ライフサイエンスコーパス: cognitive dysfunction

1 e leading preventable developmental cause of cognitive dysfunction.

2 ith IAH, and attenuates hypoglycemia-induced cognitive dysfunction.

3 rovascular disease are at increased risk for cognitive dysfunction.

4 lain why TBI patients are more vulnerable to cognitive dysfunction.

5 FC) is augmented in a genetic mouse model of cognitive dysfunction.

6 HOMA-IR >2.6) had 47% (9-99%) larger odds of cognitive dysfunction.

7 radiations that put them at risk for severe cognitive dysfunction.

8 n patients with chronic fatigue syndrome and cognitive dysfunction.

9 sed risk of neurological disease, cancer and cognitive dysfunction.

10 tic targets for preventing infection-induced cognitive dysfunction.

11 id in adolescence does not produce long-term cognitive dysfunction.

12 l features and appear to interact in driving cognitive dysfunction.

13 importance in a model of 22q11.2-associated cognitive dysfunction.

14 factor for development of schizophrenia and cognitive dysfunction.

15 glycemia and attenuates hypoglycemia-induced cognitive dysfunction.

16 etic risk of schizophrenia may contribute to cognitive dysfunction.

17 environmental cues is a major cause of human cognitive dysfunction.

18 ovel therapeutic approaches for ameliorating cognitive dysfunction.

19 could have a key role in the development of cognitive dysfunction.

20 ally linking Abeta pathology to neuronal and cognitive dysfunction.

21 such treatments are ineffective for treating cognitive dysfunction.

22 lications such as delirium and postoperative cognitive dysfunction.

23 to investigate the function of Calstabin2 in cognitive dysfunction.

24 improve our understanding of other forms of cognitive dysfunction.

25 can prevent anesthesia-induced postoperative cognitive dysfunction.

26 PAMs) are currently being developed to treat cognitive dysfunction.

27 cial for Abeta-induced synaptic toxicity and cognitive dysfunction.

28 disorders and may be related to symptoms of cognitive dysfunction.

29 es, which result in brain growth defects and cognitive dysfunction.

30 peptide in the brain, loss of synapses, and cognitive dysfunction.

31 antial evidence linking these alterations to cognitive dysfunction.

32 plicated in psychopathology characterized by cognitive dysfunction.

33 ands harboured additional phenotypes such as cognitive dysfunction.

34 njury-induced neuroinflammatory sequelae and cognitive dysfunction.

35 for PD, in parallel with the development of cognitive dysfunction.

36 docannabinoid signaling and cannabis-induced cognitive dysfunction.

37 umented association between chemotherapy and cognitive dysfunction.

38 that otherwise leads to neuronal injury and cognitive dysfunction.

39 depressive disorder (MDD) who self-reported cognitive dysfunction.

40 zures that may be fundamentally connected to cognitive dysfunction.

41 tor for the development of schizophrenia and cognitive dysfunction.

42 strongly predicts psychiatric disorders and cognitive dysfunction.

43 ission, have been associated with persistent cognitive dysfunction.

44 aviours are a popular feature in theories of cognitive dysfunction.

45 related psychiatric diseases associated with cognitive dysfunction.

46 compensate for tissue damage and to prevent cognitive dysfunction.

47 tients and correlate with disease-associated cognitive dysfunction.

48 ect against neurodegeneration and associated cognitive dysfunction.

49 nxiety, or compensatory processes related to cognitive dysfunction.

50 nsive synapse loss, which has been linked to cognitive dysfunction.

51 ive cognitive change (POCC) or postoperative cognitive dysfunction.

52 e incidence, severity, and duration of acute cognitive dysfunction.

53 be a therapeutic target for the treatment of cognitive dysfunction.

54 resolved), and 1 (5%) patient developed mild cognitive dysfunction.

55 mins has been linked to mood disturbance and cognitive dysfunction.

56 onship between poor physical performance and cognitive dysfunction.

57 ay represent a promising approach to reverse cognitive dysfunction.

58 ism by which chronic stress may promote mPFC cognitive dysfunction.

59 and their alterations are linked to various cognitive dysfunction.

60 chemokine CCL11 shown to be associated with cognitive dysfunction.

