ライフサイエンスコーパス: DLPFC

1 DLPFC activity is modulated by the ascending cholinergic

2 DLPFC and insula GMV represent promising biomarkers for

3 DLPFC GABA content did not predict performance sensitivi

4 DLPFC may be an important target for neurostimulation th

5 DLPFC neurons encoded signals related to both task-relev

6 DLPFC rTMS reduced punishment for wrongful acts without

7 and Glu (neuron-related metabolites) in ACC, DLPFC, hippocampus, and thalamus.

8 They underwent 7T (1)H-MRS of the ACC, DLPFC, hippocampus, and thalamus and performed a visuosp

9 In addition, DLPFC virtual lesion eradicated any modulation of motor

10 (WGCNA) was applied to RNA-quality-adjusted DLPFC RNA-Seq data from the LIBD Postmortem Human Brain

11 Altered DLPFC activation is implicated in a number of human psyc

12 groups had significantly decreased amygdala-DLPFC FC.

13 The altered FC of amygdala-DLPFC is associated with duration of IA.

14 n between DLPFC GSH and both whole-brain and DLPFC-specific gray matter FW in SZ (r = -.48 and -.47,

15 DLPFC NAA and anterior cingulate cortex and DLPFC Glu levels.

16 ith schizophrenia within the hippocampus and DLPFC, with little overlap between the brain regions.

17 rity, increased activation in the insula and DLPFC, and decreased DLPFC Glx.

18 gnitude of LDX-induced change in insular and DLPFC activation.

19 fficulties include modulation of insular and DLPFC recruitment as well as decrease in DLPFC Glx conce

20 tly changed, in parvalbumin interneurons and DLPFC gray matter.

21 ctivation in the insula, dorsomedial PFC and DLPFC increased over time.

22 diated by top-down inputs from both pSTS and DLPFC.

23 us, but also by top-down input from pSTS and DLPFC.SIGNIFICANCE STATEMENT Observation of object lifti

24 icant deactivation across both the VLPFC and DLPFC (P < 0.05).

25 confirmed decision-making predicts VLPFC and DLPFC deactivation (z = -2.62, P < 0.05).

26 We applied DLPFC and 12 GTEx-brain predictors to 40,299 schizophren

27 xibility, and thus the collaboration between DLPFC and TPJ might serve as a more appropriate mechanis

28 s a significant negative correlation between DLPFC GSH and both whole-brain and DLPFC-specific gray m

29 However, to what extent L3PNs differ between DLPFC and other association cortical areas is less clear

30 the previously observed differences between DLPFC and PPC neuron activity during working memory task

31 Our findings reveal a link between DLPFC structure and an individual's propensity to gain f

32 or the differences in L3PN phenotype between DLPFC and PPC.

33 ecreased repetition suppression in bilateral DLPFC.

34 to be differentially expressed, and in both DLPFC and hippocampus none of the individual immune path

35 We found that in both DLPFC and PPC, L3PNs were divided into regular spiking (

36 HD-tDCS than under sham stimulation in both DLPFC groups.

37 itional, yet crucial role of TPJ: a combined DLPFC/TPJ activity predicted flexibility, regardless of

38 in humans and implicate factors controlling DLPFC GABA content in the neural mechanisms of WM and it

39 Among controls, DLPFC stimulation led to a reciprocal attenuation of MPF

40 postmortem Dorso-Lateral Pre-Frontal Cortex (DLPFC) samples in the CommondMind Consortium (CMC) and t

41 pathways in dorsolateral prefrontal cortex (DLPFC) (144 schizophrenia and 196 control subjects) and

42 maller right dorsolateral prefrontal cortex (DLPFC) (i.e., middle and superior frontal gyri) and insu

43 ncluding the dorsolateral prefrontal cortex (DLPFC) and appear to arise during the protracted maturat

44 ver the left dorsolateral prefrontal cortex (DLPFC) and cathodal tDCS over the right DLPFC for 30 min

45 in both the dorsolateral prefrontal cortex (DLPFC) and orbitofrontal cortex (OFC).

