ライフサイエンスコーパス: cognitive deficit

1 ysfunctions of Dravet Syndrome: Epilepsy and cognitive deficit.

2 network function in humans was important for cognitive deficit.

3 on tau phosphorylation and accumulation, and cognitive deficit.

4 ut alterations could play some role in these cognitive deficits.

5 ating Setd1a expression in adulthood rescues cognitive deficits.

6 syndrome (DS) results in various degrees of cognitive deficits.

7 nses, blood-brain barrier leakage (BBB), and cognitive deficits.

8 in the hippocampus, leading to male-specific cognitive deficits.

9 ng both increased seizure susceptibility and cognitive deficits.

10 ic and neuronal EAAT2 results in age-related cognitive deficits.

11 ing stereotyped behaviour, impulsiveness and cognitive deficits.

12 in disorders, including major depression and cognitive deficits.

13 ot be the underlying causes for the observed cognitive deficits.

14 ed with earlier age at onset and more severe cognitive deficits.

15 elated layer 2/3 mitochondrial, circuit, and cognitive deficits.

16 mation, lessened Abeta load, and ameliorated cognitive deficits.

17 d as a predictor of treatment resistance and cognitive deficits.

18 er that manifests with seizures, autism, and cognitive deficits.

19 utcomes than psychotic symptoms or nonsocial cognitive deficits.

20 with schizophrenia (SCZ) experience chronic cognitive deficits.

21 rse serum lipids, and smoking associate with cognitive deficits.

22 roduction, in turn leading to depression and cognitive deficits.

23 as a promising therapeutic approach to treat cognitive deficits.

24 ment is an important factor underlying these cognitive deficits.

25 l-documented evidence that obesity can cause cognitive deficits.

26 be a promising new drug target for different cognitive deficits.

27 s in youth, and is sometimes associated with cognitive deficits.

28 ficantly improved lipopolysaccharide-induced cognitive deficits.

29 hat is, sleepiness, depression, anxiety, and cognitive deficits.

30 avenue to combat head trauma-induced chronic cognitive deficits.

31 from the general population have significant cognitive deficits.

32 ion between neonatal complications and adult cognitive deficits.

33 if such losses are apparently independent of cognitive deficits.

34 r developing optimal strategies for treating cognitive deficits.

35 f CBD on THC-induced anxiety, psychosis, and cognitive deficits.

36 n the absence of depressive-like behavior or cognitive deficits.

37 d alpha-synuclein in the CNS and ameliorated cognitive deficits.

38 can be precisely mapped onto behavioral and cognitive deficits.

39 ment poverty and slowness, tremor and subtle cognitive deficits.

40 at result from their use are associated with cognitive deficits.

41 titive behavior, and is also associated with cognitive deficits.

42 for other neurodevelopmental disorders with cognitive deficits.

43 ufficiency of ATXN1 do not cause significant cognitive deficits.

44 nd impaired cBF integrity results in lasting cognitive deficits.

45 s, attenuates synapse loss, and thus rescues cognitive deficits.

46 acology prevents the pHFD-induced prefrontal cognitive deficits.

47 ith neurodegenerative disorders in aging and cognitive deficits.

48 n vehicle emissions result in behavioral and cognitive deficits.

49 5q13.3 manifest neuropsychiatric disease and cognitive deficits.

50 ecreased hippocampal neuron loss and rescued cognitive deficits.

51 es in the medial frontal cortex that lead to cognitive deficits.

52 nnovative strategy to improve age-associated cognitive deficits.

53 mpaired in the hippocampus of aged mice with cognitive deficits.

54 analogs of depression and schizophrenia-like cognitive deficits.

55 d neuronal damage, microglia activation, and cognitive deficits.

56 pyramidal movements, spasticity, ataxia, and cognitive deficits.

57 sk (p = 0.019), which may reflect IE-related cognitive deficits.

58 rder characterized by myoclonic epilepsy and cognitive deficits.

59 arly phase of schizophrenia and may underlie cognitive deficits.

60 fects of HIV- and methamphetamine-associated cognitive deficits.

61 y modulate neurodevelopment and cause psycho-cognitive deficits.

62 e a correspondingly heterogeneous profile of cognitive deficits.