61 on of microRNAs in psychiatric disorders and cognitive dysfunction.

62 the molecular and cellular bases underlying cognitive dysfunction.

63 ore the onset of age-related gross motor and cognitive dysfunction.

64 sing a model of anticholinergic drug-induced cognitive dysfunction.

65 relating HSV-1 infection to postencephalitic cognitive dysfunction.

66 post-AT psychopathologies including PTSD and cognitive dysfunction.

67 ase onset and are more likely to demonstrate cognitive dysfunction.

68 -related cerebral injury could contribute to cognitive dysfunction.

69 ology of neuropsychiatric disease-associated cognitive dysfunction.

70 e commonly of more advanced ages with milder cognitive dysfunction.

71 hat affect sleep, including chronic pain and cognitive dysfunction.

72 tabolic functions of astrocytes and leads to cognitive dysfunction.

73 Conversely TDF protected gp120-tg mice from cognitive dysfunction.

74 lities including epileptogenic responses and cognitive dysfunction.

75 , and attentional deficits are a hallmark of cognitive dysfunction.

76 FC hyperactivity contributes to OCD-relevant cognitive dysfunction.

77 titute an effective therapeutic approach for cognitive dysfunction.

78 logues of mouse NAP genes are known loci for cognitive dysfunction.

79 e, enhances synaptic plasticity, and reduces cognitive dysfunction.

80 nce to dementia, delirium and post-operative cognitive dysfunction.

81 l blood flow, correlating with intradialytic cognitive dysfunction.

82 epresent a novel target for the treatment of cognitive dysfunction.

83 sitive correlation with disease severity and cognitive dysfunction.

84 physiology of schizophrenia and may underlie cognitive dysfunction.

85 mong these precursors of type 2 diabetes and cognitive dysfunction.

86 iated with 44% (9-91%) larger probability of cognitive dysfunction.

87 of oxidative stress, neurodegeneration, and cognitive dysfunctions.

88 localization of hTau-S199-P, which improves cognitive dysfunctions.

89 at correlate with disability progression and cognitive dysfunctions.

90 seases such as cardiovascular, metabolic, or cognitive dysfunctions.

91 barrier (BBB) is an early biomarker of human cognitive dysfunction(7), including the early clinical s

92 In the present study we focus on cognitive dysfunction, a core feature of schizophrenia (

93 onditions such as polypharmacy, frailty, and cognitive dysfunction-a combination rarely addressed in

94 known whether these shared manifestations of cognitive dysfunction across diagnostic categories also

95 microglial activation, neuronal damage, and cognitive dysfunction after GCI.

96 ce had exacerbated neuronal damage and worse cognitive dysfunction after global cerebral ischemia.

97 le cognitive subscale scores as a measure of cognitive dysfunction (Alzheimer's Disease Neuroimaging

98 Diabetes is associated with cognitive dysfunction and an increased risk of dementia.

99 ted with the 22q11DS, which may be linked to cognitive dysfunction and an increased risk to develop s

100 disease (PD) develop dementia in addition to cognitive dysfunction and are diagnosed as PD with demen

101 in sensory processing underlie more complex cognitive dysfunction and are in turn affected by higher

102 likely explanation for its association with cognitive dysfunction and ASD.

103 dely used in breast cancer treatment, causes cognitive dysfunction and changes in CNS metabolism, hip

104 These changes may contribute to the cognitive dysfunction and circuit hyperexcitability asso

105 mimics DS/AD pathology, notably age-related cognitive dysfunction and degeneration of basal forebrai

106 sk for postoperative complications including cognitive dysfunction and delirium.

107 nt LRRK2 pathogenesis.SIGNIFICANCE STATEMENT Cognitive dysfunction and dementia are common features o

108 ongoing neurodegeneration interact to induce cognitive dysfunction and episodes of delirium.