46 cells in the dorsolateral prefrontal cortex (DLPFC) appears to contribute to cognitive dysfunction in

47 and the left dorsolateral prefrontal cortex (DLPFC) as our regions of interest, we found no differenc

48 of the left dorsolateral prefrontal cortex (DLPFC) as well as left M1.

49 of the left dorsolateral prefrontal cortex (DLPFC) as well as on the integrity of the left arcuate f

50 us (pSTS) or dorsolateral prefrontal cortex (DLPFC) before having participants perform the task.

51 of the left Dorsolateral Prefrontal Cortex (DLPFC) can improve implicit, procedural learning of word

52 e postmortem dorsolateral prefrontal cortex (DLPFC) derived from 17 patients and age-matched and sex-

53 ation of the dorsolateral prefrontal cortex (DLPFC) during WM performance and the association with gl

54 ion state in dorsolateral prefrontal cortex (DLPFC) from 22 pairs of SZ and matched comparison subjec

55 signal, and dorsolateral prefrontal cortex (DLPFC) glutamate+glutamine (Glx) were measured using a c

56 obtained for dorsolateral prefrontal cortex (DLPFC) gray matter and layer 3 and layer 5 pyramidal neu

57 CS) over the dorsolateral prefrontal cortex (DLPFC) has been effective in modulating attention.

58 Although the dorsolateral prefrontal cortex (DLPFC) has long been considered critical for WM, we stil

59 how that the dorsolateral prefrontal cortex (DLPFC) implements a flexible value code based on object-

60 role of the dorsolateral prefrontal cortex (DLPFC) in regulating aggression.

61 mes that the dorsolateral prefrontal cortex (DLPFC) is causally involved in this adjustment.

62 Dorsolateral prefrontal cortex (DLPFC) maintains goal representations in a context-depen

63 sed genes of dorsolateral prefrontal cortex (DLPFC) neurons.

64 teins in the dorsolateral prefrontal cortex (DLPFC) of 22 matched pairs of elderly SCZ and comparison

65 amate in the dorsolateral prefrontal cortex (DLPFC) of patients with schizophrenia.

66 orted in the dorsolateral prefrontal cortex (DLPFC) of schizophrenia subjects.

67 these TFs in dorsolateral prefrontal cortex (DLPFC) of SCZ patients.

68 hways in the dorsolateral prefrontal cortex (DLPFC) of subjects with schizophrenia and control subjec

69 of the right dorsolateral prefrontal cortex (DLPFC) on working memory performance, while measuring ta

70 he extent of dorsolateral prefrontal cortex (DLPFC) plasticity in Alzheimer disease (AD) and its asso

71 The dorsolateral prefrontal cortex (DLPFC) plays a pivotal role in automating this process o

72 The dorsolateral prefrontal cortex (DLPFC) plays a pivotal role in executive function, inclu

73 of the left dorsolateral prefrontal cortex (DLPFC) predicted an individual's response to training.

74 a, and right dorsolateral prefrontal cortex (DLPFC) regions supported the stress processing and react

75 the primate dorsolateral prefrontal cortex (DLPFC) supports a range of cognitive functions.

76 ere lower in dorsolateral prefrontal cortex (DLPFC) tissue from donors with SCZ compared with control

77 nel for the dorso-lateral prefrontal cortex (DLPFC) to create a set of gene expression predictors and

78 of the left dorsolateral prefrontal cortex (DLPFC) to subgenual anterior cingulate cortex (sgACC) ci

79 ack from the dorsolateral prefrontal cortex (DLPFC) to V1.