63 of traumatic brain injury-induced persistent cognitive deficits.

64 but they are not very effective in reversing cognitive deficits.

65 ed the compromised reactive astrogliosis and cognitive deficits.

66 may be a misnomer because BECTS is linked to cognitive deficits, a more severe phenotype with intract

67 und that they developed hippocampus-mediated cognitive deficits accompanied by an age-dependent reduc

68 minobutyric acid type A receptors attenuated cognitive deficits after traumatic brain injury and enha

69 Cognitive deficits after traumatic brain injury are a le

70 dict variability in the type and severity of cognitive deficits after traumatic brain injury.

71 ive facial abnormalities, reduced growth and cognitive deficits along with hair anomalies.

72 Ischemia-induced brain neuronal death and cognitive deficits also increase in these mice.

73 Sleep loss produces well-characterized cognitive deficits, although there are large individual

74 In addition to cognitive deficits, Alzheimer's disease (AD) is associat

75 Furthermore, elevating miR-195 ameliorates cognitive deficits, amyloid plaque burden, and tau hyper

76 Aging rhesus monkeys naturally develop cognitive deficits, amyloid plaques, and the same qualit

77 disturbances, anxiety-like behaviour, severe cognitive deficit and an increased risk of fatality.

78 te matter (WM) connectivity in pathogenesis, cognitive deficit and psychopathology of schizophrenia.

79 nic mice displayed exacerbated Abeta-induced cognitive deficits and a selective decrease in synapsins

80 ith type 1 diabetes (T1D) has been linked to cognitive deficits and altered brain anatomy and connect

81 stress during adolescence may cause enduring cognitive deficits and anxiety in both humans and animal

82 after B-TBI prevented the induction of both cognitive deficits and B-TBI induced changes in SYP stai

83 in Alzheimer's Disease (AD), driving initial cognitive deficits and clinical manifestation.

84 for patients experiencing the combination of cognitive deficits and depression associated with AD.

85 and female wild-type and TgF344-AD rats from cognitive deficits and depressive-like behavior.

86 ific pathology, resulting in protection from cognitive deficits and depressive-like behavior.

87 Anti-LGI1 encephalitis is associated with cognitive deficits and disability as a result of structu

88 GluD1 expression in striatal neurons elicits cognitive deficits and disrupts the thalamostriatal syst

89 mice developed more severe sensorimotor and cognitive deficits and greater axonal and myelin injury

90 core features of schizophrenia (SCZ) include cognitive deficits and impaired sensory gating represent

91 n-robot interaction, partly accounted for by cognitive deficits and medication.

92 ence suggests that soluble tau species cause cognitive deficits and memory impairment.

93 , including cancer, reproductive impairment, cognitive deficits and obesity.

94 ial agonist of nAChR, for 1 day would affect cognitive deficits and P50 inhibition deficits in SCZ pa

95 se, which is associated with domain-specific cognitive deficits and relatively spared episodic memory

96 6p11.2(dp/+) mice ameliorated the social and cognitive deficits and reversed GABAergic synaptic impai

97 (TBI), yet whether these cells contribute to cognitive deficits and secondary inflammatory pathology

98 und that repression of AMPKalpha1 alleviated cognitive deficits and synaptic failure displayed in 2 s

99 poE4-associated brain PIP(2) dyshomeostasis, cognitive deficits, and AD pathology.

100 behavioral phenotypes, including social and cognitive deficits, and exhibit altered synaptic functio

101 tal re-experiencing of the trauma, long-term cognitive deficits, and PTSD-associated hippocampal dysf

102 shed children, involving growth stunting and cognitive deficits, and significant growth and productio

103 redictive coding contributes to symptoms and cognitive deficits, and this dysfunction is further posi

104 Cognitive deficits are a common feature of psychiatric d

105 Cognitive deficits are among the most severe and pervasi

106 for a scientific commentary on this article.Cognitive deficits are common among epilepsy patients.

107 the exact mechanistic underpinnings of these cognitive deficits are largely unknown, deficits in cort

108 The pathways underlying T2DM-induced cognitive deficits are not known.

109 Cognitive deficits are not observed in males of either g

110 molecular mechanisms underlying age-related cognitive deficits are not yet fully elucidated.

