ライフサイエンスコーパス: MCI

1 MCI patients with low-normal VitB12 showed a significant

2 MCI performance was better with constant words versus va

3 MCI subjects showed a trend for decreased BDNF levels co

4 ffects) were identified, which included 1993 MCI patients and 2861 healthy older adults (HOA).

5 es from patients with DLB (n=37), AD (n=20), MCI with DLB profile (n=38), MCI with AD profile (n=20)

6 Of 28 MCI patients, 9 developed dementia due to AD, 2 develope

7 37), AD (n=20), MCI with DLB profile (n=38), MCI with AD profile (n=20) and healthy control subjects

8 A total of 69 healthy controls, 86 SMD, 45 MCI, and 38 AD patients were included.

9 ed with executive function decline in Abeta+ MCI participants and AD dementia patients.

10 thout a statistical difference among the AD, MCI, and control groups.

11 The AD, MCI, and SCD groups were divided into a sex- and age-mat

12 ed as having normal cognition, MCI (amnestic MCI [aMCI] and nonamnestic MCI [naMCI]), and dementia.

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

14 al diagnoses were varied: 39.2% died with an MCI diagnosis, 46.8% with a dementia diagnosis, and 13.9

15 ssion Scale over time were similar in AD and MCI subjects among the 3 TSPO binding groups.

16 No differences were found between AD and MCI subjects in BDNF levels (11 studies, Hedges' g=0.058

17 B) have same level of amyloid load in AD and MCI subjects.

18 empted to develop fused predictors of AD and MCI.

19 ce intermediate between healthy controls and MCI.

20 ose of patients with Alzheimer's disease and MCI, possess effective phagocytosis for Abeta and protec

21 APOE-e4 and MCI was also associated with higher cortical iron.

22 Both MBL and MCI were assessed from panoramic radiographs.

23 regenerated bone are correlated with MBL and MCI.

24 Prespecified outcomes were incident MCI and MCI progression to dementia.

25 potential utility for screening for MCI and MCI that is likely to progress.

26 veloping mild cognitive impairment (MCI) and MCI progression to dementia is not well established.

27 etween the presence of diabetes mellitus and MCI (P <0.01).

28 get learning and probe trials, hAPP mice and MCI-AD patients showed similar deficits in learning and

29 und between the presence of osteoporosis and MCI (P <0.001) and between the presence of diabetes mell

30 o differentiate between patients with PD and MCI and patients with PD without MCI.

31 At P < .01, patients with PD and MCI did not show network alterations relative to patient

32 e used to differentiate patients with PD and MCI from healthy control subjects and patients with PD w

33 ve to control subjects, patients with PD and MCI had a large basal ganglia and frontoparietal network

34 ients with PD without MCI, those with PD and MCI had a network with decreased FA, including basal gan

35 Results Patients with PD and MCI had global network alterations when compared with bo

36 (i.e. in amyloid positive controls, SCD and MCI) plasma concentration of Abeta42 was just moderately

37 tions by the European Commission have banned MCI-MI in all leave-on body products as of July 16, 2015

38 studies, Hedges' g=-0.492, P<0.001; between MCI and HC: 11 studies, Hedges' g=-0.339, P=0.003).

39 ls of IL-10, IL-1beta, IL-4 and IL-2 in both MCI groups (P<0.001), while there was no significant dif

40 ed with semantic tasks in patients with both MCI and AD, but was only associated with executive funct

41 Osteoporosis (as evaluated by MCI) does not pose a risk for the development of greater

42 were classified as having normal cognition, MCI (amnestic MCI [aMCI] and nonamnestic MCI [naMCI]), a

43 for cognitive outcomes of normal cognition, MCI, or dementia at baseline and prospectively assessed

44 -MCI stage and could discriminate converting MCI and AD from nonconverting MCI with an accuracy of 83

45 ments to prevent or delay cognitive decline, MCI, or clinical Alzheimer-type dementia in adults with

46 tions to prevent or delay cognitive decline, MCI, or dementia in adults with normal cognition or MCI.

47 f the brain and, furthermore, that defective MCI macrophages recover phagocytic function via omega-3.

48 sion (6.2 times higher likelihood to develop MCI, dementia or die than healthy controls).