80 red from the dorsolateral prefrontal cortex (DLPFC) using combined transcranial magnetic stimulation

81 ion in human dorsolateral prefrontal cortex (DLPFC) using spectral imaging and dotdotdot to mask lipo

82 ex and right dorsolateral prefrontal cortex (DLPFC) were compared via 4-tesla proton single volume ma

83 la, pACC and dorsolateral prefrontal cortex (DLPFC)) to test the effects of forest, urban green, wate

84 in the left dorsolateral prefrontal cortex (DLPFC), a region of the brain that plays a key role in t

85 e, bilateral dorsolateral prefrontal cortex (DLPFC), and bilateral middle temporal gyrus.

86 amygdala and dorsolateral prefrontal cortex (DLPFC), and had increased negative FC between amygdala a

87 rain regions-dorsolateral prefrontal cortex (DLPFC), hippocampus, and caudate.

88 role for the dorsolateral prefrontal cortex (DLPFC), relatively intact function of ventrolateral pref

89 ganglia, the dorsolateral prefrontal cortex (DLPFC), the dorsal anterior cingulate cortex (dACC), the

90 post-mortem dorsolateral prefrontal cortex (DLPFC), we found striking decreases in tyrosine phosphor

91 ified in the dorsolateral prefrontal cortex (DLPFC), we observed lower complexity and substantial dep

92 (L5) of the dorsolateral prefrontal cortex (DLPFC), we sought to determine if transcriptome alterati

93 ity from the dorsolateral prefrontal cortex (DLPFC), which is of considerable interest in MDD.

94 erved by the dorsolateral prefrontal cortex (DLPFC).

95 of GAD25 in dorsolateral prefrontal cortex (DLPFC).

96 ction of the dorsolateral prefrontal cortex (DLPFC).

97 the primate dorsolateral prefrontal cortex (DLPFC).

98 eft or right dorsolateral prefrontal cortex (DLPFC).

99 ncluding the Dorsolateral Prefrontal Cortex (DLPFC).

100 tDCS) of the dorsolateral prefrontal cortex (DLPFC).

101 ivity in the dorsolateral prefrontal cortex (DLPFC).

102 between left dorsolateral prefrontal cortex (DLPFC)/inferior frontal gyrus (IFG) and posterior cingul

103 essed in the dorsolateral prefrontal cortex (DLPFC): UNC5C, ENC1, and TMEM106B.

104 d (bilateral dorsolateral prefrontal cortex, DLPFC) rsFC analysis was performed.

105 ocampi and dorsolateral prefrontal cortices (DLPFCs) from 551 individuals (286 with schizophrenia).

106 ation in the insula and DLPFC, and decreased DLPFC Glx.

107 and a potential treatment target to enhance DLPFC function and working memory in patients with AD.

108 and GSH/creatine ratios were calculated for DLPFC (SZ: n = 33, HC: n = 37) and visual cortex (SZ: n

109 EEG to assess inhibition and excitation from DLPFC.

110 l and morphological phenotypes of L3PNs from DLPFC and PPC.

111 L3PNs from DLPFC had greater diversity of physiological properties

112 medicated patient group demonstrated higher DLPFC activation (P = .02) and better behavioral perform

113 tern of genes coexpressed with DRD2 in human DLPFC.

114 ficial and middle laminar zones of the human DLPFC.

115 s superficial and middle layers of the human DLPFC.

116 ions of each PV neuronal population to human DLPFC function requires a detailed examination of their

117 Participants with AD had impaired DLPFC plasticity (mean [SD] potentiation, 1.18 [0.25]) c

118 ne whether participants with AD had impaired DLPFC plasticity compared with healthy control participa

119 of cognitive deficits in Sz, where impaired DLPFC-related cognitive control has a broad impact acros

120 In DLPFC gray matter, 41% of mitochondrial-related genes we

121 In DLPFC L3 and L5 pyramidal cells, transcriptome alteratio

122 In DLPFC, 23 immune genes were found to be differentially e

123 (RS-L3PN:B-L3PN, 94:6), but were abundant in DLPFC (50:50), showing greater physiological diversity.

