ライフサイエンスコーパス: memory deficit

1 ty, impaired social interaction, and working memory deficit.

2 d full-length species that could explain the memory deficit.

3 novel object recognition task as a model of memory deficit.

4 at results in increased tonic inhibition and memory deficit.

5 pairment of long-term potentiation (LTP) and memory deficit.

6 e (JNK) activation, which is associated with memory deficits.

7 of synaptic F-actin contributes directly to memory deficits.

8 sensorimotor gating, albeit without profound memory deficits.

9 we demonstrate that only Abeta1-42 leads to memory deficits.

10 ng-lasting hyper-excitability and persistent memory deficits.

11 missorting into dendritic spines followed by memory deficits.

12 in the aged mice was accompanied by spatial memory deficits.

13 cits, including intellectual, executive, and memory deficits.

14 rological conditions, or basic perceptual or memory deficits.

15 AD patients underestimated their memory deficits.

16 h microinfusion of DCS restored meth-induced memory deficits.

17 n the behavioral phenotypes of AD, including memory deficits.

18 ing of lifespan and no worsening of motor or memory deficits.

19 anifested a significant improvement of their memory deficits.

20 trition in PL pyramidal neurons, and working memory deficits.

21 n, the levels of inflammatory cytokines, and memory deficits.

22 erable to dementia and frequently experience memory deficits.

23 signaling, and prevents synaptic injury and memory deficits.

24 E4 inhibitors for depression and concomitant memory deficits.

25 quitin, and tau, and improved the associated memory deficits.

26 ng reduced amyloid-beta deposits and rescued memory deficits.

27 GABAergic interneuron loss and learning and memory deficits.

28 sphorylation and rescued hippocampal LTP and memory deficits.

29 e models and humans, leading to learning and memory deficits.

30 its deletion in mice results in learning and memory deficits.

31 stitute a sensitive biomarker of forthcoming memory deficits.

32 e fibers in striatum, and improved motor and memory deficits.

33 that both CCI and S-CCI produced persisting memory deficits.

34 uced obesity, hypogonadism, and learning and memory deficits.

35 umber and synaptic plasticity, and prevented memory deficits.

36 n of both in the same mouse produced working memory deficits.

37 ce Hypothesis in the context of mTBI related memory deficits.

38 re a relevant cause for pain-related working memory deficits.

39 sting that our model can also produce graded memory deficits.

40 genitors showed improvements in learning and memory deficits.

41 mnesic patients to compensate for relational memory deficits.

42 ped exploratory behavior and novelty-related memory deficits.

43 isplayed stereotyped exploratory behavior or memory deficits.

44 ne decreased Abeta pathology and ameliorated memory deficits.

45 s Abeta generation and improves learning and memory deficits.

46 se (AD) and contributes to the AD-associated memory deficits.

47 ts of donepezil in 27 older adults with mild memory deficits.

48 nnate immune response, resulting in profound memory deficits.

49 ith Abeta lack neuronal loss at the onset of memory deficits.

50 underlies olfactory associative learning and memory deficits.

51 ecies and attenuated the loss of neurons and memory deficits.

52 tered neurogenesis, as well as cognitive and memory deficits.

53 icant reversal in the observed cognitive and memory deficits.

54 .0 [1.96]; controls, 25.86 [1.24]; P < .001) memory deficits.

55 , r = -0.41; P = .04) correlated with verbal memory deficits.

56 ewy pathology, but not CA2, in causing these memory deficits.

57 on neurogenesis and associated learning and memory deficits.

58 al (ROCF delayed recall, r = -0.46; P = .03) memory deficits.

59 measurements in populations with progressing memory deficits.

60 gy, neuronal death, and exacerbates synaptic/memory deficits.

61 fore and during MWM rescued the learning and memory deficits.

62 hy, neuron loss, dendritic degeneration, and memory deficits.

63 ng-term depression, and induces learning and memory deficits.

64 erconnection may be a trigger to age-related memory deficits.

65 ed tau and amyloidogenic Abeta-peptides, and memory deficits.