111 Although cognitive deficits are one of the factors most strongly

112 sleep problems even before memory and other cognitive deficits are reported.

113 notype that can aid repair and alleviate the cognitive deficits arising from brain injury.

114 ebrospinal fluid of HIV-infected people with cognitive deficits as compared with infected people with

115 FOXP1 is additionally linked to cognitive deficits, as is FOXP4.

116 and/or cGMP activities, which may ameliorate cognitive deficits associated with AD.

117 a decrease in DBN levels is correlated with cognitive deficits associated with ageing and dementia,

118 5 is distributed to the brain and can rescue cognitive deficits associated with aging in mice.

119 rom recent LTM, which may have relevance for cognitive deficits associated with aging, temporal lobe

120 ls of amyloid-beta (Abeta) and contribute to cognitive deficits associated with Alzheimer's disease (

121 potential nicotine-related masking effect on cognitive deficits associated with cannabis use, yet the

122 t common complication of long-term diabetes, cognitive deficits associated with encephalopathy and my

123 s as a potential therapeutic target to treat cognitive deficits associated with MS.SIGNIFICANCE STATE

124 Network and cognitive deficits associated with neurological disorder

125 p75(NTR) as a promising target to limit the cognitive deficits associated with SD.

126 y, yet the mechanisms underlying the chronic cognitive deficits associated with TBI remain unknown.

127 ase-modifying treatments to prevent or treat cognitive deficits associated with the disease.

128 therapeutic targets to mitigate or delay the cognitive deficits associated with this devastating dise

129 Altogether, these findings suggest that cognitive deficits attributable to adversity during earl

130 Consistent with cognitive deficits being core features of the phenotype

131 Abeta and correlates with the development of cognitive deficits better than the number of plaques.

132 bate Abeta pathology, neuroinflammation, and cognitive deficits, but it is unknown how the loss of LC

133 Temporal lobe epilepsy causes severe cognitive deficits, but the circuit mechanisms remain un

134 in FXS, and enriched environment may rescue cognitive deficits by improving network activation accur

135 hagy contributes to synaptic dysfunction and cognitive deficits by triggering Abeta and Tau accumulat

136 , was death or disability, defined as any of cognitive deficit, cerebral palsy, or severe visual or h

137 esis of neurodevelopmental abnormalities and cognitive deficits commonly observed in psychiatric diso

138 1q-Flox mice exposed to cranial RT showed no cognitive deficits compared with irradiated WT mice.

139 ring the Persian Gulf War and is notable for cognitive deficits, depression, muscle pain, weakness, i

140 Cognitive deficits during nicotine withdrawal may contri

141 involved in these effects is crucial because cognitive deficits during nicotine withdrawal may predic

142 connectivity in prefrontal-limbic circuits), cognitive deficits (e.g., executive function and memory

143 as an FTD-associated tau variant can lead to cognitive deficits even in the absence of tangles.

144 en with sickle cell disease (SCD) experience cognitive deficits even when unaffected by stroke.

145 intracranial transplantation can ameliorate cognitive deficits following 9 Gy head-only irradiation.

146 ippocampal neuronal loss, and behavioral and cognitive deficits following BCAS.

147 e effects of proton radiotherapy, a model of cognitive deficits from conventional proton exposure is

148 It encompasses the full range of cognitive deficits from mild cognitive impairment to dem

149 s (n = 101) using model-based predictions of cognitive deficits generated from the Iowa cohort lesion

150 Modelling supported earlier findings that cognitive deficit has a putatively causal role in schizo

151 both endogenous C9orf72 alleles exacerbated cognitive deficits, hippocampal neuron loss, glial activ

152 adult neurogenesis in the hippocampus causes cognitive deficits; however, the underlying molecular me

153 eutic effects of PDD005 for the treatment of cognitive deficit in aging mice.

154 over, a battery of tests revealed a specific cognitive deficit in older adults with geometric prefere

155 ts of variable severity in five individuals, cognitive deficit in two individuals, and various unusua

156 We show that cognitive deficits in 7-month-old 3xTg-AD mice are assoc

157 ted the effects of EC-DBS on the progressive cognitive deficits in a genetically-based mouse model of

158 3 overexpression prevented synaptic loss and cognitive deficits in a mouse model of neurodegeneration

159 estation produce communication, learning and cognitive deficits in a rat model that can be prevented

160 a potential network correlate for persistent cognitive deficits in absence epilepsy despite effective

161 such as losartan restore cerebrovascular and cognitive deficits in AD is unknown.