124 lysis we established that neural activity in DLPFC is high both when 'on-task' under demanding condit

125 ndings suggest that molecular alterations in DLPFC L3 and L5 pyramidal cells might be characteristic

126 he activity of excitatory pyramidal cells in DLPFC layer 3 and, to a lesser extent, in layer 5.

127 c single-neuron and population value code in DLPFC that advances from reward experiences to economic

128 association with glutamate concentration in DLPFC depending on medication status.

129 and DLPFC recruitment as well as decrease in DLPFC Glx concentration.

130 ated inhibitory neurotransmission deficit in DLPFC could lead to hyperexcitability and, potentially n

131 any studies have profiled gene expression in DLPFC gray matter in schizophrenia, little is known abou

132 These oscillations are generated in DLPFC layer 3 (L3) via reciprocal connections between py

133 oscopy ((1)H-MRS) investigating glutamate in DLPFC.

134 ealed that children with larger increases in DLPFC activity from middle to late childhood showed stro

135 in the proportion of intragenic novel L1s in DLPFC of PDS.

136 e ARP2/3 complex were significantly lower in DLPFC layer 3 and 5 pyramidal cells in schizophrenia.

137 oup were observed for myo-inositol (mIns) in DLPFC and hippocampus and total choline (tCho) in ACC.

138 Results indicate similar modulation in DLPFC as seen previously.

139 r levels of glutamate (Glu) were observed in DLPFC.

140 ater complexity of computations performed in DLPFC.

141 r memory-related cortical regions, including DLPFC, thus supporting a specific hippocampal contributi

142 rain-behavior analyses showed that increased DLPFC activation after negative feedback was associated

143 orm a reward-based foraging task, individual DLPFC neurons signal the value of specific choice object

144 white matter structural integrity between L-DLPFC and thalamus, two key components of the neuromodul

145 .0001), and a positive correlation between l-DLPFC GABA levels, but not Glx, and minimal oxygen satur

146 , there was a negative correlation between l-DLPFC GABA levels, but not Glx, and SDB severity by AHI

147 n the left dorsolateral prefrontal cortex (l-DLPFC) and bilateral hippocampal regions of 19 older adu

148 Left dorsolateral prefrontal cortex (L-DLPFC) tDCS induced an analgesic effect, which was expla

149 In subjects with SDB, levels of l-DLPFC GABA, but not Glx, were significantly lower than i

150 higher task-related frontal activation (left DLPFC, N2>N0), which disappeared after real-rTMS.

151 orsal anterior cingulate cortex (dACC), left DLPFC, hippocampus, and left insula, suggested a stress

152 ncreased withdrawal symptoms, decreased left DLPFC and increased PCC BOLD percent signal change (abst

153 Specific decreases of activity from left DLPFC in the end compared to beginning or middle of impr

154 OLD responses in the right hippocampus, left DLPFC, left ACC during encoding; and in the bilateral hi

155 tion of abstinence-induced decreases in left DLPFC activation and reduced suppression of PCC may be a

156 up-regulating the cortical function in left DLPFC and left M1 with tDCS.

157 significantly reduced WM activation in left DLPFC in medicated patients and a trendwise reduction in

158 onance imaging, and local activation in left DLPFC was measured.

159 mate concentration and WM activation in left DLPFC, with a positive association in unmedicated patien

160 We estimated glutamate in left DLPFC.

161 isational performance and modulation in left DLPFC.

162 ving simultaneous anodal stimulation of left DLPFC and cathodal stimulation of right DLPFC (bipolar-b

163 changes following tDCS over left M1 or left DLPFC in learning a complex bimanual task.

164 ree separate sessions of HD-tDCS (sham, left DLPFC and right DLPFC) for 20 min.

165 Given that left DLPFC has been proposed as an explicit target of depress

166 er repeated anodal tDCS targeted at the left DLPFC (compared with sham tDCS) has an immediate effect

167 We collected MRS measurements in the left DLPFC and left striatum during tDCS and an additional MR

168 orrelated with Glx concentration in the left DLPFC at baseline.