109 CFS) have similar profiles of pain, fatigue, cognitive dysfunction and exertional exhaustion.

110 al adverse events included transient grade 3 cognitive dysfunction and grade 1-2 seizures (n=3 [17%])

111 evidence of an association between mood and cognitive dysfunction and hippocampal pathology epitomiz

112 mulation in aging blood promotes age-related cognitive dysfunction and impairs neurogenesis, in part

113 rrent epileptiform discharge, which provoked cognitive dysfunction and memory deficits without affect

114 variants predict a more rapid progression of cognitive dysfunction and motor symptoms in patients wit

115 pha7 nicotinic receptor partial agonists for cognitive dysfunction and negative symptoms in schizophr

116 otinic receptor partial agonist, TC-5619, on cognitive dysfunction and negative symptoms in subjects

117 d expression of imprinted genes is linked to cognitive dysfunction and neuropsychological disorders,

118 s little to suggest how reduced Glut1 causes cognitive dysfunction and no optimal treatment for Glut1

119 ted mild traumatic insult is associated with cognitive dysfunction and other chronic co-morbidities.

120 therapies to prevent or treat postoperative cognitive dysfunction and other forms of cognitive decli

121 Cognitive dysfunction and reactive microglia are hallmar

122 sparing of TBI-induced hippocampal-dependent cognitive dysfunction and reduced proinflammatory activa

123 of the most common genetic risk factors for cognitive dysfunction and schizophrenia, we found that g

124 e rats produced depression-like changes with cognitive dysfunction and selective cell death in the in

125 Deltatau314 proteins and their relevance to cognitive dysfunction and shed light on the contribution

126 enic mice were also resistant to HFD-induced cognitive dysfunction and were protected against deficit

127 2 potassium channel has been associated with cognitive dysfunction and with schizophrenia, yet little

128 repetitive behaviors, sociability deficits, cognitive dysfunction, and abnormal dendritic morphogene

129 i detected by serial/extended EEG, transient cognitive dysfunction, and good seizure control and tole

130 read changes to brain networks contribute to cognitive dysfunction, and grey matter atrophy is an ear

131 ts corresponding to general psychopathology, cognitive dysfunction, and impulsivity.

132 Tau PET uptake was tied to the onset of cognitive dysfunction, and there was a higher amount, an

133 chizophrenia that is broadly associated with cognitive dysfunction, and they support hippocampal acti

134 ecify the pattern and severity of persistent cognitive dysfunctions, and to examine the potential mod

135 sorders including delirium and postoperative cognitive dysfunction are common postanesthesia complica

136 rapeutic interventions for the management of cognitive dysfunction are ongoing, as well as numerous p

137 n, neurodegeneration-associated changes, and cognitive dysfunction arising after sepsis recovery.

138 exposed to Al and EWH did not show memory or cognitive dysfunction as was observed in Al-treated anim

139 atal exposure, can initiate neurological and cognitive dysfunction, as well as memory impairment.

140 lusion: Disability, chair-stand performance, cognitive dysfunction, as well as psychoactive medicatio

141 In mice, a salt-rich diet leads to cognitive dysfunction associated with a nitric oxide def

142 and provide new insights into the origin of cognitive dysfunction associated with developmental inte

143 ogenic role of PVMs in the neurovascular and cognitive dysfunction associated with hypertension and i

144 the contributions of these modulators to the cognitive dysfunction associated with neuropsychiatric i

145 identify the neural substrates that mediate cognitive dysfunctions associated with a majority of MS

146 fering from psychosis and has been linked to cognitive dysfunction, audiovisual hallucinations, and n

147 rationale for survival of humans with severe cognitive dysfunction bearing a truncating mutation in t

148 as promising compounds in the management of cognitive dysfunction, but clinical experience of their

149 order is associated with variable degrees of cognitive dysfunction, but no consistent functional biom

150 rbidities including anxiety, depression, and cognitive dysfunction, but the mechanism for these is no

151 The findings suggest that cognitive dysfunction can be considered a sign of prodro

152 y contributors to the clinical expression of cognitive dysfunction caused by other pathologies, inclu

153 Cognitive dysfunction characterizes all the various form

154 s with non-NET cancer also demonstrated some cognitive dysfunction compared with norms, the patients

155 Sarcopenia, cognitive dysfunction, depression, and nutrition are oth

156 spinal fluid (CSF) and developed progressive cognitive dysfunction despite ventricular drainage.

