ライフサイエンスコーパス: neurocognitive

1 The neurocognitive ability of children with konzo over time

2 represent structural brain underpinnings of neurocognitive abnormalities and respiratory-related abn

3 quently develop various metabolic disorders, neurocognitive abnormalities, and cardiovascular disease

4 aglobulinemia, hepatopathy and a spectrum of neurocognitive abnormalities.

5 dverse events (OR, 1.01; 95% CI, 0.87-1.13), neurocognitive adverse events (OR, 1.29; 95% CI, 0.64-2.

6 tudies did suggest an increased incidence of neurocognitive adverse events (OR, 2.85; 95% CI, 1.34-6.

7 However, the overall incidence of neurocognitive adverse events and stroke was <1%, wherea

8 tributable to study drug, which were grade 2 neurocognitive adverse events comprising slowed speech a

9 erse events, musculoskeletal adverse events, neurocognitive adverse events, and stroke.

10 Neurocognitive AEs were infrequent and balanced during t

11 tients (0.3%) in the control groups reported neurocognitive AEs.

12 dings challenge the conventional approach to neurocognitive aging by showing that the neural underpin

13 infection and its link to the development of neurocognitive alternations are still poorly understood.

14 We present findings from morphometric and neurocognitive analyses of 1381 subjects (SZ probands, n

15 The potential neurocognitive and behavioral effects of anesthesia expo

16 ting sleep problems can add substantially to neurocognitive and behavioural comorbidities.

17 s; however, whether mild OSA has significant neurocognitive and cardiovascular complications is uncer

18 evidence regarding whether long-term adverse neurocognitive and cardiovascular outcomes are attributa

19 tive at preventing or reducing these adverse neurocognitive and cardiovascular outcomes, delineate th

20 To compare neurocognitive and endocrine functional outcomes and sur

21 e acute changes predict beneficial clinical, neurocognitive and functional outcomes.

22 sociated psychosis (MAP) involves widespread neurocognitive and molecular deficits, however accurate

23 Clinical, neurocognitive and mood assessments using the PRIME-MD a

24 limb malformation syndrome, associated with neurocognitive and motor delay, via a proposed gain-of-f

25 SCRT compared with ConvRT achieves superior neurocognitive and neuroendocrine functional outcomes ov

26 evaluated 12 primary and other supplementary neurocognitive and neurophysiological endophenotypes in

27 emia, mild deficiency may be associated with neurocognitive and other consequences.

28 te leukoencephalopathy and neurobehavioural, neurocognitive, and brain white matter imaging outcomes

29 posttraumatic stress or anxiety, somatoform, neurocognitive, and eating disorders, as well as prolong

30 tion used machine learning with demographic, neurocognitive, and neuroimaging data in substance-naive

31 al disorders and rheumatic, ear-nose-throat, neurocognitive, and ophthalmologic complications.

32 However, the neurocognitive architecture giving rise to this interdep

33 onstrate a flexible division of labor in the neurocognitive architecture that underpins size knowledg

34 served striking contextual modulation of the neurocognitive architecture: when human participants jud

35 structured clinical neurological assessment, neurocognitive assessment (Wechsler Abbreviated Scale of

36 prior randomized clinical trial underwent a neurocognitive assessment battery pretransplantation and

37 andardized average differences in individual neurocognitive assessment scores over the 5.6-year (rang

38 Neurocognitive assessment was conducted at baseline, wit

39 f 9498 youths who underwent genomic testing, neurocognitive assessment, and neuroimaging.

40 HIV-infected adults underwent comprehensive neurocognitive assessments and had anti-Toxoplasma gondi

41 Participants underwent MRI, clinical, and neurocognitive assessments before and after training (4-

42 ic schools and underwent polysomnography and neurocognitive assessments of intellectual, attention, m

43 Patients underwent neurocognitive assessments, and the debris captured was

44 Main Outcomes and Measures: Neurocognitive associations with transition to psychosis

45 osognosia can offer unique insights into the neurocognitive basis of awareness.

46 ARIC-NCS), participants underwent a detailed neurocognitive battery, informant interviews, and adjudi

47 ale-Third Edition, and the Penn Computerized Neurocognitive Battery.