49 and 95% confidence intervals for developing MCI and AD were calculated for men and women across APOE

50 POE genotype affect the risks for developing MCI and AD.

51 % CI, 1.43-1.81) in their risk of developing MCI between the ages of 55 and 85 years, but women had a

52 itive impairment due to Alzheimer's disease (MCI-AD) to evaluate the sensitivity of performance measu

53 ly less brain atrophy (p=0.037, adjusted for MCI status) in the IVIG group (5.87%) when compared with

54 r sentence recognition but were marginal for MCI.

55 de from midlife to late life is a marker for MCI and may help identify persons at increased risk for

56 other multi-class classification methods for MCI prediction (PPV: 0.80 vs. 0.67, 0.63).

57 to identify cases missed by testing only for MCI-MI.

58 UC, 0.89; P < .01), and poor performance for MCI versus SCD (AUC, 0.63; P = .06).

59 ce); high-dose raloxifene decreased risk for MCI but not for dementia (1 trial, low strength of evide

60 help identify persons at increased risk for MCI.

61 sts have potential utility for screening for MCI and MCI that is likely to progress.

62 ence estimate, nor did the criteria used for MCI diagnosis or MCI subtype.

63 and women in their risks for converting from MCI to AD between the ages of 55 and 85 years.

64 seful in predicting midterm progression from MCI to AD dementia.

65 etween risk factors and the progression from MCI to AD were found for abnormal cerebrospinal fluid (C

66 ns of markers could predict progression from MCI to AD within 1 to 6 years, the elastic net algorithm

67 Main Outcomes and Measures: Progression from MCI to AD within 1 to 6 years.

68 rm SSRI treatment may delay progression from MCI to Alzheimer's dementia.

69 ited use for predicting the progression from MCI to dementia due to AD in short-term follow-up, irres

70 923-1687] pg/mL), and progressive MCI group (MCI with progression to AD dementia during follow-up; 13

71 elated to cognitive status (normocognitive > MCI > AD; P < 0.0001).

72 is in patients initially diagnosed as having MCI or subjective cognitive impairment (SCI).

73 Melodic contour identification (MCI) was measured using sung speech in which the words w

74 positive (Abeta+) mild cognitively impaired (MCI) and cognitively normal (CN) participants.

75 th AD (n = 95) or mild cognitive impairment (MCI) (n = 192) and in cognitively normal individuals (n

76 ts with diagnosed mild cognitive impairment (MCI) and 30 patients with Alzheimer's disease (AD) in ea

77 of patients with mild cognitive impairment (MCI) and Alzheimer disease (AD) are defective in phagocy

78 hy controls (HC), mild cognitive impairment (MCI) and Alzheimer's participants from the well characte

79 nt association of mild cognitive impairment (MCI) and APOE has not been established.

80 individuals with mild cognitive impairment (MCI) and cognitively normal individuals receiving care a

81 line, and risk of mild cognitive impairment (MCI) and dementia; (2) whether this association differs

82 disease (PD) and mild cognitive impairment (MCI) and in patients with PD without MCI.

83 individuals with mild cognitive impairment (MCI) and may confer a higher likelihood of progression t

84 isk of developing mild cognitive impairment (MCI) and MCI progression to dementia is not well establi

85 disease (AD) and mild cognitive impairment (MCI) and subjects with subjective cognitive decline (SCD

86 mer's disease and mild cognitive impairment (MCI) are defective in amyloid-beta1-42 (Abeta) phagocyto

87 e introduction of mild cognitive impairment (MCI) as a diagnostic category adds to the challenges of

88 itive function in mild cognitive impairment (MCI) due to Alzheimer's disease (AD).

89 ith diabetes with mild cognitive impairment (MCI) from those with normal cognition and those with Alz

90 562 subjects with mild cognitive impairment (MCI) from two national studies (ADNI) using a novel mult

91 specially for the Mild Cognitive Impairment (MCI) group.

92 OE-e4) allele and mild cognitive impairment (MCI) in elderly subjects.

93 Because mild cognitive impairment (MCI) is a prodromal stage for dementia, we sought to eva

94 Mild cognitive impairment (MCI) is common in early Parkinson's disease (PD).

95 mer's disease and mild cognitive impairment (MCI) is deregulated with highly increased or decreased t

96 g to AD-including mild cognitive impairment (MCI) not converting or converting to AD-to disclose the

97 of progression to mild cognitive impairment (MCI) or AD.

98 delay or prevent mild cognitive impairment (MCI) or Alzheimer disease (AD) dementia, markers of earl

99 ed odds of having mild cognitive impairment (MCI) or Alzheimer disease have been reported.