66 done and dibenzoylmethane treatment restored memory deficits, abrogated development of neurological s

67 ed corticosterone, depressive-like behavior, memory deficits, accompanied with decreased cAMP-PKA-CRE

68 n of alpha5GABA(A)Rs completely reversed the memory deficits after anesthesia.

69 esting a mechanism to account for persistent memory deficits after general anesthesia.

70 -42 and completely rescued spatial reference memory deficits after passive immunization.

71 nts the loss of dendritic spines and rescues memory deficits after TBI.

72 be a potential therapeutic target to restore memory deficits after TBI.SIGNIFICANCE STATEMENT Traumat

73 ed WT mice developed spatial and recognition memory deficits, aged Pdyn(-/-) mice performed similarly

74 ; 50, 100 and 200mg/kg, p.o. for 10 days) on memory deficit and cerebral oxidative stress induced by

75 , but not control CSF, developed progressive memory deficit and depressive-like behavior along with d

76 ed at a subanesthetic dose, produces working memory deficit and other schizophrenia-like symptoms in

77 glial activation correlates with the spatial memory deficit and spread of tau pathology in the anatom

78 Removal of tau oligomers reversed memory deficits and accelerated plaque deposition in the

79 TgCRND8 mice exhibited spatial memory deficits and altered anxiety that were rescued af

80 escued the early contextual fear and spatial memory deficits and decreased subsequent plaque load in

81 ic excitability, which may contribute to the memory deficits and epilepsy that are prominent in patie

82 diated PGRN overexpression prevented spatial memory deficits and hippocampal neuronal loss in AD mice

83 K281 acetylation (tauKQ) exhibit AD-related memory deficits and impaired hippocampal long-term poten

84 irmed that Kir6.2 mutant mice exhibit severe memory deficits and impaired hippocampal LTP, impairment

85 tional knockout of Deaf1 in the brain showed memory deficits and increased anxiety-like behavior.

86 sory changes translated into domain-specific memory deficits and increased compulsive-like behaviors,

87 of MiR-223 leads to contextual, but not cued memory deficits and increased neuronal cell death follow

88 as been implicated previously in recognition-memory deficits and is expressed in subcortical structur

89 stereotypic behaviors, anxiety, learning and memory deficits and motor defects.

90 nction in cultured neurons, and it prevented memory deficits and neurodegeneration in mice.

91 ant Tau transgenic mice restores the spatial memory deficits and normalizes the basic synaptic transm

92 lays a causal role in stress-induced working memory deficits and pointing to a potential new avenue t

93 tau acetylated at K174, rescued tau-induced memory deficits and prevented hippocampal atrophy.

94 ce, both drugs were neuroprotective, rescued memory deficits and reduced hippocampal atrophy.

95 PP/PS1 transgenic mice fully rescues spatial memory deficits and synaptic depletion, without altering

96 Processing speed and working memory deficits and white-matter abnormalities may serve

97 s (PCBs) and have both central (learning and memory deficits) and peripheral (motor dysfunction) neur

98 r pathological features of the AD phenotype: memory deficits, and Abeta and tau neuropathology.

99 l cerebrospinal fluid, developed progressive memory deficits, and anhedonic and depressive-like behav

100 anized communication, suspiciousness, verbal memory deficits, and decline in social functioning durin

101 of the RPSV, increased synaptic depression, memory deficits, and epilepsy.

102 Dnmt3a2; re-expression in aged mice reverses memory deficits, and knockdown in young mice impairs mem

103 6K1 improved synaptic plasticity and spatial memory deficits, and reduced the accumulation of amyloid

104 reduced prepulse inhibition (PPI), long-term memory deficits, and spontaneous locomotor hyperactivity

105 e found that specific effects of THC such as memory deficits, anxiolytic-like effects, and social int

106 Working memory deficits are characteristic for many psychiatric

107 Learning and memory deficits are early clinical manifestations of Hun

108 structural hippocampal damage and associated memory deficits are important long-term sequelae of the

109 Hippocampus-based learning and memory deficits are key symptoms of FASD.

110 changes, the molecular mechanisms leading to memory deficits are not clear.

111 ophrenia are worsened by stress, and working memory deficits are often a central feature of illness.