162 OPC cell senescence in neuroinflammation and cognitive deficits in AD, and a potential therapeutic be

163 inks between AD pathology and behavioral and cognitive deficits in AD.

164 CANCE STATEMENT Clinical research identified cognitive deficits in alcoholic individuals as a risk fa

165 ion is an early event in the pathogenesis of cognitive deficits in Alzheimer's disease (AD).

166 tor transcription underlies the synaptic and cognitive deficits in Alzheimer's disease, and targeting

167 al changes in network function that underlie cognitive deficits in Alzheimer's disease.

168 and aggregation, are considered hallmarks of cognitive deficits in Alzheimer's disease.

169 s measured with 18F-AV-1451-PET imaging, and cognitive deficits in Alzheimer's disease.

170 plored as promising targets for ameliorating cognitive deficits in Alzheimer's disease.

171 n protein antagonist can rescue synaptic and cognitive deficits in Alzheimer's mice overexpressing am

172 fied Abeta oligomers during the evolution of cognitive deficits in an aggressive model of Abeta amylo

173 el for understanding the biological bases of cognitive deficits in AN and provides context for new tr

174 that increasing brain p62 expression rescues cognitive deficits in APP/PS1 mice, a widely used animal

175 t the lack of Nrf2 significantly exacerbates cognitive deficits in APP/PS1, without altering gross mo

176 We confirmed cognitive deficits in Atxn1154Q/2Q knock-in mice with br

177 The biomarkers that predict cognitive deficits in BD are largely unknown, however re

178 posure to antipsychotic medications leads to cognitive deficits in both schizophrenia patients and an

179 which intermittent seizures drive persistent cognitive deficits in conditions accompanied by recurren

180 esting state networks (RSNs) associated with cognitive deficits in different frequency bands in 25 PP

181 Compound 28 robustly reversed the cognitive deficits in episodic/working memory in both ti

182 ges might be involved in the pathogenesis of cognitive deficits in ET.

183 trophic lateral sclerosis (ALS) exhibit mild cognitive deficits in executive functions, language and

184 apies are underway, with the aim of treating cognitive deficits in fetal alcohol spectrum disorders.

185 -driven Sema5a deregulation may underlie the cognitive deficits in FUS transgenic mice.

186 inappropriate engram reactivation underlies cognitive deficits in FXS, and enriched environment may

187 It is also not clear whether cognitive deficits in Gambling Disorder extend to those

188 toluene) misuse is linked to behavioral and cognitive deficits in humans, yet preclinical studies of

189 abuse that cause devastating behavioral and cognitive deficits in humans.

190 dy showed significant gender differences for cognitive deficits in immediate and delayed memory in sc

191 The physiological basis of cognitive deficits in LD is thus largely unexplored.

192 ng PDE4D activity using an inhibitor rescues cognitive deficits in male mice but has no effect on fem

193 Hypofrontality is considered a main cause of cognitive deficits in mental disorders, yet the underlyi

194 er metabolic impairment and a wider array of cognitive deficits in middle-aged females than males.

195 bilobalide has been linked to the rescue of cognitive deficits in mouse models of Down syndrome(5).

196 neural substrates that link demyelination to cognitive deficits in MS, we investigated hippocampal ne

197 bral cortical association areas may underlie cognitive deficits in neurodevelopmental disorders, incl

198 load and microglia activation, and improved cognitive deficits in old Gen-1 and Gen-2 APP/PS1 mice.

199 Indeed, depression often precedes cognitive deficits in patients with AD.

200 molecular and cellular mechanisms underlying cognitive deficits in patients with cancer, novel treatm

201 mation integration and organization and thus cognitive deficits in patients with PD.

202 frequency bands in brain networks underlying cognitive deficits in primary-progressive multiple scler

203 ination also prevented age-related motor and cognitive deficits in PS19 mice and significantly reduce

204 Cognitive deficits in psychiatric and age-related disord

205 as been implicated in the pathophysiology of cognitive deficits in psychiatric disorders.

