ライフサイエンスコーパス: amnestic

1 degeneration patients (five amnestic; 59 non-amnestic).

2 nfusion (3 patients), epileptic (1 patient), amnestic (1 patient), and a severe form of fulminant enc

3 There were 21 amnestic, 12 non-amnestic, and seven non-specific amyloi

4 mnestic); 19.4% had mixed pathologies (22.7% amnestic; 15.3% nonamnestic).

5 hort of 118 Alzheimer's disease patients (98 amnestic; 20 non-amnestic) and 64 frontotemporal lobar d

6 fusion (12 patients), epileptic (1 patient), amnestic (3 patients), and fulminant encephalitis (2 pat

7 n percent were classified as having MCI (36% amnestic, 37% amnestic multidomain, 28% nonamnestic).

8 54.4% had pathologically diagnosed AD (58.7% amnestic; 49.2% nonamnestic); 19.4% had mixed pathologie

9 totemporal lobar degeneration patients (five amnestic; 59 non-amnestic).

10 at estrogen was highly effective against the amnestic action of scopolamine when tested in young-adul

11 Moreover, the amnestic actions of etomidate were selectively potentiat

12 ning GABAARs contributes to the hypnotic and amnestic actions of the intravenous anesthetics, etomida

13 cid (GABA)(A) receptor is critical for these amnestic actions, knowledge of the neuronal localization

14 sence of left parietal features and AOS, and amnestic AD could be differentiated from bvFTD, svPPA an

15 clinically subclassified at presentation as amnestic AD dementia versus atypical AD dementia.

16 of primary progressive aphasia, differ from amnestic AD in distributions of tau aggregates and neuro

17 ApoE4 is less prevalent in non-amnestic AD variants suggesting a direct effect on the c

18 e Disorders Clinic, Oxford, UK, including 29 amnestic AD, 12 posterior cortical atrophy (PCA), 12 log

19 ostic value of tau PET in typical late-onset amnestic AD, its utility in predicting clinical decline

20 evalence of limb apraxia was highest in PCA, amnestic AD, lvPPA and nfvPPA.

21 e examine the use of the naturally occurring amnestic agent garcinol to manipulate an established coc

22 es) and a comparison cohort of patients with amnestic Alzheimer's disease (n = 20, eight female, aged

23 zheimer's disease, temporo-parietal areas in amnestic Alzheimer's disease and frontotemporal areas in

24 area under the curve when discriminating non-amnestic Alzheimer's disease from frontotemporal lobar d

25 degeneration, compared to discrimination of amnestic Alzheimer's disease from frontotemporal lobar d

26 Medial temporal sparing in non-amnestic Alzheimer's disease may thus be due in part to

27 Results show that non-amnestic Alzheimer's disease patients were less likely t

28 nificantly lower in non-amnestic compared to amnestic Alzheimer's disease patients.

29 Alzheimer's disease (n = 12), as well as 17 amnestic Alzheimer's disease patients.

30 ay thus result in misclassifications for non-amnestic Alzheimer's disease patients.

31 biomarker provides better sensitivity to non-amnestic Alzheimer's disease than either the ATN framewo

32 ed with Alzheimer's disease (18 with typical amnestic Alzheimer's disease, 17 with posterior cortical

33 1-42 did not differ between amnestic and non-amnestic Alzheimer's disease, and receiver operating cha

34 ar whether such models are applicable in non-amnestic Alzheimer's disease, which is associated with d

35 wed by behavioural Alzheimer's disease, then amnestic Alzheimer's disease.

36 of ATN designations for identifying true non-amnestic Alzheimer's disease.

37 biomarkers differed between amnestic and non-amnestic Alzheimer's disease; standard cut-offs for phos

38 n primary progressive aphasia but not in the amnestic Alzheimer-type dementia (P < 0.05).