112 large sample of wild sea lions, that spatial memory deficits are predicted by the extent of right dor

113 Working memory deficits are present in several psychiatric disor

114 Working memory deficits are prominent in stress-related mental d

115 t-term memory, but exhibited broad long-term memory deficits as revealed by several behavioral paradi

116 (+/+) showed more severe spatial and working memory deficits as well as worse motor performance than

117 r the development of CAA, negated short-term memory deficits, as assessed by object-recognition tests

118 t correlated with the extent of learning and memory deficits, as determined by Morris water maze (MWM

119 rease, working memory impairment, and social memory deficits, as well as synaptic and structural plas

120 be directly responsible for the synaptic and memory deficits associated with fetal alcohol spectrum d

121 fficacy of this mechanism to correct working memory deficits associated with NMDA hypofunction.

122 ic M1 receptors is thought to worsen working memory deficits associated with schizophrenia.

123 at time points late after injury can reverse memory deficits associated with TBI.

124 the precise role of dopamine transmission in memory deficits associated with these disorders and thei

125 A53T mice also exhibit spatial memory deficits at 6 and 12 months, as demonstrated by Y

126 te compensation of EC lesion-induced spatial memory deficit before a slower glutamatergic reinnervati

127 Are memory deficits better explained by damage to individual

128 ns exhibit amyloid-beta-induced synaptic and memory deficits but they do not fully recapitulate other

129 to ameliorate schizophrenia-spectrum working memory deficits, but has yet to be rigorously evaluated

130 tic plasticity impairments, and learning and memory deficits, but not apoptosis.

131 c pain patients commonly complain of working memory deficits, but the mechanisms and brain areas unde

132 beta-amyloid levels, plaque deposition, and memory deficits by 2-3 mo of age.

133 reverses Abeta-induced spatial learning and memory deficits by restoring a specific subset of Crtc1

134 n that an anti-A2AR therapy reverts age-like memory deficits, by reestablishment of the hypothalamic-

135 overexpression not only failed to rescue the memory deficit caused by APPL loss of function, it exace

136 for olfactory memory, is able to rescue the memory deficit caused by APPL partial loss of function.

137 mutant APPL form is sufficient to rescue the memory deficit caused by APPL reduction, revealing for t

138 ), AMPAR potentiators reduce spatial working memory deficits caused by the nonselective NMDAR antagon

139 emory processes, with orthographic long-term memory deficits centred in either the left posterior inf

140 ohen d = 1.24; P = 6.91 x 10-30) and working memory deficits (Cohen d = 0.83; P = 1.10 x 10-14) as we

141 ed sleep time, diminished sleep rebound, and memory deficits comparable to those after sleep loss.

142 Individuals with DS often exhibit working memory deficits coupled with degeneration of the locus c

143 cits may lead to the variety of learning and memory deficits defining ID is still unknown.

144 mpus of adult Fmr1(-/y) mice rescued working memory deficits, demonstrating reversal of this FXS phen

145 stresses, which might be relevant to spatial memory deficits described in posttraumatic stress disord

146 Conversely, memory deficits displayed by dAbeta-expressing flies are

147 g progressive terminal neurodegeneration and memory deficits due to a disruption of hippocampal choli

148 In spite of their memory deficit during free reporting, after accuracy mon

149 e evidence that CRTC1 deregulation underlies memory deficits during neurodegeneration.

150 n may underlie persistent age-related source memory deficits, even when encoding is supported via dir

151 d a role in impaired synaptic plasticity and memory deficits exhibited by AS model mice.

152 ic Sirt1 knock-out closely recapitulated the memory deficits exhibited by obese mice, consistent with

153 Autobiographic memory deficits exist in HR individuals, suggesting that

154 empts to prevent such stress-induced working memory deficits focused mainly on pharmacological interv

155 disorders are characterized by learning and memory deficits, for which cognitive enhancement is cons

156 Targeting Fyn can reverse memory deficits found in AD mouse models, and rescue syn

157 Memory deficits gradually worsened until Day 18 (4 days

158 eurons (Ctcf CKO mice) have spatial learning/memory deficits, impaired fine motor skills, subtly alte

159 rological disturbances including hippocampal memory deficits, implicating CD44 in the processes under

160 id negative feedback inhibition, but not the memory deficit, implying that the memory deficit is an i

161 pus after cohousing underlie the reversal of memory deficit in APP/PS1 mice.

