurotransmission and neuroinflammation may underlie some of these cognitive c

245 tau pathology (measured by 18F-AV-1451 PET), neuroinflammation (measured by 11C-PK11195 PET) and brai

246 ion in the developing brain across models of neuroinflammation-mediated injury (mouse, zebrafish) and

247 Cirr-Hum mice had greater neuroinflammation, microglial/glial activation, and GABA

248 ntional cirrhotic mice had higher degrees of neuroinflammation, microglial/glial activation, GABA sig

249 causality, our study suggests that targeting neuroinflammation might represent a novel therapeutic st

250 nant strain of MHV-A59)-induced experimental neuroinflammation model to compare the disease in CD4(-/

251 ing, and has synergistic effects in inducing neuroinflammation, monocytic infiltrates, synaptic defec

252 e model profoundly reduced Tau accumulation, neuroinflammation, neuronal and synaptic loss, and also

253 ponses and could therefore contribute to the neuroinflammation observed in various neurodegenerative

254 neurons to model the effects of hypoxia and neuroinflammation on BBB function.

255 and tau pathologies as well as the effect of neuroinflammation on the disease trajectory in AD.

256 lation, glutamate/NMDA receptor dysfunction, neuroinflammation or redox imbalance, all appear to conv

257 nabolic metabolism fail to induce autoimmune neuroinflammation or to develop into T(H)1-like cells, b

258 odendroglia did not affect clinical disease, neuroinflammation, or demyelination, yet there was incre

259 Neuroinflammation orchestrated by activated microglia/ma

260 iptome and altered gene pathways involved in neuroinflammation, oxidative stress, and neuroplasticity

261 -m represents a new therapeutic strategy for neuroinflammation pain associated with mixed neuropathie

262 cascade of cellular responses, which produce neuroinflammation, partly due to microglial activation.

263 Astrocytes are pivotal regulators of neuroinflammation, playing either detrimental or benefic

264 ons, and a growing body of evidence suggests neuroinflammation plays a crucial role in HF.

265 Neuroinflammation plays a key role in neuronal injury af

266 and microglia or astrocytes, suggesting that neuroinflammation plays a less causal role in PD than AD

267 parietal tau pathology and anterior temporal neuroinflammation predict cognitive decline in patients

268 n innate immune response that contributes to neuroinflammation processes.

269 cal tau pathology (R = 0.667, p = 0.003) and neuroinflammation (R = 0.788, p < 0.001).

270 n to investigate the underlying mechanism of neuroinflammation, rather than focusing on peripheral im

271 ggest that future studies should address how neuroinflammation relates to network function as AD prog

272 We investigated how neuroinflammation relates to the localization of tau and

273 periphery, but the role of the core clock in neuroinflammation remains poorly understood.

274 l Mfn2, this study centered on Mfn2-mediated neuroinflammation reveals novel molecular mechanisms tha

275 l risk for developing MS, showed subclinical neuroinflammation (SCNI) with small MRI lesions.

276 ith the glucocorticoid receptor singling and neuroinflammation signaling pathways.

277 h1 activation pathways and downregulation of neuroinflammation signaling pathways.

278 ls, a type of innate lymphocytes, alleviates neuroinflammation, stimulates neurogenesis, and improves

279 Brain damage, neuroinflammation, stroke-induced neurogenesis, and atro

280 he fibrinogen binding motif to CD11b reduced neuroinflammation, synaptic deficits, and cognitive decl

281 Moreover, in neuroinflammation, the stimulation of CB2R, overexpresse

282 neurons are thought to trigger glia-mediated neuroinflammation, thus increasing neuronal death.

283 d exists for reliable in-vivo measurement of neuroinflammation to better characterise the inflammator

284 The contribution of neuroinflammation to the pathogenesis of neurological co

285 O has yielded valuable clinical data linking neuroinflammation to various neurodegenerative diseases,

286 d the relationship between tau pathology and neuroinflammation using [(11) C]PK11195 and [(18) F]AV-1

287 ctional relationship between SVD and in vivo neuroinflammation using [(11)C]PK11195 positron emission

288 ism in which gamma-secretase is modulated by neuroinflammation via IFITM3 and the risk of Alzheimer's

289 tability via glutamate receptor function and neuroinflammation via other KP metabolites.

290 Neuroinflammation was assessed using [(11)C]PK11195 PET

291 157 (or PERK knockdown) the whole cascade of neuroinflammation was attenuated and improved cognitive

292 d histopathological data.RESULTSEvidence for neuroinflammation was observed in 32% (n = 16 of 50) of

293 n did 18F-AV-1451: distinct spatial modes of neuroinflammation were associated with different frontot

294 at the 4-month level, while LB formation and neuroinflammation were significantly, though incompletel

295 er induction of IFNbeta has any influence on neuroinflammation, which is the primary reason for morbi

296 -synuclein processing and microglia-mediated neuroinflammation, which may initiate the disease proces

297 taining was performed to correlate extent of neuroinflammation with [(64)Cu]Cu-c[E(4)W(5)C] PET signa

298 ggests the therapeutic potential of treating neuroinflammation with an oral inhibitor of the NLRP3 in

299 Chronic neuroinflammation with sustained microglial activation o

300 in human microglial cells and contributes in neuroinflammation within the CNS.