206 stones of clinical neurology, behavioral and cognitive deficits in psychiatry remain impervious to th

207 as a therapeutic target in the treatment of cognitive deficits in psychosis.

208 xn1154Q/2Q mice, supporting the concept that cognitive deficits in SCA1 arise from a combination of c

209 a potential therapeutic target for improving cognitive deficits in schizophrenia and other disorders.

210 ved in both neurodevelopment and severity of cognitive deficits in schizophrenia are associated with

211 onnectivity is responsible for 2 of the core cognitive deficits in schizophrenia- reduced information

212 al neural target for the treatment of social cognitive deficits in schizophrenia.

213 reversing cortical-related symptoms, such as cognitive deficits in schizophrenia.

214 residual positive and negative symptoms and cognitive deficits in schizophrenia.

215 be understood within the broader context of cognitive deficits in Sz, where impaired DLPFC-related c

216 The findings indicate that mood and cognitive deficits in T2DM patients has brain structural

217 au) forms neurotoxic aggregates that promote cognitive deficits in tauopathies, the most common of wh

218 pressive-like behavior occurred earlier than cognitive deficits in TgF344-AD rats, consistent with AD

219 n of amyloid deposits, neuroinflammation and cognitive deficits in the AD mouse model.

220 rodegenerative disorder that leads to severe cognitive deficits in the elderly population.

221 e prevents N-CAD proteolysis and ameliorates cognitive deficits in the mice.

222 , suggesting they were not biased by general cognitive deficits in the patients.

223 loid beta (Abeta)-associated pathologies and cognitive deficits in two mouse models of Alzheimer's di

224 However, the observed cognitive deficits in victimized individuals were largel

225 ty and attenuated long-term sensorimotor and cognitive deficits in wild-type mice, as revealed by his

226 beta1-40 ratio, prevented the development of cognitive deficits in Y-maze test and improved synaptic

227 ght underlie some of the symptoms, including cognitive deficits, in LD.

228 aspects, including microglial reactivity and cognitive deficits, in the brains of aged mice.

229 Patients also display cognitive deficits including impairments in working memo

230 my 21 is a developmental disorder leading to cognitive deficits, including disruption of hippocampus-

231 Aging is accompanied by cognitive deficits, including impairments in long-term m

232 th schizophrenia typically suffer a range of cognitive deficits, including prominent deficits in work

233 und participants with celiac disease to have cognitive deficit, indications of worsened mental health

234 Thus, some perceptual and cognitive deficits induced by developmental hearing loss

235 thalamocortical pathway, some perceptual and cognitive deficits induced by developmental hearing loss

236 the ISR, reversed the hippocampal-dependent cognitive deficits induced by TBI in two different injur

237 gh-energy, heavy particle radiation, and the cognitive deficits induced by this exposure are not well

238 Many of these cognitive deficits involve dysfunction of the newly evol

239 This cognitive deficit is consecutive to PKA deregulation in

240 Cognitive deficit is thought to represent, at least in p

241 r understanding of the pathogenesis of these cognitive deficits is needed.

242 We examined cognitive deficits, kynurenine pathway mediators, TXNIP,

243 dings imply that first-episode patients with cognitive deficits may gain from glutamate-modulating co

244 s of SCZ pathogenesis, especially related to cognitive deficits, may lead to improved treatments.

245 nogen induces spine elimination and promotes cognitive deficits mediated by CD11b-CD18 microglia acti

246 usation models to assess the extent to which cognitive deficit mediates some of the effect of polygen

247 Substantial evidence suggests that cognitive deficits might persist after remission of a ma

248 gic system to demonstrate an exacerbation of cognitive deficits, neuroinflammation, neurodegeneration

249 To examine whether the general cognitive deficit observed across psychotic disorders is

250 etwork efficiency play a role in the general cognitive deficit observed across the psychosis spectrum

251 ac1 hyperactivity in synaptic plasticity and cognitive deficits observed in Cc2d1a cKO mice and revea

252 ynapse function, which may contribute to the cognitive deficits observed in pathological mitochondria

253 thought to contribute to the development of cognitive deficits observed in schizophrenia.