39 estive of another degenerative disorder, the amnestic amyloid-negative cases had subtle atrophy and h

40 Amnestic amyloid-negative cases were most often reclassi

41 diagnosis in most cases (90%), including in amnestic amyloid-negative cases whose post-positon emiss

42 diagnosis was not made in about half of the amnestic amyloid-negative cases, highlighting the need f

43 In contrast, in the subgroup of amnestic amyloid-negative cases, the clinical presentati

44 predicted all-cause dementia in people with amnestic and any-type MCI, respectively.

45 t AD, visual-variant AD and AD patients with amnestic and dysexecutive deficits.

46 Amyloid-beta1-42 did not differ between amnestic and non-amnestic Alzheimer's disease, and recei

47 , T and N status biomarkers differed between amnestic and non-amnestic Alzheimer's disease; standard

48 Still, differences in CSF levels across amnestic and non-amnestic variants or due to co-occurrin

49 While the non-amnestic and non-specific amyloid-negative cases usually

50 including 48% of amnestic versus 94% of non-amnestic and non-specific cases.

51 toms of dementia (BPSDs) in association with amnestic and nonamnestic cognitive phenotypes have not b

52 We also used subcategories of MCI (amnestic and nonamnestic), and dementia (probable Alzhei

53 elated Disorders Association criteria), MCI (amnestic and nonamnestic), or no cognitive impairment.

54 the overall category of delirium, dementia, amnestic and other cognitive disorders (OR = 1.90, 95% C

55 Experiments 1 to 3 investigated amnestic and performance effects of NO inhibitor L-NAME

56 Cirrhotics were impaired on non-amnestic and selected amnestic tests, HRQOL and systemic

57 imer's disease patients (98 amnestic; 20 non-amnestic) and 64 frontotemporal lobar degeneration patie

58 There were 21 amnestic, 12 non-amnestic, and seven non-specific amyloid-negative Alzhei

59 ation of the fimbria-fornix increased TGC in amnestic animals and partially rescued memory performanc

60 reclassified as frontotemporal dementia, non-amnestic as frontotemporal dementia or corticobasal dege

61 ssociated with reversal of transgene-related amnestic behavior, reduction in anxiety, reduction in le

62 d we can reinstate a forgotten memory in the amnestic brain by stimulating the memory engram.

63 and plaques were greater in the aphasic than amnestic cases (P < 0.05), especially in neocortical are

64 ern was not seen in any of the predominantly amnestic cases.

65 ments under the influence of scopolamine (an amnestic cholinergic antagonist) or vehicle (saline).

66 ent in its prototypical presentation and non-amnestic cognitive impairment in its less common variant

67 dic neurodegenerative disease that causes an amnestic cognitive impairment in its prototypical presen

68 ker levels, APOE epsilon4 carriership and an amnestic cognitive impairment.

69 The most prevalent non-amnestic cognitive manifestations in participants in the

70 Non-amnestic cognitive manifestations were less prevalent in

71 mer's disease is associated with greater non-amnestic cognitive symptoms and neuropathological burden

72 oid-beta1-42 were significantly lower in non-amnestic compared to amnestic Alzheimer's disease patien

73 largely on two fundamental discoveries: the amnestic consequences of removing the hippocampus and as

74 ppocampus and is associated with progressive amnestic decline in individuals with a neurodegenerative

75 ypically manifests clinically as an isolated amnestic deficit that progresses to a characteristic dem

76 Two months after ECT, retrograde amnestic deficits were greatest among patients treated w

77 6 patients who had the clinical diagnosis of amnestic dementia and autopsy-confirmed AD (AMN-AD) were

78 Both cancer and amnestic dementia are prevalent and potentially lethal c

79 ompared between Abeta(+) PPA and an Abeta(+) amnestic dementia groups (n = 22).

80 redominance of entorhinal NFT typical of the amnestic dementia of the Alzheimer type.

81 /AD cases and four AD cases with the typical amnestic dementia of the Alzheimer type.

82 clinical entity in 2019, is characterized by amnestic dementia resembling AD dementia and occurring m

83 mon TDP-43 proteinopathy, associated with an amnestic dementia syndrome that mimicked Alzheimer's-typ

84 Alzheimer's disease (AD) is a progressive amnestic dementia that involves post-translational hyper

85 Alzheimer's disease (AD) is a progressive amnestic dementia typified by abnormal modifications of

86 itive impairment, amnestic dementia, and non-amnestic dementia).

