ライフサイエンスコーパス: memory deficit

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

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

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

4 at results in increased tonic inhibition and memory deficit.

5 n intrahippocampal injection, caused spatial memory deficit.

6 nuclei produced the severest spatial working memory deficit.

7 ts in late-onset spatial reference long-term memory deficit.

8 eases and DMN degeneration in early stage of memory deficit.

9 -cortical networks could account for spatial memory deficits.

10 e long term effects, including cognitive and memory deficits.

11 systemic IL-1beta replicated, these working memory deficits.

12 l polyribosome aggregations and learning and memory deficits.

13 levels is sufficient to reverse age-related memory deficits.

14 s, such as through neurodegeneration, causes memory deficits.

15 displayed hippocampal-dependent learning and memory deficits.

16 sociability, as well as learning and working memory deficits.

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

18 measurements in populations with progressing memory deficits.

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

20 ibited in aged mice, coinciding with spatial memory deficits.

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

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

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

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

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

26 icant reversal in the observed cognitive and memory deficits.

27 .0 [1.96]; controls, 25.86 [1.24]; P < .001) memory deficits.

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

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

30 on neurogenesis and associated learning and memory deficits.

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

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

33 hanges and prevented associated learning and memory deficits.

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

35 progressive neurodegeneration, and motor and memory deficits.

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

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

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

39 sensorimotor gating, albeit without profound memory deficits.

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

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

42 missorting into dendritic spines followed by memory deficits.

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

44 rological conditions, or basic perceptual or memory deficits.

45 AD patients underestimated their memory deficits.

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

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

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

49 anifested a significant improvement of their memory deficits.

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

51 erable to dementia and frequently experience memory deficits.

52 signaling, and prevents synaptic injury and memory deficits.

53 E4 inhibitors for depression and concomitant memory deficits.

54 . propose a dual-process model to understand memory deficits.

55 Mice treated with a G4 stabilizer develop memory deficits.

56 rsus low risk of presurgical or postsurgical memory deficits.

57 t the effective therapeutic dose for spatial memory deficits.

58 ch as developmental delays and cognitive and memory deficits.

59 and were consistent with the behavioral and memory deficits.

60 comotion, synapse morphology, and short-term memory deficits.

61 ts into the nature of memory and age-related memory deficits.

62 n of Pyk2 rescues synaptic loss and learning/memory deficits.

63 D-associated neuropathology and learning and memory deficits.

64 electively vulnerable to LPS-induced working memory deficits.

65 hology, gradually developing age-progressive memory deficits.

66 D910A) mice exhibited no spatial learning or memory deficits.

67 d driven synaptic dysfunction and underlying memory deficits.

68 generation, impaired neuronal signaling, and memory deficits.

69 cal synaptic dynamics accompanied by working memory deficits.

70 -term inhibition in Rett mice rescued social memory deficits.

71 rescued adult neurogenesis and learning and memory deficits.

72 /-) mice exhibit profound phenotypic spatial memory deficits, a DAGL inhibitor selectively impairs th

73 rebrain (Upf2 fb-KO mice) show impaired NMD, memory deficits, abnormal long-term potentiation (LTP),

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

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

76 AD mice exhibited memory deficits across age and these memory deficits wer

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

78 -42 and completely rescued spatial reference memory deficits after passive immunization.

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

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

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

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

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

84 The pattern of the contextual memory deficit and the disruption of local PL firing dur

85 Our results suggest that memory deficits and accelerated cognitive decline report

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

87 uced by bacterial LPS, produces both working-memory deficits and acute brain injury in the degenerati

88 urthermore, ISRIB treatment reverses spatial memory deficits and ameliorates working memory in old mi

89 puncture mice exhibited spatial and aversive memory deficits and anxiety-like behavior.

90 Thus, we conclude that the memory deficits and anxiety-related behaviors in patient

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

92 on of pyramidal cells successfully corrected memory deficits and did so in a regionally specific mann

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

94 Aergic neurons (NS-V mice) recapitulated the memory deficits and had reduced GABA(A) receptor subunit

95 iated eEF2 hyperphosphorylation and improved memory deficits and hippocampal long-term potentiation (

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

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

98 ta and have been successful in understanding memory deficits and in linking to neural data.

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

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

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

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

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

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

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

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

107 ssing Cav-1 (AAV-Cav-1) rescues learning and memory deficits and reduces pathology (i.e., APP, BACE-1

108 In addition to memory deficits and reduction of NMDARs, CSF antibodies

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

110 no effective treatment that counteracts the memory deficits and the underlying synaptic malfunction

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

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

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

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

115 6K1 improved synaptic plasticity and spatial memory deficits, and reduced the accumulation of amyloid

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

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

118 Memory deficits are common in epilepsy patients.

119 Episodic memory deficits are consistently documented as a core as

120 Age-related memory deficits are correlated with neural hyperactivity

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

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

123 strong links to both MHPG and p-tau, whereas memory deficits are linked to MHPG via a combination of

124 Recent studies suggest that memory deficits are more susceptible to phosphorylated t

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

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

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

128 Together, results showed that older adults' memory deficits are related to reduced discriminability

129 abetic mice and corresponds with recognition memory deficits as well as the upregulation of amyloid p

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

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

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

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

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

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

136 , mild anxiety-like behavior and substantial memory deficits associated with the presence of extraute

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

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

139 Are memory deficits better explained by damage to individual

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

141 rmal gait and locomotor activity, tremor and memory deficits, but human disorders related to KCNN2 va

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

143 We observed a borderline recognition memory deficit by novel object recognition in aged Tmprs

144 during early stages may prevent progressive memory deficits by preserving memory mechanisms.