162 y drugs, we first identified an early object memory deficit in APPSwe-PS1DeltaE9 mice that preceded p

163 Importantly, the pattern of memory deficit in both patient groups was specifically e

164 factors that may contribute to the semantic memory deficit in semantic variant primary progressive a

165 Moreover, we found that the memory deficit in the ApoE KO mice was specific to femal

166 Rats fed on an n-3 deficient diet showed memory deficits in a Barnes maze, which were further exa

167 amatically reduced Abeta levels and restored memory deficits in a mouse model of AD.

168 was sufficient to reverse both locomotor and memory deficits in a mouse model of tauopathy for 60 d,

169 ration of human recombinant CSF1 ameliorates memory deficits in a transgenic mouse model of Alzheimer

170 neural mechanisms underlying anosognosia of memory deficits in AD by combining measures of regional

171 an reduce Abeta neuropathology and alleviate memory deficits in AD model mice.

172 ndings suggest that the lack of awareness of memory deficits in AD results from a disruption of the c

173 molecular mechanism underlying synaptic and memory deficits in AD.

174 pse damage, neurodegeneration, learning, and memory deficits in AD.

175 ed by trisomy 21 contribute significantly to memory deficits in adult life in DS.

176 with a vulnerable genotype results in subtle memory deficits in adulthood, which might develop before

177 nal loss at P14, and (4) cerebral myelin and memory deficits in adulthood.

178 cial transcription factor PSD95-VP64 rescued memory deficits in aged and Alzheimer's disease mice.

179 In addition to reducing memory deficits in aged rats, FKBP1b selectively counter

180 o suggest that caffeine consumption prevents memory deficits in aging and Alzheimer's disease through

181 Synaptopathy underlying memory deficits in Alzheimer's disease (AD) is increasin

182 ases could alleviate synaptic plasticity and memory deficits in Alzheimer's disease model mice.

183 vated retinoid X receptors (RXRs) ameliorate memory deficits in Alzheimer's disease mouse models, inc

184 We confirm the reversal of memory deficits in APP/PS1DeltaE9 mice expressing human

185 ion protein (PrP(C)) prevents development of memory deficits in APPswe/PS1DeltaE9 mice, a model of fa

186 DNF rescues theta-LTP and cocaine-associated memory deficits in BAF53b transgenic mice.

187 has been successfully used to model working memory deficits in both rodents and nonhuman primates, b

188 show that hippocampal-dependent learning and memory deficits in CDKL5 deficiency have origins in glut

189 ow that 14 prevents manifestation of spatial memory deficits in chimeric EcoHIV-infected mice, a mode

190 R192Q mice showed significant spatial memory deficits in contextual fear-conditioning and Morr

191 Memory deficits in Drosophila nalyot mutants suggest tha

192 We find spatial learning and memory deficits in FE65-KO and FE65L1-KO mice.

193 dorsal hippocampus resulted in learning and memory deficits in fear conditioning, whereas CREB delet

194 s provide evidence of hippocampus-associated memory deficits in HD and demonstrate that p75(NTR) medi

195 could contribute to synaptic dysfunction and memory deficits in HD.

196 urons is a critical component underlying the memory deficits in hippocampus-dependent learning tasks

197 make these assays sensitive to learning and memory deficits in humans with MCI-AD and in mouse model

198 mug/kg) induced acute and transient working memory deficits in lesioned animals without effect in un

199 approach for disordered sleep physiology and memory deficits in MCI patients and advance our understa

200 rgic interneurons that leads to learning and memory deficits in mice and provides a novel target for

201 critical synaptic proteins, which results in memory deficits in mice but also decreases seizure susce

202 Finally, synaptic tagging and long-term memory deficits in mice lacking translin/trax are mimick

203 impairments and distraction alleviates these memory deficits in patients with hippocampal injury and

204 efficacious, and safe treatment for working memory deficits in patients with schizophrenia.

205 ion are associated with long-term contextual memory deficits in PS cDKO mice.