87 inical phenotype (mild cognitive impairment, amnestic dementia, and non-amnestic dementia).

88 her primary progressive aphasia or a typical amnestic dementia.

89 conditions that can manifest clinically with amnestic dementia; the amygdala region is often affected

90 lower incidence of Alzheimer's disease-type (amnestic) dementia among individuals with a diagnosis of

91 the dementia phenotype (amnestic versus non-amnestic) did not affect this conclusion.

92 Alzheimer's disease (AD) is a progressive amnestic disorder typified by the pathological misfoldin

93 is underwent cognitive testing (amnestic/non-amnestic domains), quality of life (HRQOL), multi-modal

94 Typical amnestic-dominant AD patients also exhibited 3D shape de

95 ith diffuse Lewy body dementia (DLBD) and an amnestic-dominant phenotype of AD, respectively.

96 lts indicate that intraseptal infusion of an amnestic dose of the BDZ ligand, chlordiazepoxide, decre

97 Other research indicates that the amnestic drug midazolam impairs recollection more than f

98 eived shock after systemic injections of the amnestic drug scopolamine at a dose (1 mg/kg) that impai

99 ion can be disrupted either by administering amnestic drugs in conjunction with a memory reactivation

100 The amnestic effect of AM251 was rescued by coadministration

101 administration of quinpirole potentiated the amnestic effect of mecamylamine infused into the ventral

102 ereas it was previously found to reverse the amnestic effect of systemically administered mecamylamin

103 Thus, amnestic effects of [Leu]- or [Met]enkephalin administra

104 olateral amygdala (ABL) is essential for the amnestic effects of benzodiazepines in aversive learning

105 gs indicating that the amygdala mediates the amnestic effects of benzodiazepines on aversive learning

106 context before drug treatment eliminated the amnestic effects of DHEA-S, suggesting that, like adrena

107 The present study compared amnestic effects of dizocilpine maleate (MK-801), an NMD

108 The amnestic effects of ECT are greatest and most persistent

109 The present study investigated the amnestic effects of microinjections of the NMDA receptor

110 The present study investigated the amnestic effects of N-methyl-D-aspartate (NMDA) receptor

111 g SNAP significantly ameliorated anterograde amnestic effects of pretraining L-NAME.

112 ion of NO donor SNAP ameliorated anterograde amnestic effects of pretraining NO inhibitor L-NAME.

113 Our results suggest that (1) the amnestic effects of protein synthesis inhibitors are con

114 emory formation is consistent with localized amnestic effects produced by [Met]enkephalin administrat

115 Bilateral ECT produces more profound amnestic effects than RUL ECT, particularly for memory o

116 Late-onset DLB had more amnestic features, but this was accounted for by a highe

117 e, and 50 mg/kg for aminoglutethimide) being amnestic for the task.

118 zed amyloid uptake in the PPA group than the amnestic group (p < 0.007), consistent with the left lat

119 logic substrate in a subset of patients with amnestic impairments.

120 ex was only observed among prodromal (mildly amnestic) individuals.

121 stable and highly resistant to disruption by amnestic influences.

122 24 older adults with amnestic MCI (aMCI) due to possible Alzheimer's disease

123 Amnestic MCI (aMCI) was defined by a composite episodic

124 (MDD), non-amnestic MCI (naMCI), MDD+naMCI, amnestic MCI (aMCI), and MDD+aMCI.

125 nam Era Twin Study of Aging (VETSA): 7% with amnestic MCI (aMCI); 4% with non-amnestic MCI (naMCI).

126 Subjects diagnosed with amnestic MCI (n = 12) and normal controls (n = 23) recei

127 ain imaging characteristics of patients with amnestic MCI (n = 26), patients with dysexecutive MCI (n

128 We studied subjects with amnestic MCI (n = 41: 28 SD, 13 MD), Alzheimer's disease

129 ing dementia- remitted depression (MDD), non-amnestic MCI (naMCI), MDD+naMCI, amnestic MCI (aMCI), an

130 A): 7% with amnestic MCI (aMCI); 4% with non-amnestic MCI (naMCI).

131 classified as having normal cognition, MCI (amnestic MCI [aMCI] and nonamnestic MCI [naMCI]), and de

132 al magnetic resonance hippocampal data of 31 amnestic MCI and 34 Alzheimer's disease subjects.