157 We also detected a subgroup with no cognitive dysfunction, despite having substantial TDP-43

158 Our data show that individuals with early cognitive dysfunction develop brain capillary damage and

159 Traumatic brain injury (TBI) can induce cognitive dysfunction due to the regional accumulation o

160 e significant implications for management of cognitive dysfunction during acute illness.

161 in, contributing to the onset/progression of cognitive dysfunction during aging.

162 Many healthy women with no history of cognitive dysfunction experience subjective executive di

163 Patient-reported outcomes related to cognitive dysfunction (F = 7.27; P = .002) and psycholog

164 erative side-effects (including delirium and cognitive dysfunction, fatigue, dizziness, pain, and gas

165 reased hospital readmissions and substantial cognitive dysfunction for 1 year following surgery.

166 at is characterized by acute inattention and cognitive dysfunction, for which prior dementia is the m

167 sufficient dexterity, visual impairment, and cognitive dysfunction, found commonly in older adults sh

168 This HO-1 deficiency correlated with cognitive dysfunction, HIV replication in the CNS, and n

169 E knock-out (KO) mice have synaptic loss and cognitive dysfunction; however, these findings are compl

170 that elevated CRP is associated with a broad cognitive dysfunction in affectively remitted BD patient

171 od-brain barrier has long been implicated in cognitive dysfunction in aging and neurodegeneration, bu

172 Patients with CS reported greater cognitive dysfunction in all cognitive domains than both

173 es, neuronal and synaptic loss, and eventual cognitive dysfunction in Alzheimer disease.

174 ggesting a novel target for the treatment of cognitive dysfunction in Alzheimer's disease.

175 novel potential target for the treatment of cognitive dysfunction in Alzheimer's disease.

176 is protein exacerbates neuroinflammation and cognitive dysfunction in an AD mouse model whereas ablat

177 homeostasis as key mechanisms important for cognitive dysfunction in children with NF1.

178 Persistent cognitive dysfunction in depression and bipolar disorder

179 (OFC) that we have used previously to model cognitive dysfunction in depression.

180 es findings with brain MRI that may underlie cognitive dysfunction in diabetes.

181 se of selective GABA(A) alpha5 NAMs to treat cognitive dysfunction in DS.

182 inflammatory events often precipitate acute cognitive dysfunction in elderly and demented population

183 tracerebral hemorrhage, ischemic stroke, and cognitive dysfunction in elderly patients with and witho

184 Cognitive dysfunction in fibromyalgia patients has been

185 Cognitive dysfunction in first-degree relatives is more

186 Cognitive dysfunction in HIV has decreased, but milder f

187 tions for improving how we measure and model cognitive dysfunction in human disorders in animals, thu

188 Cognitive dysfunction in human immunodeficiency virus (H

189 their levels correlate with the severity of cognitive dysfunction in humans.

190 bute to the circuitry alterations underlying cognitive dysfunction in individuals with SZ.

191 iring prolonged oxygen therapy often develop cognitive dysfunction in later life.

192 in proteins link Abeta and hyperglycaemia to cognitive dysfunction in MetS/T2DM and AD.

193 uces hyperphosphorylation of tau followed by cognitive dysfunction in mice, and that these effects ar

194 However, the mechanisms underlying severe cognitive dysfunction in MS are not well understood.

195 of CXCL12/CXCR4 as a contributing factor to cognitive dysfunction in neuroAIDS.

196 that altered O-GlcNAc levels could underlie cognitive dysfunction in neurological diseases.

197 This is significant because cognitive dysfunction in normative and pathological agin

198 Increased focus on symptoms of cognitive dysfunction in older patients with rosacea may

199 that PKA dysregulation in the mPFC underlies cognitive dysfunction in Ophn1-deficient mice, as assess

200 l connectivity (FC) are important factors in cognitive dysfunction in patients with multiple sclerosi

201 rontal cortex (PFC) has been associated with cognitive dysfunction in patients with schizophrenia and

202 terventions that may slow the progression of cognitive dysfunction in PD.

203 abnormal pattern of neural activity underlie cognitive dysfunction in PP-MS, and that CLs possibly pl

204 elopmental processes and has been related to cognitive dysfunction in psychiatric disorders.