206 bodied cognition, and clinical research into memory deficits in psychiatric disorders.

207 t SAR218645 improved MK-801-induced episodic memory deficits in rats and attenuated working memory im

208 on results in novel object recognition (NOR) memory deficits in rats.

209 ntrol participants revealed disproportionate memory deficits in schizophrenia for relational vs item-

210 glutamate and GABA in MMN and verbal working memory deficits in schizophrenia has been frequently deb

211 o standardized treatment options for working memory deficits in schizophrenia.

212 ic neurobiologic correlates of attention and memory deficits in school-age survivors of neonatal extr

213 Blocking GluA2 endocytosis rescues memory deficits in stathmin mutant and aged wild-type mi

214 onths old) was also sufficient to rescue the memory deficits in Tg mice.

215 significantly improved spatial learning and memory deficits in Tg19959 mice, diminished Abeta plaque

216 logical lesions, and slows down learning and memory deficits in Tg2576 mice.

217 of large boutons indicate that learning and memory deficits in the aged brain arise not through an i

218 and plaque deposits, gliosis, and behavioral memory deficits in the disease-established 5xFAD mice.

219 n and neuritic plaque formation, and rescued memory deficits in the double transgenic AD model mice.

220 was associated with a reversal of contextual memory deficits in the drug-treated mice.

221 tides play a key role in synaptic damage and memory deficits in the early pathogenesis of Alzheimer's

222 rally accepted that neuronal dysfunction and memory deficits in the early stages of AD are caused by

223 normal circadian behavior and to rescue the memory deficits in the fragile X mutant fly.

224 I/KI);Psen2(-/-) mice exhibited mild spatial memory deficits in the Morris water maze task.

225 ese changes are associated with learning and memory deficits in the Morris Water Maze.

226 , 30 years after the initial injury, working memory deficits in the PBI group would remain, despite c

227 inflammatory processes contribute to spatial memory deficits in the rodent social defeat model that c

228 tor agonist LY379268 ameliorated the working memory deficits in the transgenic mice, suggesting that

229 that daily scheduled feeding rescued spatial memory deficits in these arrhythmic animals.

230 that preceded previously identified spatial memory deficits in this model.

231 ment impaired memory performance in wt mice, memory deficits in Ts65Dn mice were unchanged.

232 NF signaling rescued synaptic plasticity and memory deficits in Ts65Dn mice.

233 ed 3R-tau expression and rescued anxiety and memory deficits in Ts65Dn mouse brains.

234 4X and its Fab fragment also rescued working memory deficits in wild type mice induced by intraventri

235 tradiol synthesis, are suspected of inducing memory deficits in women.

236 , which plays a crucial role in learning and memory; deficits in this process have been associated wi

237 t, only male Nf1 GEM showed spatial learning/memory deficits, increased Ras activity, and reduced dop

238 ciated with memory and learning, and rescues memory deficits independently of its immunosuppressive a

239 PERK phosphorylation rescues spine loss and memory deficits independently of phosphorylation of eIF2

240 T4 and metformin alleviated contextual fear memory deficit induced by FAE, and reversed the hippocam

241 On the other hand, memory deficit induced by HMW AbetaOs (10 pmol) was foun

242 evel of the neprilysin 1 peptidase overcomes memory deficits induced by amyloid peptide in young flie

243 mory-enhancing properties and it ameliorated memory deficits induced by scopolamine.

244 Whether or not episodic memory deficit is a characteristic of behavioral variant

245 Episodic memory deficit is a common cognitive disorder in human t

246 ut not the memory deficit, implying that the memory deficit is an independent post-AT clinical entity

247 In schizophrenia patients, working memory deficit is highly debilitating and currently with

248 DMN-HC alterations in aging and concomitant memory deficits is largely unknown.

249 Here we examined visual short-term memory deficits--long associated with Parkinson's diseas

250 Years before clinical memory deficits manifest, amyloid-beta deposits in the c

251 tective effects of BAY against Abeta-induced memory deficits might involve the regulation of neuroinf

252 sensory disturbances, and verbal and spatial memory deficits, not only in complicated HSP but also in

253 on in aged animals ameliorated the long-term memory deficits observed in control animals.