133 Twenty cognitively normal, 17 amnestic MCI and 8 probable Alzheimer's disease subjects

134 eristics of two single-domain MCI subgroups: amnestic MCI and dysexecutive MCI.

135 eline projected risk of probable dementia or amnestic MCI gained greater absolute cognitive benefit f

136 In contrast, patients with amnestic MCI had significantly lower scores on tests of

137 risk, there was no difference in the rate of amnestic MCI or PD among new users of an ARB compared wi

138 users of an ARB vs ACEI had a lower rate of amnestic MCI or PD among those in the standard systolic

139 rs, the inverse probability-weighted rate of amnestic MCI or PD was 4.3 vs 4.6 per 100 person-years a

140 Composite of adjudicated amnestic MCI or PD.

141 were 45 vs 59 cases per 1000 person-years of amnestic MCI or probable dementia among prevalent users

142 imary outcome was a composite of adjudicated amnestic MCI or probable dementia.

143 As expected, the amnestic MCI participants demonstrated reduced episodic

144 Most amnestic MCI patients develop Alzheimer's disease.

145 We compared them to 22 stable amnestic MCI patients with similar cognitive performance

146 gions and was also detected in the brains of amnestic MCI patients, where it correlated with the abun

147 years, comprised three groups (n = 19 each): amnestic MCI patients; cognitively intact older particip

148 were recorded from 15 older controls and 15 amnestic MCI subjects (single domain).

149 Almost all amnestic MCI subjects (Z score </= -1.5) with a positive

150 from the MCSA was compared to a sample of 58 amnestic MCI subjects from the Alzheimer's Disease Neuro

151 and high hippocampal volume; and on average amnestic MCI subjects were intermediate on both PiB and

152 en high versus low PiB cognitively normal or amnestic MCI subjects.

153 A2 and CA3 hippocampal subfields relative to amnestic MCI subjects.

154 ory cortical sensory potentials differ among amnestic MCI subtypes and outcomes occurring up to 5 yea

155 rediabetes increased risk of conversion from amnestic MCI to Alzheimer's dementia; risk in treated ve

156 er documented MCI to AD conversion or stable amnestic MCI underwent three yearly magnetic resonance i

157 50 participant 50-84 years of age with amnestic MCI were administered 0.4 g/kg 10% IVIG or 0.9%

158 ctivation of memory circuits is preserved in amnestic MCI when task performance is controlled.

159 pes of MCI have an episodic memory disorder (amnestic MCI) occurring either alone [single domain (SD)

160 r absolute reduction of probable dementia or amnestic MCI) of intensive vs standard treatment across

161 ects were initially classified clinically as amnestic MCI, 7 as multidomain MCI, and 9 as nonamnestic

162 accounted for 4.5% of probable AD, 13.3% of amnestic MCI, and 18.6% of nonamnestic MCI.

163 3 patients with mild AD, 34 individuals with amnestic MCI, and 28 healthy elderly control subjects-we

164 inically diagnosed probable AD and MCI, even amnestic MCI, are pathologically heterogeneous disorders

165 In participants with amnestic MCI, compared with age-matched controls, result

166 domain deficits, rather than those with pure amnestic MCI, constituted the high-risk group.

167 creased progression from normal cognition to amnestic MCI, suggesting that anxiety may be a neuropsyc

168 the comparison of cognitively normal versus amnestic MCI, which was not significant for PiB.

169 pairment (MCI), 69 of whom had single-domain amnestic MCI.

170 omposite of adjudicated probable dementia or amnestic MCI.