48 t mice expressing a human alpha5 SNP exhibit neurocognitive behavioral deficits in social interaction

49 ork from our laboratory has demonstrated the neurocognitive benefits of human neural stem cell (hNSC)

50 schizophrenia patients; no concurrent acute neurocognitive changes were detected by the MCCB.

51 We therefore sought to determine the neurocognitive components of apathy and impulsivity in f

52 The primary outcome (the Neurocognitive Composite of the MATRICS Consensus Cognit

53 e MATRICS Consensus Cognitive Battery (MCCB) neurocognitive composite score for ABT-126 50 mg vs plac

54 nectivity properties might contribute to the neurocognitive computations underlying these abilities.

55 Delirium is a serious acute neurocognitive condition frequently occurring for hospit

56 Acute alcohol reduced 'neurocognitive coupling', the association between behavi

57 was a correlation between lesion volume and neurocognitive decline (p = 0.0022).

58 Neurocognitive decline has been observed in patients wit

59 Neurocognitive decline was assessed using standardized c

60 Patterns of neurocognitive decline were similar between participants

61 so that some older individuals evince clear neurocognitive declines whereas others are spared.

62 ssociated with long-term sequelae, including neurocognitive deficits and secondary neoplasms.

63 ient at deciphering post-concussion residual neurocognitive deficits and thus has a potential clinica

64 ct transition to psychosis, and determine if neurocognitive deficits are robust or explained by poten

65 gene is thought to have a major role in the neurocognitive deficits associated with Trisomy 21.

66 In this study, we calculated neurocognitive deficits combining EEG analysis with thre

67 with OSAS that may help explain some of the neurocognitive deficits described in these children.

68 These results suggest that neurocognitive deficits in mental perspective taking may

69 unologic and genetic factors associated with neurocognitive deficits in SM including 551 SM children,

70 term HIV-1 viral protein exposure on chronic neurocognitive deficits observed in pediatric HIV-1 (PHI

71 Long-term neurocognitive deficits occur in 15-40% of patients, whe

72 logy of the illness, and a potential link to neurocognitive deficits shaping the disorder.

73 ymphoblastic leukaemia (ALL) are at risk for neurocognitive deficits that affect development in adole

74 lymphoblastic leukemia (ALL) are at risk for neurocognitive deficits that are associated with treatme

75 unction, may combine with symptoms and other neurocognitive deficits to influence illness presentatio

76 ) exposure is associated with neuromotor and neurocognitive deficits, but the exact mechanism of Mn n

77 uals and are likely linked to HIV-associated neurocognitive deficits, including those in learning and

78 f an HSCT are at risk for severe, persistent neurocognitive deficits.

79 e, notably stunting, immune dysfunction, and neurocognitive deficits.

80 th CNS-directed chemotherapy are at risk for neurocognitive deficits.

81 al phenotypes, including cardiac defects and neurocognitive delays.

82 ffects of maternal iodine supplementation on neurocognitive development could be accelerated by the d

83 mine the roles of the social environment and neurocognitive development in adolescents' natural resil

84 -CM nutrient, choline is essential for fetal neurocognitive development, we hypothesized that choline

85 d might have long-term effects on children's neurocognitive development.

86 he benefits of early nutrition on children's neurocognitive development.

87 prenatal exposure to fluoride with offspring neurocognitive development.

88 ated to poverty interact to shape children's neurocognitive development.

89 genetic lesions that affect both kidney and neurocognitive development.

90 rrations, including mild skeletal anomalies, neurocognitive developmental delay, and cataracts.

91 eversible neuronal injury and HIV associated neurocognitive disease (HAND).

92 HIV-associated neurocognitive disorder (HAND) affects approximately hal

93 HIV-associated neurocognitive disorder (HAND) affects approximately hal

94 een HIV-1 RNA discordance and HIV-associated neurocognitive disorder (HAND) may reflect compartmental

95 tes with cognitive decline in HIV-associated neurocognitive disorder (HAND) patients.

96 Milder forms of HIV-associated neurocognitive disorder (HAND) remain common in HIV-infe

97 nodeficiency virus type-1 (HIV-1)-associated neurocognitive disorder (HAND) remains an important neur

98 long with its contribution to HIV-associated neurocognitive disorder (HAND) remains ill-defined.