100 the incidence of mild cognitive impairment (MCI) or dementia among cognitively unimpaired individual

101 their prodromal, mild cognitive impairment (MCI) phases.

102 ts in the earlier mild cognitive impairment (MCI) stage of AD in their respective versions of the maz

103 m AD patients and Mild cognitive impairment (MCI) subjects relative to healthy controls.

104 progression from mild cognitive impairment (MCI) to AD dementia by combining information from divers

105 progression from mild cognitive impairment (MCI) to Alzheimer's dementia.

106 progression from mild cognitive impairment (MCI) to Alzheimer's disease (AD).

107 progression from mild cognitive impairment (MCI) to dementia.

108 progression from mild cognitive impairment (MCI) to dementia.

109 with AD, 332 with mild cognitive impairment (MCI)) were selected from the Alzheimer's Disease Neuroim

110 in patients with mild cognitive impairment (MCI), a precursor of AD, and advances our understanding

111 ve decline (SCD), mild cognitive impairment (MCI), Alzheimer's disease (AD) dementia and cognitively

112 197 patients with mild cognitive impairment (MCI), and 180 patients with AD dementia from the Alzheim

113 ognitive decline, mild cognitive impairment (MCI), or dementia are uncertain.

114 ognitive decline, mild cognitive impairment (MCI), or dementia is uncertain.

115 in subjects with mild cognitive impairment (MCI), patients with Parkinson disease (PD), and young an

116 Mild cognitive impairment (MCI), which often precedes AD, is characterized by neuro

117 ctory deficits in mild cognitive impairment (MCI).

118 ical diagnosis of mild cognitive impairment (MCI).

119 in patients with mild cognitive impairment (MCI).

120 rmal cognition or mild cognitive impairment (MCI).

121 in patients with mild cognitive impairment (MCI).

122 t at the stage of mild cognitive impairment (MCI).

123 ients with AD and mild cognitive impairment (MCI, a prodromal stage of AD) with a meta-analytical tec

124 concerns: n = 74; mild cognitive impairment [MCI]: n = 29, AD dementia: n = 10) were administered nov

125 In MCI an association between APOE-e4 and higher Abeta-plaq

126 In MCI participants, a baseline examination, including clin

127 In MCI patients with a history of depression, long-term SSR

128 In MCI with SNAP, low APOE epsilon4 and high APOE epsilon2

129 In MCI with SNAP, sustained glucose metabolism and gray mat

130 1) and APOE-e4 carrier status (p < 0.001) in MCI.

131 mentation of VitB12 may improve cognition in MCI patients even in the absence of clinically manifeste

132 ered sleep physiology and memory deficits in MCI patients and advance our understanding of offline me

133 effects were seen for olfactory deficits in MCI relative to HOA (d=-0.76, 95% CI -0.87<delta<-0.64).

134 test is associated with incident dementia in MCI.

135 s also suggest that dentate hyperactivity in MCI patients may be directly related to EC neuronal loss

136 Odour identification is most impaired in MCI, which parallels the most prominent sensory deficit

137 Olfactory deficits are present and robust in MCI.

138 is pathology (p < 0.001) were more severe in MCI than cognitively intact controls.

139 ively normal participants developed incident MCI (50.3% were men; mean age, 78.5 years).

140 ater for participants who developed incident MCI vs those who remained cognitively normal (-2.0 [5.1]

141 ssociated with an increased risk of incident MCI (hazard ratio [HR], 1.04 [95% CI, 1.02-1.06]; P < .0

142 vities in late life and the risk of incident MCI and to evaluate the influence of the apolipoprotein

143 n about the longitudinal outcome of incident MCI as predicted by late-life (aged >/=70 years) mentall

144 .92) and toward the highest risk of incident MCI for APOE varepsilon4 carriers who do not engage in m

145 ata point toward the lowest risk of incident MCI for APOE varepsilon4 noncarriers who engage in menta

146 ssociated with an increased risk of incident MCI were MetS (hazard ratio [HR], 1.46; 95% CI, 1.02-2.0

147 were followed up to the outcome of incident MCI.

148 were followed up to the outcome of incident MCI.

149 late life have a decreased risk of incident MCI.

150 associated with a decreased risk of incident MCI.

151 d body mass index (BMI) may predict incident MCI.

152 Prespecified outcomes were incident MCI and MCI progression to dementia.

153 per decade was also associated with incident MCI (HR, 1.08 [95% CI, 1.03-1.13]; P = .003).