169 term tDCS.Short-term anodal tDCS of the left DLPFC did not have an immediate effect on ad libitum foo

170 results indicated that HD-tDCS over the left DLPFC differentially modulated right fronto-visual funct

171 nd an additional MRS measurement in the left DLPFC immediately after the end of stimulation.

172 We conclude that cathodal tDCS over the left DLPFC might facilitate the relaxation of learned constra

173 o individually target the region of the left DLPFC most anticorrelated with sgACC in each participant

174 GABA normalized by water signal) in the left DLPFC of individuals with ASD than that of TD controls.

175 Magnetic Stimulation was applied to the left DLPFC or to the control site before the Hebb task.

176 cal activity) or sham tDCS aimed at the left DLPFC.

177 ng cathodal, anodal or sham tDCS to the left DLPFC.

178 r gamma-aminobutyric acid levels in the left DLPFC.

179 Smokers showed lower DLPFC NAA, Cr, mI and Glu concentrations and lower lenti

180 We found that individuals with lower DLPFC GABA showed greater performance degradation with h

181 We used fMRI to measure DLPFC/TPJ activity recruited during moral flexibility, a

182 athway were assessed in laser-microdissected DLPFC layer 3 and 5 pyramidal cells and layer 3 parvalbu

183 athway were assessed in laser-microdissected DLPFC layer 3 and 5 pyramidal cells and layer 3 parvalbu

184 ysiology and morphology of L3PNs from monkey DLPFC and PPC.

185 e compared the properties of L3PNs in monkey DLPFC versus posterior parietal cortex (PPC), a key node

186 h previous ultrastructural studies in monkey DLPFC where Type I PV-IR synapses were not identified in

187 Supporting this interpretation, in monkey DLPFC, higher minor-to-major variant ratios predicted lo

188 d transcriptome of L3PNs from macaque monkey DLPFC and posterior parietal cortex (PPC), two key nodes

189 Moreover, DLPFC L3PNs display larger and more complex basal dendri

190 cance (P<0.05) in an independent post-mortem DLPFC data set (182 schizophrenia and 212 control subjec

191 1) recent findings regarding alterations of DLPFC layer 3 circuitry in schizophrenia, 2) the develop

192 emonstrated greater age-related decreases of DLPFC NAA and anterior cingulate cortex and DLPFC Glu le

193 tions indicated heterozygosity in genomes of DLPFC cells.

194 These results confirm the involvement of DLPFC GABA in WM load processing in humans and implicate

195 gnitive control, but that the involvement of DLPFC in control is not restricted to the left or right

196 e findings indicate a crucial involvement of DLPFC in the normalization processes of emotional attent

197 the use of DLPFC plasticity as a measure of DLPFC function and a potential treatment target to enhan

198 The presumptive added modulation of DLPFC circuitry by the thalamus in human may contribute

199 Plasticity of DLPFC was positively associated with working memory perf

200 ies in these neurophysiological processes of DLPFC in persons with MDD.

201 , or found to a lesser degree, in samples of DLPFC gray matter from the same subjects, suggesting tha

202 ay profiling to analyze the transcriptome of DLPFC L3 PV cells in 36 matched pairs of SZ and unaffect

203 The findings support the use of DLPFC plasticity as a measure of DLPFC function and a po

204 ergic stimulation has detrimental effects on DLPFC representations of task attributes.

205 ver DLPFC, sham tDCS over M1, sham tDCS over DLPFC, or no stimulation.

206 nodal tDCS applied over M1, anodal tDCS over DLPFC, sham tDCS over M1, sham tDCS over DLPFC, or no st

207 To refine optimal stimulation parameters, DLPFC stimulation using two common electrode montages wa

208 Significant dorsolateral PFC (DLPFC) activations were observed during self-paced sutur

209 ional connectivity between dorsolateral PFC (DLPFC) and temporal lobe that mediated the effect of pai

210 carbachol onto neurons in dorsolateral PFC (DLPFC) of male rhesus macaques performing rule-guided pr

211 la and ventral PFC (VPFC), dorsolateral PFC (DLPFC), and dorsal anterior cingulated cortex (dACC) amo

212 Postmortem DLPFC expression data analysis showed decreased expressi

213 cence-activated cell sorting from postmortem DLPFC of 36 PDS and 26 age-matched controls.