99 tes with cognitive decline in HIV-associated neurocognitive disorder (HAND).

100 ly relevant HIV-associated dementia and mild neurocognitive disorder sensitivity was 100% and specifi

101 s 30.7% (HIV-associated dementia, 3.2%; mild neurocognitive disorder, 12.6%; and asymptomatic neuroco

102 ocognitive disorder, 12.6%; and asymptomatic neurocognitive disorder, 15.0%; HIV- group: 13.9%; P = .

103 eted for regular screening for HIV-associate neurocognitive disorder, particularly with tests referab

104 uman immunodeficiency virus (HIV)-associated neurocognitive disorders (HAND) are not routinely assess

105 at plays an important role in HIV-associated neurocognitive disorders (HAND) by disrupting neurotrans

106 he most challenging issues in HIV-associated neurocognitive disorders (HAND) caused by HIV-1 virotoxi

107 he neurodegenerative syndrome HIV-associated neurocognitive disorders (HAND), for which there is no s

108 iduals frequently suffer from HIV-associated neurocognitive disorders (HAND), with about 30% of AIDS

109 he most prevalent features of HIV-associated neurocognitive disorders (HAND), yet their origins are u

110 licated in the development of HIV-associated neurocognitive disorders (HAND).

111 e combination antiretroviral therapy (cART), neurocognitive disorders afflict 30-50% of HIV-infected

112 Despite the possible overlap between neurocognitive disorders and glaucoma in older individua

113 pathological presentation of HIV-associated neurocognitive disorders in the post-ARV era.

114 uman immunodeficiency virus (HIV)-associated neurocognitive disorders persist despite suppressive ant

115 Neurocognitive disorders remain common among human immun

116 HIV-associated neurocognitive disorders remain prevalent among HIV type

117 t cognitive deficits in neuropsychiatric and neurocognitive disorders that are associated with altera

118 uding Alzheimer's disease and HIV-associated neurocognitive disorders where APP misprocessing to amyl

119 f synaptic connections is a hallmark of many neurocognitive disorders, including HAND.

120 ators of neurodegeneration in HIV-associated neurocognitive disorders.

121 may offer protection against HIV-associated neurocognitive disorders.

122 adaptive immune responses to HIV-associated neurocognitive disorders.

123 higher visual cortex that is consistent with neurocognitive divergence across a spectrum of primate s

124 testing had severe impairment in at least 1 neurocognitive domain at the most recent evaluation.

125 ernal iodine supplementation on the specific neurocognitive domain of memory in infants and young chi

126 negative effects of ageing were noted on all neurocognitive domains (p<0.0001 for all).

127 nimal effect in subsequent years or on other neurocognitive domains.

128 isease stage), and their interaction on five neurocognitive domains: information processing speed, ex

129 heterogeneity in the pattern and severity of neurocognitive dysfunction across individuals and tumour

130 een increased brain iron-burden and risk for neurocognitive dysfunction due to AD, and indicates that

131 Such events may underlie METH- exacerbated neurocognitive dysfunction in HIV-infected patients.

132 t approaches for prevention and reduction of neurocognitive dysfunction include avoidance of radiothe

133 k for neurocognitive impairment, but whether neurocognitive dysfunction is solely attributable to imp

134 Neurocognitive dysfunction is the leading cause of reduc

135 on framework for understanding affective and neurocognitive dysfunctions across multiple disorders, i

136 Objectives: To identify core neurocognitive dysfunctions associated with the CHR phas

137 n type-9) inhibition was not associated with neurocognitive effects in a recent phase 3 randomized tr

138 oprotein cholesterol are not associated with neurocognitive effects in blacks.