205 ng alteration in synaptic function underlies cognitive dysfunction in RAB39B-related disorders.

206 s indicate that forniceal DBS might mitigate cognitive dysfunction in RTT.

207 important link between GABA transmission and cognitive dysfunction in schizophrenia because they show

208 Identification of biomarkers for cognitive dysfunction in schizophrenia is a priority for

209 Cognitive dysfunction in schizophrenia is associated wit

210 Cognitive dysfunction in schizophrenia is one of the mos

211 consistently documented as a core aspect of cognitive dysfunction in schizophrenia patients, present

212 ecently proposed hyperfocusing hypothesis of cognitive dysfunction in schizophrenia proposes that peo

213 ectivity are critical determinants of social cognitive dysfunction in schizophrenia, and thus represe

214 ntal cortex (DLPFC) appears to contribute to cognitive dysfunction in schizophrenia, whereas psychosi

215 substrate for altered gamma oscillations and cognitive dysfunction in schizophrenia.

216 onnectivity in the pathophysiology of social cognitive dysfunction in schizophrenia.

217 ons in GABA signaling drive certain forms of cognitive dysfunction in schizophrenia.

218 ssing speed (PS; beta=0.74; P=0.003), a core cognitive dysfunction in schizophrenia.

219 d mechanistic account of multiple aspects of cognitive dysfunction in schizophrenia.SIGNIFICANCE STAT

220 ion of GIRK-dependent signaling may underlie cognitive dysfunction in some disorders.

221 aging are associated with varying degrees of cognitive dysfunction in stroke, cerebral small vessel d

222 The results show that, despite broad cognitive dysfunction in the acute phase, patients with

223 The mechanisms underlying this postoperative cognitive dysfunction in the adult brain remain poorly u

224 ts its therapeutic effects on stress-induced cognitive dysfunction in the OFC.

225 There is a hidden epidemic of cognitive dysfunction in the perioperative setting.

226 inergic deficit that contributes to gait and cognitive dysfunction in these patients.

227 Despite the prominence of cognitive dysfunction in this syndrome, little is known

228 uits may have a role in mediating aspects of cognitive dysfunction in underweight individuals with AN

229 ain nor the molecular basis of systems-level cognitive dysfunctions in AS.

230 t synaptic and circuit mechanisms underlying cognitive dysfunctions in DS.

231 s of large-scale brain networks may underlie cognitive dysfunctions in psychiatric and addictive diso

232 ness can also produce profound, maladaptive, cognitive dysfunction including delirium, but our unders

233 tween androgen deprivation therapy (ADT) and cognitive dysfunction, including Alzheimer disease.

234 Cognitive dysfunction, including significant impairments

235 BBB breakdown is an early biomarker of human cognitive dysfunction independent of Abeta and tau.

236 se (PD), with clinical features of motor and cognitive dysfunction indistinguishable from sporadic PD

237 Cognitive dysfunction is a challenging adverse effect of

238 Cognitive dysfunction is a common feature among patients

239 Cognitive dysfunction is a common symptom in many neurop

240 Cognitive dysfunction is a core feature of dementia and

241 PFC-dependent cognitive dysfunction is a core feature of multiple psyc

242 Fragmentation-induced cognitive dysfunction is a feature of many common human

243 Cognitive dysfunction is an early clinical hallmark of H

244 PFC-dependent cognitive dysfunction is associated with many psychiatri

245 Cognitive dysfunction is common in depression during bot

246 Cognitive dysfunction is common in LLD, particularly exe

247 In schizophrenia, cognitive dysfunction is highly predictive of poor patie

248 PFC cognitive dysfunction is implicated in multiple psychopa

249 on adverse effects, it is uncertain whether cognitive dysfunction is induced in humans by exposure t

250 tor in the development of treatments for PFC cognitive dysfunction is our limited understanding of th

251 Cognitive dysfunction is reported in people with cancer.

252 ng MS-related cognitive impairment; however, cognitive dysfunction is still often considered to be po

253 However, there is significant variability in cognitive dysfunction, likely reflecting biological hete

254 ngs suggest that screening and monitoring of cognitive dysfunction may be important in the assessment