171 At baseline, 108 patients met criteria for amnestic MCI: 87 had memory plus other cognitive domain

172 n integrity in 4 groups: memory-impaired PD (amnestic MCI; n = 9), PD with nonamnestic MCI (n = 10),

173 enty-six patients with MCI (13 single-domain amnestic-MCI [a-MCI], 6 multidomain a-MCI, and 7 nonamne

174 ding to their pre-scan clinical phenotype as amnestic (memory predominant), non-amnestic (predominant

175 g elderly population with cirrhosis could be amnestic (memory-related) or non-amnestic (memory-unrela

176 is could be amnestic (memory-related) or non-amnestic (memory-unrelated).

177 order: cognitively normal (1.3 cm(3)/year) < amnestic mild cognitive impairment (2.5 cm(3)/year) < Al

178 gnetic resonance imaging in 25 patients with amnestic mild cognitive impairment (aMCI) and 23 matched

179 vity of the default mode network (DMN) in 54 amnestic mild cognitive impairment (aMCI) and 46 AD.

180 h and without late-life depression (LLD) and amnestic mild cognitive impairment (aMCI) are unknown.

181 Amnestic mild cognitive impairment (AMCI) carries a high

182 In 38 older human adults with amnestic mild cognitive impairment (aMCI) or normative c

183 during non-pharmacological interventions for amnestic mild cognitive impairment (aMCI) patients.

184 cale items that exhibited change in previous amnestic Mild Cognitive Impairment (aMCI) trials.

185 lti-centre longitudinal study of people with amnestic mild cognitive impairment (aMCI) we assessed th

186 A total of 20 healthy controls and 17 amnestic mild cognitive impairment (aMCI), 6 nonamnestic

187 estion that HSP levels would be increased in amnestic mild cognitive impairment (aMCI), a transition

188 derly subjects, including 10 probable AD, 15 amnestic mild cognitive impairment (aMCI), and 10 cognit

189 nfer risk for Alzheimer's disease, including amnestic mild cognitive impairment (aMCI).

190 tion and brain connectivity in patients with amnestic mild cognitive impairment (aMCI).

191 with clinical diagnoses of ADD (n = 305) or amnestic mild cognitive impairment (aMCI, n = 909) from

192 By contrast, depression predicted amnestic mild cognitive impairment (hazard ratio=1.74, 9

193 e discrimination between cognitively normal, amnestic mild cognitive impairment (MCI) and Alzheimer's

194 eria for subjective cognitive decline (SCD), amnestic mild cognitive impairment (MCI) and probable Al

195 The concept of amnestic mild cognitive impairment (MCI) describes older

196 Amnestic mild cognitive impairment (MCI) is a clinical c

197 Amnestic mild cognitive impairment (MCI) is a relatively

198 Amnestic mild cognitive impairment (MCI) is an isolated

199 s were also measured in brain samples from 9 amnestic mild cognitive impairment (MCI) subjects.

200 bjects, 68 individuals with AD, and 156 with amnestic mild cognitive impairment (MCI), 69 of whom had

201 ognition and brain activity in patients with amnestic mild cognitive impairment (MCI), a diagnosis as

202 nty healthy controls and 25 individuals with amnestic mild cognitive impairment (MCI), an early stage

203 ed normal control subjects and patients with amnestic mild cognitive impairment (MCI), and late-stage

204 tion carriers had dementia (MUT-Dem), 12 had amnestic mild cognitive impairment (MUT-aMCI) and nine w

205 42 cognitively impaired patients with either amnestic mild cognitive impairment (n = 23) or mild and

206 d thinner left entorhinal cortex compared to amnestic mild cognitive impairment (P = 0.02).