139 There is a signal toward adverse neurocognitive effects, seen in the outcome studies with

140 Future studies should focus on long-term neurocognitive effects.

141 A neurocognitive evaluation of intellectual functioning (I

142 tic relatedness translates into differential neurocognitive evaluation of observed social interaction

143 Neurocognitive event rates were 0% (SOC alone) and 0.4%

144 close monitoring, for the increased risk of neurocognitive events in the ongoing outcome studies and

145 Despite concerns about adverse neurocognitive events raised by prior trials, pharmacolo

146 Neurological and neurocognitive events were similar among the 3 groups.

147 rse events (including new-onset diabetes and neurocognitive events), with the exception of injection-

148 ll treatment-emergent adverse event rates or neurocognitive events, although cataract incidence appea

149 inuation; adverse muscle, hepatobiliary, and neurocognitive events; and hemorrhagic stroke, heart fai

150 ovascular signals-from diving, exercise, and neurocognitive fear responses-that challenge physiologic

151 Collectively, these results provide a neurocognitive framework for understanding the pathways

152 We present a unifying neurocognitive framework of mechanisms underlying inform

153 comes were overall survival, adverse events, neurocognitive function (will be reported separately), h

154 tics causes neurotoxicity including impaired neurocognitive function and abnormal behavior.

155 We report on longitudinal change in neurocognitive function and predictors of neurocognitive

156 rates a likely pathway of effects of OSAS on neurocognitive function in children, as well as potentia

157 Drugs that rescue synapses may improve neurocognitive function in HAND.SIGNIFICANCE STATEMENT S

158 and in vivo and has been linked to impaired neurocognitive function in humans.

159 ividually or in combination on the change in neurocognitive function in persons with human immunodefi

160 These data indicate that impaired neurocognitive function in some children with CKD may be

161 use disorder is associated with dysregulated neurocognitive function in the right inferior frontal gy

162 py is associated with detrimental effects on neurocognitive function or brain imaging markers compare

163 Neurocognitive function was largely age appropriate 2 ye

164 Neurocognitive function was measured using the Brief Ass

165 e deleterious effect of genomic disorders on neurocognitive function was significantly attenuated in

166 and 5.6% in patients with devices (p = 0.25) Neurocognitive function was similar in control subjects

167 Health-related quality of life and neurocognitive function were evaluated at baseline and e

168 ata provide new insight into the genetics of neurocognitive function with relevance to understanding

169 Fourteen-day survival rate, neurocognitive function, and endothelial integrity (addi

170 ential associations between SDB severity and neurocognitive function, as well as the presence of an S

171 Neurocognitive function, neurobehavioral symptoms, emoti

172 ions between VO2Max and multiple measures of neurocognitive function.

173 d neither health-related quality of life nor neurocognitive function.

174 statins or ACEI/ARB have an effect on global neurocognitive function.

175 ized interventions to mitigate the effect on neurocognitive function.

176 ea, and also that even snoring alone affects neurocognitive function.

177 n VACS Index scores correspond to changes in neurocognitive function.

178 ebris in 99% of patients, and did not change neurocognitive function.

179 of cerebral white matter and improvement in neurocognitive function.

180 or association between these and measures of neurocognitive function.

181 l effect of statin or ACEI/ARB initiation on neurocognitive function; initial constant slope was assu

182 h bone marrow cell transplantation, MRI, and neurocognitive functional assessments, we demonstrate th

183 ethodological issues central to the study of neurocognitive functioning and genetic associations for

184 Interventions targeting the enhancement of neurocognitive functioning are warranted in this populat

185 re also associated with a steeper decline in neurocognitive functioning during the 5-year follow-up p

186 n addition, higher FW correlated with better neurocognitive functioning following 12 weeks of antipsy

187 many clinical and patient characteristics on neurocognitive functioning have been documented, but lit

188 ) and corticosteroid treatment strategies on neurocognitive functioning in children with high-risk B-

189 Impairment of neurocognitive functioning is a common result of cerebra

190 Secondary outcomes included domain-specific neurocognitive functions and behavior.

191 be causally linked to distinct and specific neurocognitive functions and suggest mechanisms for long

192 ate specific gender differences in essential neurocognitive functions with implications for clinical

193 ical battery assessed IQ and domain-specific neurocognitive functions.

194 ly underlying observed larger impairments in neurocognitive functions.

195 term data are needed to fully understand the neurocognitive impact of PBRT in survivors of pediatric

196 y, P = .28), the proportion with symptomatic neurocognitive impairment (13% and 18% in the PI-mono an

197 lobal deficit score, a continuous measure of neurocognitive impairment (both P < .01), as well as wit

198 rain function, we investigated its impact on neurocognitive impairment (NCI) in people living with HI

199 has been associated with concurrent risk for neurocognitive impairment (NCI).

