ライフサイエンスコーパス: amnestic

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

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

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

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

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

6 54.4% had pathologically diagnosed AD (58.7% amnestic; 49.2% nonamnestic); 19.4% had mixed pathologie

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

8 Moreover, the amnestic actions of etomidate were selectively potentiat

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

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

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

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

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

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

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

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

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

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

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

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

21 Amnestic amyloid-negative cases were most often reclassi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

41 Non-amnestic cognitive manifestations were less prevalent in

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

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

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

45 6 patients who had the clinical diagnosis of amnestic dementia and autopsy-confirmed AD (AMN-AD) were

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

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

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

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

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

51 her primary progressive aphasia or a typical amnestic dementia.

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

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

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

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

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

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

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

59 The amnestic effect of AM251 was rescued by coadministration

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

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

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

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

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

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

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

67 The amnestic effects of ECT are greatest and most persistent

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

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

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

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

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

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

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

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

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

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

78 stable and highly resistant to disruption by amnestic influences.

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

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

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

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

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

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

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

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

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

88 As expected, the amnestic MCI participants demonstrated reduced episodic

89 Most amnestic MCI patients develop Alzheimer's disease.

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

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

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

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

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

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

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

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

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

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

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

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

102 50 participant 50-84 years of age with amnestic MCI were administered 0.4 g/kg 10% IVIG or 0.9%

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

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

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

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

107 3 patients with mild AD, 34 individuals with amnestic MCI, and 28 healthy elderly control subjects-we

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

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

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

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

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

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

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

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

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

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

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

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

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

121 Amnestic mild cognitive impairment (AMCI) carries a high

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

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

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

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

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

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

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

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

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

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

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

133 Amnestic mild cognitive impairment (MCI) is a relatively

134 Amnestic mild cognitive impairment (MCI) is an isolated

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

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

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

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

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

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

141 42 cognitively impaired patients with either amnestic mild cognitive impairment (n = 23) or mild and

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

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

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

145 The concept of amnestic mild cognitive impairment attempts to describe

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

171 annel blocker nimodipine interferes with the amnestic outcome.

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

173 4 amnestic-"plus" and 2 (10.0%) of 20 "pure" amnestic patients converted to AD (P = .001).

174 Clearly amnestic patients with a positive amyloid scan have prod

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

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

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

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

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

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

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

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

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

184 20 somatosensory cortical activity occurs in amnestic single-domain MCI and is sensitive to modulatio

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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