214 gnificantly between dorsolateral prefrontal (DLPFC) and sensory areas.

215 primary visual and dorsolateral prefrontal (DLPFC) cortices.

216 Proper DLPFC activity is, in part, maintained by two population

217 e AX-CPT, both patient groups showed reduced DLPFC activity compared with the control group (P = .02

218 Given the roles of PV neurons in regulating DLPFC microcircuits and of PNNs in regulating PV cellula

219 lateral hippocampus, striatum, ACC and right DLPFC during retrieval.

220 The FC between left amygdala and right DLPFC had significant correlation with duration of IA.

221 e an equal involvement of the left and right DLPFC in adaptive control, whereas stimulation of a cont

222 sions of HD-tDCS (sham, left DLPFC and right DLPFC) for 20 min.

223 act of stimulation site (i.e. left and right DLPFC) on neural interactions.

224 left DLPFC and cathodal stimulation of right DLPFC (bipolar-balanced montage) showed reduced vigilanc

225 ed to four HD-tDCS conditions: left or right DLPFC or left or right primary motor cortex (M1).

226 theta band compared to HD-tDCS of the right DLPFC and further, specifically modulated the oscillator

227 caused by dysconnectivity between the right DLPFC and several cortical regions.

228 0) functional connectivity between the right DLPFC and the right caudate nucleus and bilateral (para)

229 tex (DLPFC) and cathodal tDCS over the right DLPFC for 30 minutes, one of the most common montages us

230 ion was observed on BOLD signal in the right DLPFC such that TD increased activation in high ACE subj

231 n and functional connectivity with the right DLPFC were calculated.

232 , real-rTMS (10 Hz) was applied to the right DLPFC.

233 rovement was negatively associated with rsFC DLPFC-putamen changes across all subjects.

234 his study, we tested whether an individual's DLPFC gamma-aminobutryic acid (GABA) content predicts in

235 ings, and fMRI revealed punishment-selective DLPFC recruitment, suggesting that these two facets of n

236 nteers received 20 minutes of active or sham DLPFC stimulation before completing computerized emotion

237 These data suggest that smaller DLPFC and insula GMV plausibly represent genetically con

238 OR signaling cascade are downregulated in SZ DLPFC.

239 rmal mTOR expression in both complexes in SZ DLPFC.

240 ance sensitivity to other components tested; DLPFC glutamate + glutamine and visual cortical GABA con

241 t serve as a more appropriate mechanism than DLPFC alone.

242 ociations are genetically conferred and that DLPFC GMV prospectively predicts future use and initiati

243 The finding that DLPFC tDCS acutely alters the processing of threatening

244 The DLPFC-disrupted group showed enhanced learning of the no

245 the anterior cingulate cortex (ACC) and the DLPFC during REM sleep.

246 theta and beta activities in the ACC and the DLPFC, two relatively distant but reciprocally connected

247 d a significant decrease in rsFC between the DLPFC and the left putamen and insula.

248 d a significant decrease in rsFC between the DLPFC and the left superior frontal gyrus (SFG) and ante

249 ur study examined TMS-EEG responses from the DLPFC in persons with MDD compared with those in healthy

250 related via excitatory projections from the DLPFC to the ventral mesencephalon, the location of dopa

251 Across the sample, higher NAA and Glu in the DLPFC and NAA concentrations in multiple lobar gray matt

252 ts that were preferentially expressed in the DLPFC and was associated with replicable differential ge

253 ge change in binding potential (BPND) in the DLPFC following amphetamine, BOLD activation during the

254 for the major PNN protein, aggrecan, in the DLPFC from schizophrenia and matched comparison subjects

255 tcome was the difference in glutamate in the DLPFC in cases versus controls.