200 proportion of participants with symptomatic neurocognitive impairment (score >1 standard deviation b

201 e association between PCSK9 LOF variants and neurocognitive impairment and decline among black REGARD

202 lower low-density lipoprotein cholesterol on neurocognitive impairment and decline.

203 To evaluate the association between global neurocognitive impairment and visual field variability i

204 strategies designed to slow or even prevent neurocognitive impairment associated with AIDS.

205 D, 9), 62% were women, and the prevalence of neurocognitive impairment at any assessment was 6.3% by

206 s are most susceptible to the progression of neurocognitive impairment caused by ageing in individual

207 herapy, chronic inflammation with underlying neurocognitive impairment continues to afflict almost 50

208 Adjusted odds ratios for neurocognitive impairment for participants with versus w

209 f pediatric CNS tumors are at risk of severe neurocognitive impairment in adulthood.

210 Previous studies have documented neurocognitive impairment in children with severe anemia

211 rovides the first objective data documenting neurocognitive impairment in long-term survivors of chil

212 identifies a potential mechanism underlying neurocognitive impairment in patients recovering from WN

213 PI monotherapy does not increase the risk of neurocognitive impairment in stable human immunodeficien

214 Odds ratios for neurocognitive impairment per 20 mg/dL low-density lipop

215 With improved acute care in these patients, neurocognitive impairment represents the major contribut

216 Symptomatic neurocognitive impairment was associated with higher GCA

217 Neurocognitive impairment was associated with these imag

218 Neurocognitive impairment was defined as a score >/=1.5

219 Neurocognitive impairment was significantly associated w

220 , may enable timely intervention and prevent neurocognitive impairment, but conventional techniques a

221 Children with CKD are at increased risk for neurocognitive impairment, but whether neurocognitive dy

222 disability was significantly associated with neurocognitive impairment, lower education, Medicare/Med

223 rm survivors of osteosarcoma are at risk for neurocognitive impairment, which is related to current c

224 ray matter and a high incidence of long-term neurocognitive impairment.

225 es of aging, like cardiovascular disease and neurocognitive impairment.

226 ause widespread neuronal apoptosis and later neurocognitive impairment.

227 t predispose them to organ malformations and neurocognitive impairment.

228 the processes of ageing and HIV infection in neurocognitive impairment.

229 ities may play a relevant role for long-term neurocognitive impairments associated with premature del

230 ver, there is a continuing problem of milder neurocognitive impairments in treated HIV(+) patients th

231 viduals have an increased risk for long-term neurocognitive impairments.

232 contributing to neocortical dysfunction and neurocognitive impairments.

233 s that govern the association between a core neurocognitive measure-processing speed-and neurobiologi

234 developmental trajectory and the underlying neurocognitive mechanisms are still little understood.

235 essions and advance our understanding of the neurocognitive mechanisms that may underlie propensity t

236 At present, little is known about the neurocognitive mechanisms that underlie this adaptive ph

237 emotional SFRs may be the result of complex neurocognitive mechanisms which lead to partial mimicry

238 demonstrated that behavioral goal shapes the neurocognitive network underpinning object size.

239 oup differences in either trial in any other neurocognitive or pregnancy outcomes or in the incidence

240 The primary endpoint was favorable neurocognitive outcome (cerebral performance category of

241 To evaluate the association between Vt and neurocognitive outcome after OHCA.

242 RATIONALE: Neurocognitive outcome after out-of-hospital cardiac arr

243 ative dietary treatment strategy to optimize neurocognitive outcome in patients with phenylketonuria.

244 ative dietary treatment strategy to optimize neurocognitive outcome in phenylketonuria and has been s

245 was independently associated with favorable neurocognitive outcome in propensity-adjusted analysis (

246 A is independently associated with favorable neurocognitive outcome, more ventilator-free days, and m

247 eir depletion attenuates secondary injury or neurocognitive outcome.

248 ping--has been proposed as a cause of poorer neurocognitive outcome.