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

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

147 We propose that memory deficits can be understood within the broader con

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

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

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

151 allosteric modulator of NMDAR, reverted the memory deficit caused by phencyclidine (a non-competitiv

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

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

154 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

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

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

157 rozygous mNGF(+/-) mice, show no learning or memory deficits, despite a reduction in secretion and br

158 ression is acutely knocked down in adult MB, memory deficits displayed by amn hypomorphic mutants are

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

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

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

162 a core feature of cognitive decline-working-memory deficits-emerges from disconnected local and long

163 foundations for pathology-specific models of memory deficits, enhancing the development of precision

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

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

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

167 -state hippocampal connectivity and episodic memory deficits following one night of total sleep depri

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

169 Memory deficits gradually worsened until Day 18 (4 days

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

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

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

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

174 ventricular injection exhibit a learning and memory deficit in object recognition, fear conditioning,

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

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

177 ivity in control mice could recapitulate the memory deficits in a regionally specific manner.

178 prevents hippocampal neuron loss and spatial memory deficits in a transgenic AD mouse model with Abet

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

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

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

182 molecular mechanism underlying synaptic and memory deficits in AD.

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

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

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

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

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

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

189 been linked to amnesia in humans and spatial memory deficits in animal models.

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

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

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

193 ac1 activity rescues synaptic plasticity and memory deficits in Cc2d1a cKO mice.

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

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

196 scharges (IEDs) are thought to be a cause of memory deficits in chronic epilepsy patients, but the un

197 in memory in order to make predictions about memory deficits in clinical populations.

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

199 escued the synaptic plasticity and long-term memory deficits in DS mice.

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

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

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

203 ase in young adult male mice led to age-like memory deficits in hippocampus-dependent memory tasks.

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

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

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

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

208 arying magnitudes of behavioral learning and memory deficits in mice.

209 ecrosis factor alpha correlated with spatial memory deficits in middle-aged females, but not males.

210 g per kg) reversibly induced spatial working memory deficits in monkeys expressing hM4Di in the prefr

211 (GABA) or CA3(GABA) neuron activity reversed memory deficits in NS-V mice.

212 in young adult mice, recapitulating observed memory deficits in old adult mice, whereas knocking down

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

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

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

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

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

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

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

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

221 dual neurons by IEDs to specific declarative memory deficits in specific cell types, thereby revealin

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

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

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

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

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 Memory deficits in TLE are associated with specific morp

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

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

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

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

239 We show that DBS rescues memory deficits induced by GI and produces changes in sy

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

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

242 Unawareness, or anosognosia, of memory deficits is a challenging manifestation of Alzhei

243 of hippocampal abnormalities and associated memory deficits is controversial, and functional MRI stu

244 aging, or stress are most likely to produce memory deficits-knowledge that could eventually help in

245 ts ameliorates early-life adversity-provoked memory deficits later in life.

246 s use can result in cognitive impairment and memory deficits long after its use is discontinued.

247 the brain non-uniformly, causing hippocampal memory deficits long before wide-spread brain degenerati

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

249 work examining implicit memory suggests that memory deficits may be better understood by separating a

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

251 nd allocentric learning and caused reference memory deficits (Morris water maze), but did not affect

252 g showed locomotor hyperactivity and working memory deficit not observed in fathers.

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

254 ing was impaired, consistent with the social memory deficit observed in these mice; in contrast, spat

255 ion could be responsible for the progressive memory deficits observed following irradiation.

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

257 ormal circuit anatomy, recapitulated spatial memory deficits observed in epileptic mice.

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

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

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

263 a progressive decrease in self-awareness of memory deficits, reaching anosognosia approximately 3 ye

264 w that mice with DAD knock-in mutations have memory deficits, reduced anxiety levels, and reduced soc

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

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

267 cluding hot flashes, depression/anxiety, and memory deficits severe enough for many women to disconti

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

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

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

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

272 Beyond memory deficits, the most common AD co-morbidities inclu

273 r thinking about the structure of memory and memory deficits, their distinction between entities and

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

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

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

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

278 Thus, by relating older adults' memory deficits to age-specific visual exploration patte

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

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

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

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

283 The memory deficits we observed in mouse prion disease were

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

285 hibited memory deficits across age and these memory deficits were also seen in naturally aged mice.

286 Remarkably, working memory deficits were restored by optogenetic stimulation

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

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

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

290 genetic activation of this projection caused memory deficits, whereas targeted manipulation of LH(GAB

291 Dementia is associated with severe spatial memory deficits which arise from dysfunction in hippocam

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

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

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

295 ent mouse, and identify a significant social memory deficit, with no change in sociability, olfaction

296 uence of dendritic spine density and spatial memory deficits, with reduced spine density only in mice

297 F, and treated with vehicle developed severe memory deficit without locomotor alteration, accompanied

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

299 synthesis and was protective against working memory deficits, without blocking brain IL-1beta synthes

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