207 healthy cognitively normal subjects, 32 with amnestic mild cognitive impairment and 8 with Alzheimer'

208 rom four tertiary epilepsy surgical centres; amnestic mild cognitive impairment and control subjects

209 contrast to the reverse pattern reported in amnestic mild cognitive impairment and incipient Alzheim

210 e-matched healthy controls and patients with amnestic mild cognitive impairment and mild AD, we found

211 People with amnestic mild cognitive impairment and probable Alzheime

212 The concept of amnestic mild cognitive impairment attempts to describe

213 language and memory encoding, patients with amnestic mild cognitive impairment demonstrated poorer d

214 ostly uses glucose for energy, but in AD and amnestic mild cognitive impairment glucose metabolism is

215 Both temporal lobe epilepsy and amnestic mild cognitive impairment groups showed signifi

216 older adults with temporal lobe epilepsy and amnestic mild cognitive impairment highlights the risks

217 There is growing evidence that amnestic mild cognitive impairment is associated with bi

218 ood that predicted phenoconversion to either amnestic mild cognitive impairment or Alzheimer's diseas

219 (TYM-MCI) in the diagnosis of patients with amnestic mild cognitive impairment or mild Alzheimer's d

220 ely normal HE subjects, 4 AD subjects, and 2 amnestic mild cognitive impairment subjects after a bolu

221 pPKR concentrations were elevated in AD and amnestic mild cognitive impairment subjects.

222 le Alzheimer disease (AD), and subjects with amnestic mild cognitive impairment were characterized in

223 Sixty-four patients with amnestic mild cognitive impairment who later converted t

224 ipants were 25 patients who met criteria for amnestic mild cognitive impairment, 27 patients with mil

225 nitively average same-aged peers, those with amnestic mild cognitive impairment, and - remarkably - e

226 mal elders, 26 patients who met criteria for amnestic mild cognitive impairment, and 22 patients who

227 ts clinically characterized as PD, PDD, DLB, amnestic mild cognitive impairment, and AD.

228 with preclinical to late-stage AD, including amnestic mild cognitive impairment, and age-matched cont

229 tive impairment, three with multi-domain non-amnestic mild cognitive impairment, and three with multi

230 group (n = 535), 54 (10.1%) had dementia or amnestic mild cognitive impairment, including 33 biomark

231 NA isolated from vulnerable brain regions in amnestic mild cognitive impairment, the earliest clinica

232 in 70 healthy controls and 79 patients with amnestic mild cognitive impairment, the prodromal stage

233 resented include: two with single domain non-amnestic mild cognitive impairment, three with multi-dom

234 eta1-40 is found only in patients with AD or amnestic mild cognitive impairment.

235 derly individuals, and five individuals with amnestic mild cognitive impairment.

236 ated with the rate of hippocampal atrophy in amnestic mild cognitive impairment.

237 onamnestic mild cognitive impairment but not amnestic mild cognitive impairment.

238 tive impairment, and three with multi-domain amnestic mild cognitive impairment.

239 685), 70 individuals (10.2%) had dementia or amnestic mild cognitive impairment.

240 magnitude of medial temporal lobe atrophy to amnestic mild cognitive impairment.

241 the CSF of 91 patients were studied (AD: 45; amnestic mild cognitive impairment: 11; neurological dis

242 classified as having MCI (36% amnestic, 37% amnestic multidomain, 28% nonamnestic).

243 investigated the prevalences of various non-amnestic neurological symptoms and the contributions of

244 iterature to estimate the prevalences of non-amnestic neurological symptoms in participants with ADAD

245 s disease (ADAD) is a rare disorder with non-amnestic neurological symptoms in some clinical presenta

246 thout cirrhosis underwent cognitive testing (amnestic/non-amnestic domains), quality of life (HRQOL),

247 uropsychological performance (amnestic-type, amnestic/non-amnestic-type and unimpaired).

248 Using the neuropsychological classification amnestic/non-amnestic-type individuals were majority cir

249 annel blocker nimodipine interferes with the amnestic outcome.

250 formance in the right PHG and left insula of amnestic patients and with executive performance in the

251 4 amnestic-"plus" and 2 (10.0%) of 20 "pure" amnestic patients converted to AD (P = .001).

252 In the medial temporal lobes, non-amnestic patients had less atrophy at their initial scan

253 ion patterns and clinical trajectories among amnestic patients is not well understood.

254 nset of medial temporal degeneration than in amnestic patients rather than different rates of atrophy

255 the anatomical progression of disease in non-amnestic patients remains understudied.