249 in neurocognitive function and predictors of neurocognitive outcomes 2 years after completing therapy

250 assignment were unrelated to differences in neurocognitive outcomes after controlling for ethnicity,

251 the association between aerobic fitness and neurocognitive outcomes at young adult age, along with t

252 Most studies evaluating neurocognitive outcomes in children with congenital hear

253 on between various genes and risk of adverse neurocognitive outcomes in patients with brain tumours.

254 rstanding the effect of genetic variation on neurocognitive outcomes in patients with brain tumours.

255 To characterize neurocognitive outcomes of boys with cALD and early-stag

256 imate = 0; P = .45) were not associated with neurocognitive outcomes.

257 nt of survivors and the neurobehavioural and neurocognitive outcomes.

258 itiated to mitigate the impact of therapy on neurocognitive outcomes.

259 r Intake Level (UL) (>/=1000 mug/d) on child neurocognitive outcomes.The objective of the study was t

260 lutamate, subclinical psychopathological and neurocognitive parameters were examined.

261 ntly associated with worse global and domain neurocognitive performance (Ps < .01), as well as increa

262 Tolerability as measured by neurocognitive performance (reported elsewhere) was asse

263 icipants with genomic disorders had impaired neurocognitive performance at enrollment.

264 correlations between clinical variables and neurocognitive performance suggest a basis for heterogen

265 Worse neurocognitive performance was associated with discordan

266 In summary, although modest declines in neurocognitive performance were seen in single domains w

267 s 1-5 post-ICH, and long-term improvement in neurocognitive performance, as quantified by reduced Mor

268 association of GM-NDI with disease state and neurocognitive performance, its potential utility for bi

269 groups and to assess their relationship with neurocognitive performance.

270 ich was fully mediated by inhibitory control neurocognitive performance.

271 d network dysfunction that may be related to neurocognitive problems in this devastating disorder.

272 velopment, and have a high risk of long-term neurocognitive problems.

273 Extant research has addressed the neurocognitive processes associated with aggression in s

274 knowledge acquired during studying and basic neurocognitive processes that establish durable memories

275 exible goal-directed behavior and underlying neurocognitive processes.

276 of mucopolysaccharidosis type III syndromes, neurocognitive progression was improved in all patients,

277 We assessed tolerance, neurocognitive progression, brain growth, NAGLU enzymati

278 s that Bbeta15-42 improves survival rate and neurocognitive recovery after cardiopulmonary resuscitat

279 NTROL; 11/26 vs 6/26; p < 0.05) and fastened neurocognitive recovery in the Water-Maze test (15/26 vs

280 e radiotherapy techniques in minimisation of neurocognitive sequelae in children with brain tumours,

281 The neurocognitive sequelae of a sport-related concussion an

282 and allowed patients to avoid the potential neurocognitive sequelae of WBRT.

283 iotherapy is one of the main contributors to neurocognitive sequelae.

284 Neurocognitive status was plotted over time using demogr

285 ost recently, in 2011-2013, through the ARIC Neurocognitive Study (ARIC-NCS), participants underwent

286 ormative means in >/=2 cognitive domains and neurocognitive symptoms).

287 vide evidence for engagement of the relevant neurocognitive systems.

288 esponses involving complex physiological and neurocognitive systems.

289 Longitudinal neurocognitive test performance in 4 domains (verbal com

290 Baseline and follow-up neurocognitive test performance was analyzed for all boy

291 Patients received neurocognitive testing before, 1, and 6 months after car

292 nts (67%) with available long-term follow-up neurocognitive testing had severe impairment in at least

293 FA maps were obtained and neurocognitive testing was performed in 74 patients with

294 s after their diagnosis, survivors completed neurocognitive testing, another brain MRI, and their par

295 is, 18 years [11 to 42 years]) and completed neurocognitive testing.

296 Neurocognitive tests included the Consortium to Establis

297 d with the CHR phase, measure the ability of neurocognitive tests to predict transition to psychosis,

298 standardized continuous scores on individual neurocognitive tests.

299 tcomes were neuroendocrine toxic effects and neurocognitive toxic effects, assessed by intention-to-t

300 d toxicities associated with WBRT, including neurocognitive toxicity.

301 D, yet there is limited understanding of the neurocognitive trajectory of patients who undergo HSCT.