256 ecific defect in glucose utilization, in the DLPFC in schizophrenia.

257 support the idea that spine deficits in the DLPFC may contribute to subcortical hyperdopaminergia in

258 Relative HDAC expression was lower in the DLPFC of patients with SCZ/SAD compared with controls, a

259 hermore, conflict-related activations in the DLPFC of those CHR individuals who ultimately developed

260 tal evidence that modulating activity in the DLPFC reduces vigilance to threatening stimuli.

261 Furthermore, dopamine release in the DLPFC relates to working memory-related activation of th

262 of neural signals are flexibly routed in the DLPFC so as to favor actions that maximize reward.

263 Pools of L3 and L5 pyramidal cells in the DLPFC were individually captured by laser microdissectio

264 nd phosphofructokinase (PFK) activity in the DLPFC, as well as decreased PFK1 mRNA expression.

265 In the DLPFC, cortical inhibition was significantly decreased i

266 e DLPFC in the control group, but not in the DLPFC-disrupted group.

267 plicable differential gene expression in the DLPFC.

268 ly higher full-length GAD1 expression in the DLPFC.

269 pect to the lateralization of control in the DLPFC.

270 are similar mitochondrial alterations in the DLPFC.

271 ated abnormalities in TMS-EEG markers in the DLPFC.

272 schizophrenia-associated alterations in-the DLPFC circuitry that subserves working memory could prov

273 CS, to clarify the causal involvement of the DLPFC in conflict adaptation.

274 ies have suggested causal involvement of the DLPFC in this phenomenon, such evidence is currently lac

275 Plasticity of the DLPFC measured as potentiation of cortical-evoked activi

276 n-containing basket cells) in layer 3 of the DLPFC.

277 ed with executive functions that rely on the DLPFC in the control group, but not in the DLPFC-disrupt

278 ese observations indicate that tDCS over the DLPFC has fast excitatory effects, acting on prefrontal

279 mulation (1 mA, 20 min) was applied over the DLPFC.

280 Since the DLPFC and the ACC are implicated in memory and emotional

281 Furthermore the striatum, the DLPFC, the insula and the vmPFC appeared to be central '

282 estigated the possibility of suppressing the DLPFC by transcranial direct current stimulation (tDCS)

283 timulation (HD-tDCS) to demonstrate that the DLPFC is causally involved in conflict adaptation in hum

284 n sum, the present results indicate that the DLPFC plays a causal role in adaptive cognitive control,

285 , counter to current prevailing thought, the DLPFC is active during REM sleep and likely interacting

286 xecutive control network associated with the DLPFC might be an integral part of mind-wandering neural

287 g the posterior supratemporal plane with the DLPFC.

288 the neural elements and pathways within the DLPFC that support WM in humans.

289 ural phenotype appears correlated within the DLPFC with the development of psychosis and with functio

290 The subjects then had their DLPFC GABA content measured by single-voxel proton magne

291 V neurons and their PNNs could contribute to DLPFC dysfunction in schizophrenia.

292 The dorsal striatal BOLD response to DLPFC stimulation however was not significantly differen

293 yer 3 parvalbumin interneurons, and in total DLPFC gray matter.

294 yer 3 parvalbumin interneurons, and in total DLPFC gray matter.

295 ng cognition with their personal goals using DLPFC.

296 This study demonstrated impaired in vivo DLPFC plasticity in patients with AD.

297 th AD and controls, and to determine whether DLPFC plasticity was associated with working memory.

298 ond step, in the subset of participants with DLPFC DNA methylation data (n = 648), we found that resi

299 ird step, in the subset of participants with DLPFC RNA sequencing data (n = 469), brain transcription

300 tasks and lateral regions of the DMN within DLPFC, as well as less cortical grey matter in regions s