256 Clearly amnestic patients with a positive amyloid scan have prod

257 and brain microstructure abnormalities in 13 amnestic patients with mild cognitive impairment (MCI),

258 ncluded 109 cognitively normal subjects, 192 amnestic patients with mild cognitive impairment and 98

259 had less atrophy at their initial scan than amnestic patients, but longitudinal rate of change did n

260 rapid atrophy of left insula than other non-amnestic patients.

261 Each non-amnestic phenotype displayed unique patterns of initial

262 n present clinically with either the typical amnestic phenotype or with atypical phenotypes, such as

263 In 3 years, 32 (50.0%) of 64 amnestic-"plus" and 2 (10.0%) of 20 "pure" amnestic pati

264 notype as amnestic (memory predominant), non-amnestic (predominant language, visuospatial or frontal

265 Patients with an amnestic-predominant presentation (n = 5) showed highest

266 ogeneity of tau in typical AD, atypical (non-amnestic-predominant) AD variants with distinct tau patt

267 h matched autopsy/biomarker-defined typical (amnestic-predominant) Alzheimer's disease (typical Alzhe

268 au deposition that are distinct from typical amnestic presentations of Alzheimer's disease.

269 ns in patients with Alzheimer's disease-like amnestic presentations.

270 tients with Alzheimer's disease present with amnestic problems; however, a substantial proportion, ov

271 e realistation that subjects pass through an amnestic prodrome which is thought to reflect dysfunctio

272 iated rejection (AMR) that occurs during the amnestic response within the first month posttransplant

273 to a booster vaccine suggests a long-lasting amnestic response.

274 iconvulsants devoid of sedative, ataxic, and amnestic side effects.

275 20 somatosensory cortical activity occurs in amnestic single-domain MCI and is sensitive to modulatio

276 A safe and acceptable analgesic/amnestic state for these procedures can be provided by t

277 cognitive impairment (MCI), particularly the amnestic subtype (aMCI), is considered as a transitional

278 -blind study, we evaluated subjects with the amnestic subtype of mild cognitive impairment.

279 that d-serine deficiency is important in the amnestic symptoms of temporal lobe epilepsy.

280 Compared with initial amnestic symptoms, executive symptoms were associated wi

281 d 35 (97%) with APP mutations presented with amnestic symptoms, making atypical cognitive presentatio

282 ized deficit, but the pattern was unlike the amnestic syndrome and probably reflects different mechan

283 nt Primary Progressive Aphasia (n = 15); and amnestic syndrome with multi-domain impairment and young

284 nt AD (31 [94%]) initially presented with an amnestic syndrome, but fewer patients with hippocampal-s

285 be epilepsy (TLE), but may be complicated by amnestic syndromes.

286 s were impaired on non-amnestic and selected amnestic tests, HRQOL and systemic inflammation compared

287 r labile according to whether they withstand amnestic treatment, or not.

288 f 117 mild cognitive impairment patients (45 amnestic type and 72 subcortical vascular type), from wh

289 cal performance (amnestic-type, amnestic/non-amnestic-type and unimpaired).

290 uropsychological classification amnestic/non-amnestic-type individuals were majority cirrhosis and ha

291 lso based on neuropsychological performance (amnestic-type, amnestic/non-amnestic-type and unimpaired

292 rences in CSF levels across amnestic and non-amnestic variants or due to co-occurring pathologies mig

293 trophy and later disease spread in three non-amnestic variants, including logopenic-variant primary p

294 f amyloid-negative patients including 48% of amnestic versus 94% of non-amnestic and non-specific cas

295 Comparisons of ADNC in typical amnestic versus atypical aphasic dementia and of TDP in

296 The nature of the dementia phenotype (amnestic versus non-amnestic) did not affect this conclu

297 he cell-to-cell propagation framework in the amnestic, visuospatial, language, and behavioral/dysexec

298 I diagnosis (cognitive vs global measure and amnestic vs nonamnestic).

299 [Leu]enkephalin was amnestic when administered in the IMHV but not in the LP

300 In contrast, [Met]enkephalin may be amnestic when administered in the LPO but not in the IMH