254 re consistently and robustly associated with cognitive deficits of ASD and ID in humans, and overexpr

255 hibitor of 2-AG biosynthesis O7460 abolished cognitive deficits of nicotine abstinence, whereas the i

256 ource allocation may contribute to the early cognitive deficits of Parkinson's disease.

257 e of glucose metabolism may be implicated in cognitive deficits of schizophrenia in its early phases.

258 ysarthria, dysphagia, cerebellar ataxia, and cognitive deficits, often accompanied by exotropia and m

259 efore study enrollment with either objective cognitive deficits or subjective cognitive complaints we

260 s of neuroinflammation correlated with worse cognitive deficits.Our study suggests that neuroinflamma

261 inued post-HSCT; however, the progression in cognitive deficits, overall functional status and gait i

262 ation therapy of brain tumors often produces cognitive deficits, particularly in children.

263 However, clinical reports of long-lasting cognitive deficits, particularly in subjects who discont

264 e association between brain connectivity and cognitive deficits post-TBI.

265 At more advanced ages (16-19 months), cognitive deficits progressed in conjunction with restin

266 have employed lighting conditions that cause cognitive deficits rather than improvements.

267 anied by recurrent seizures, the severity of cognitive deficits reflects the degree of calbindin redu

268 ce (16p11.2(dp/+)) and identified social and cognitive deficits reminiscent of ASD and ID phenotypes.

269 stemic inflammation produces both reversible cognitive deficits, resembling delirium, and acute brain

270 elevant contributing factor for the onset of cognitive deficits resulting from abnormal increases of

271 mic responses and EEG abnormalities, improve cognitive deficits, revert autistic-like behaviors and p

272 the cellular mechanisms mediating RT-induced cognitive deficits (RICD) are poorly understood.

273 campal mitochondrial changes may account for cognitive deficits seen in children and adolescents born

274 Clinically, cognitive deficits should be conceptualized as individua

275 identification of treatments for age-related cognitive deficits.SIGNIFICANCE STATEMENT People and mic

276 rodegeneration, as well as related motor and cognitive deficits.SIGNIFICANCE STATEMENT Traumatic brai

277 The profile of mild cognitive deficits specifically predicts regional cerebr

278 as a therapeutic strategy for conditions of cognitive deficit such as neurodegeneration.

279 ormance (r = 0.182; P = .184) and related to cognitive deficits such as attention and perception (rho

280 Cognitive deficits such as working memory (WM) impairmen

281 sed protein-transport systems often underlie cognitive deficits, such as those associated with aging

282 re more likely to develop mood disorders and cognitive deficits than women in the general population.

283 a promising strategy to limit the memory and cognitive deficits that accompany sleep loss.SIGNIFICANC

284 This dysfunction is manifest as cognitive deficits that appear to arise from disturbance

285 ropathic pain and underlie the mPFC-specific cognitive deficits that are comorbid with neuropathic pa

286 on is thought to be a critical factor in the cognitive deficits that are observed in diseases such as

287 companying these changes were behavioral and cognitive deficits that could be rescued by either desig

288 lae from their treatments, including serious cognitive deficits that impair daily function.

289 imized individuals were largely explained by cognitive deficits that predated childhood victimization

290 Schizophrenia is associated with cognitive deficits that reflect impaired cortical inform

291 are often unaware of their sensorimotor and cognitive deficits, there is a critical need for non-inv

292 f nicotine and related agonists for treating cognitive deficits, these data suggest that daily dosing

293 This suggests that tau pathology may lead to cognitive deficits through a variety of mechanisms, incl

294 gen leads to dendritic spine elimination and cognitive deficit via microglial CD11b/CD18.

295 Cognitive deficit was found in spatial memory and explor

296 e of -0.7% (95% CI, -4.3% to 2.9%; P = .70), cognitive deficit was observed in 154/410 (37.6%) vs 148

297 Cognitive deficits were observed in both CNV groups, wit

298 ecipitation of nicotine withdrawal, when the cognitive deficits were still present.

299 unclear whether these changes are related to cognitive deficits, which have been described in ET pati

300 een associated with psychiatric symptoms and cognitive deficits, yet we have almost no knowledge of t