255 rtant clinical implications, suggesting that cognitive dysfunction may not be useful targets of preve

256 (measured using [(18)F]Florbetapir-PET) and cognitive dysfunction (measured using ADAS-cog) by condu

257 Because MMSE could be impaired in several cognitive dysfunctions, more specific test should be use

258 espread nervous system dysfunction including cognitive dysfunction, neuropathy and susceptibility to

259 This paper highlights a dimension of cognitive dysfunction not well documented in neurodegene

260 Sickness behavior and cognitive dysfunction occur frequently by unknown mechan

261 Cognitive dysfunction occurs in many debilitating condit

262 dies have implications for understanding the cognitive dysfunction of psychiatric illnesses and certa

263 sts a possible neurobiological mechanism for cognitive dysfunction of this type of PTSD.

264 senting one potential therapeutic target for cognitive dysfunctions of Alzheimer's disease and schizo

265 at a range of malignancies can elicit severe cognitive dysfunction often referred to as "chemobrain,"

266 ety and probable behaviour disorder, but not cognitive dysfunction or motor severity.

267 P = .04) and were more likely to demonstrate cognitive dysfunction (P = .001).

268 go general anesthesia and surgery experience cognitive dysfunction, particularly memory deficits that

269 iminary evidence suggests that postoperative cognitive dysfunction (POCD) is common after lung transp

270 POD can lead to postoperative cognitive dysfunction (POCD), a more prolonged cognitive

271 ue to their potential role in post-operative cognitive dysfunction (POCD).

272 tion can reduce some measures of age-related cognitive dysfunction, possibly through an improvement i

273 CHI3L1 correlated with degree of cognitive dysfunction (r=-0.25, p=0.038).

274 nisms within the white matter accounting for cognitive dysfunction remain unclear.

275 CNS malignancy, progressive and debilitating cognitive dysfunction remains a pressing unmet medical n

276 but its protective effect on diabetes-driven cognitive dysfunction remains elusive.

277 owever, how the genetic elimination leads to cognitive dysfunction remains unknown.

278 SAE, which ultimately leads to delirium and cognitive dysfunction, remains elusive.

279 Radiation-induced cognitive dysfunction (RICD) is a progressive and debili

280 o be a particularly important determinant of cognitive dysfunction seen in well-treated HIV-infected

281 e showed that LPS (100 ug/kg) produced acute cognitive dysfunction, selectively in those animals.

282 new developments for treatments that address cognitive dysfunction should be a priority so that all m

283 potential target for treating frontostriatal cognitive dysfunction.SIGNIFICANCE STATEMENT The dorsome

284 e were associated with more severe motor and cognitive dysfunction, supporting a specific contributio

285 uding those associated with chronic pain and cognitive dysfunction syndrome.

286 al WM damage may have a greater relevance to cognitive dysfunction than physical disability in MS, an

287 brain cancer elicits progressive and severe cognitive dysfunction that is associated with significan

288 5(E218A) protein leads to survival rates and cognitive dysfunction that mirror human WNV neuroinvasiv

289 g stress and this may underlie affective and cognitive dysfunctions that characterize stress-related

290 linked adolescent cannabis use to long-term cognitive dysfunction, there are negative reports as wel

291 uggesting an association between obesity and cognitive dysfunction, this phenomenon has received rela

292 myofascitis (MMF) and the relationship with cognitive dysfunction through the use of PET with (18)F-

293 rebromicrovascular pathology associated with cognitive dysfunction using APPSwDI transgenic mice expr

294 n this study of MDD adults who self-reported cognitive dysfunction, vortioxetine significantly improv

295 t cascade activation, neuroinflammation, and cognitive dysfunction, we used a genetic approach-condit

296 losed that status epilepticus, psychosis and cognitive dysfunction were statistically significant var

297 ric symptoms, seizures, movement disorder or cognitive dysfunction, were identified from 111 paediatr

298 as been shown to specifically replicate this cognitive dysfunction, which has limited its translation

299 HIIT attenuated hypoglycemia-induced cognitive dysfunction, which was mainly driven by change

300 rly individuals without clinical evidence of cognitive dysfunction who were randomly assigned to cons