254 representations could explain the long-term memory deficits observed in previous behavioral studies.

255 f retrieval was the major contributor to the memory deficit of DLB.

256 We found that 7,8-DHF rescued memory deficits of 5XFAD mice in the spontaneous alterna

257 the neuroanatomical defects and learning and memory deficits of Osteocalcin(-/-) mice is determined b

258 expressing 5LO manifested an exacerbation of memory deficits, plaques, and tangle pathologies.

259 ates spine numbers resulting in learning and memory deficits, possibly as a result of its essential r

260 The pattern of visual short-term memory deficit potentially provides a cognitive marker o

261 ic model of AD, PirB not only contributed to memory deficits present in adult mice, but also mediated

262 al temporal cortex, and orthographic working memory deficits primarily arising from lesions of the le

263 sease severity correlated with larger verbal memory deficits (RAVLT delayed recall, r = -0.40; P = .0

264 prevents hippocampus-dependent learning and memory deficits, restores motor function after brain tra

265 In fact, the working memory deficits resulting from reduced GABAergic transmi

266 naptic plasticity and is contributing to the memory deficits seen in Alzheimer's disease.

267 logical injury, gray matter volume loss, and memory deficits seen in children born extremely prematur

268 -dependent neurodegeneration or learning and memory deficits seen in gamma-secretase deficient mice.

269 Moreover, both groups with working memory deficits shared an inability to suppress parahipp

270 The patients exhibited a broad memory deficit that markedly reduced the value of both p

271 of Abeta and potentially contributes to the memory deficit that occurs in AD.

272 ) and aged mice display spatial learning and memory deficits that are absent from young mice.

273 ed with dentate gyrus-dependent learning and memory deficits that are manifested in adulthood.

274 perience cognitive dysfunction, particularly memory deficits that can persist for days to months.

275 ch could contribute to hippocampus-dependent memory deficits that occur during aging.

276 ence in sleep and quiet wakefulness, and the memory deficits that result from their interruption, sug

277 Similar to the memory deficits, theta-induced long-term potentiation (t

278 APP/PS1 mice with exogenous CART ameliorated memory deficits; this effect was associated with improve

279 circuit model for stress-induced hippocampal memory deficits through BLA activity-dependent p25 gener

280 , leading to aggravated spatial learning and memory deficits, thus emphasizing the importance of syst

281 The synaptic plasticity and memory deficits triggered by GR in the hippocampus are a

282 e beneficial effects of NTR1 on synaptic and memory deficits under the Abeta-enriched conditions in v

283 s a causative role in aging- or tau-mediated memory deficits via IL-1beta upregulation in mice.

284 has been suggested to underlie learning and memory deficits via the basolateral amygdala (BLA) and t

285 In schizophrenia, working memory deficit was mostly accounted for by processing sp

286 The memory deficits we observed in mouse prion disease were

287 eatment on Abeta accumulation and associated memory deficit were studied in APPSW /PS1dE9 AD transgen

288 ts revealed that age-related spatial working memory deficits were exacerbated by increased HPA activi

289 ing Pip18 for 4 months, spatial learning and memory deficits were not rescued, plaque-associated spin

290 Surprisingly, ISRIB corrected TBI-induced memory deficits when administered weeks after the initia

291 BAergic interneuron decline and learning and memory deficits, when examined at 16 month of age.

292 DG D1R KOs displayed significant fear memory deficits, whereas DG D5R KOs did not.

293 rilysin overexpression improves learning and memory deficits, whereas neprilysin deficiency aggravate

294 IV infection of the CNS causes cognitive and memory deficits, which have become more prevalent in the

295 campus of WT mice reproduced HD learning and memory deficits, while knockdown of p75(NTR) in the hipp

296 We modelled prevention of this memory deficit with ibuprofen, and found that ibuprofen

297 plasticity, leading to hippocampus-dependent memory deficit with intact olfactory function.

298 ge, which provoked cognitive dysfunction and memory deficits without affecting bidirectional synaptic

299 We hypothesized that older adults with mild memory deficits would show behavioral and functional net

300 patients with the emergence of learning and memory deficits, yet a clear understanding of the events