154 s measured by the mandibular cortical index (MCI), and MBL and 2) to assess how various systemic dise

155 Microcirculation inflammation (MCI = g + ptc score) was higher in patients with a posit

156 INTERPRETATION: MCI diagnosis usually was associated with comorbid neuro

157 endent components first appeared in the late-MCI stage and could discriminate converting MCI and AD f

158 Individuals with LLD+MCI also showed greater white matter hyperintensity burd

159 s were stratified into early and late (LMCI) MCI stages.

160 ation of methylchloroisothiazolinone and MI (MCI-MI) has increased significantly, with a frequency of

161 on, MCI (amnestic MCI [aMCI] and nonamnestic MCI [naMCI]), and dementia.

162 insula and right ACC compared to nonamnestic MCI patients.

163 ate converting MCI and AD from nonconverting MCI with an accuracy of 83.5%.

164 follow-up, there were 250 incident cases of MCI among 1430 cognitively normal participants.

165 algorithm identified homogenous clusters of MCI subjects with markedly different prognostic cognitiv

166 y and predict diagnosis of AD, conversion of MCI to AD, stable MCI, and SCD with good to excellent ac

167 ing those with a final clinical diagnosis of MCI.

168 , which leads to the increased expression of MCI, Myb, and FoxJ1, transcriptional regulators necessar

169 as associated with an increased incidence of MCI and progression to dementia.

170 ormant-based, or self-report), and method of MCI diagnosis (cognitive vs global measure and amnestic

171 d risk for dementia or a combined outcome of MCI or dementia (1 trial, low strength of evidence); hig

172 sus SCD discrimination map for prediction of MCI subgroups resulted in good performance for patients

173 measure) remained a significant predictor of MCI (HR, 1.10 [95% CI, 1.04-1.16]; P < .001) and improve

174 After adjusting for key predictors of MCI risk, B-SIT (as a continuous measure) remained a sig

175 did not improve prediction of progression of MCI group, the predictive ability of SNP information ext

176 d neuropathologies; less than one-quarter of MCI cases showed "pure" AD at autopsy.

177 ade corresponds to a 24% increase in risk of MCI (HR, 1.24).

178 Risk of MCI and dementia; global and domain-specific cognitive d

179 ng risk of mortality, and determined risk of MCI and/or dementia by genotype and baseline age.

180 Estimates of the absolute risk of MCI or dementia, particularly over short time intervals,

181 ristics associated with an increased risk of MCI progression to dementia were MetS (HR, 4.25; 95% CI,

182 ate of change in weight and BMI with risk of MCI was investigated using proportional hazards models.

183 t, were associated with an increased risk of MCI.

184 tion concerning the structural substrates of MCI in patients with PD and may offer markers that can b

185 Lifetime incidence (to age 80-85 y) of MCI or dementia for the APOE-e4/e4 individuals in the lo

186 strengthen the clinical evidence that AD or MCI is accompanied by reduced peripheral blood BDNF leve

187 Positive patch test reaction to MI and/or MCI-MI and identification of the relevance of contact al

188 patch testing, contact allergy to MI and/or MCI-MI occurred in 57 patients (8.1%), with 35 reactions

189 Contact allergy to MI and/or MCI-MI was occupationally related in 4 cases.

190 h positive patch test reactions to MI and/or MCI-MI.

191 dementia in adults with normal cognition or MCI but no dementia diagnosis.

192 dementia in adults with normal cognition or MCI.

193 rotection in adults with normal cognition or MCI.

194 otection in persons with normal cognition or MCI.

195 fects on clinical Alzheimer-type dementia or MCI, and those that did suggested no benefit.

196 r did the criteria used for MCI diagnosis or MCI subtype.

197 duals followed longitudinally from normal or MCI status to death, derived from 4 Alzheimer Disease (A

198 PD-MCI level I criteria may have greater clinical convenien

199 PD-MCI was classified using Movement Disorders Society Task

200 cipants reverted to normal cognition from PD-MCI.

201 We evaluated the stability of PD-MCI over time to determine its clinical utility as a mar

202 d a dementia all of which were previously PD-MCI.

203 biomarkers of AD in a well-characterized pre-MCI population.

204 incident dementia cases among 221 prevalent MCI cases.

205 -up; 1182 [923-1687] pg/mL), and progressive MCI group (MCI with progression to AD dementia during fo

206 DNI cohort also showed significantly reduced MCI or AD conversion among APOE4 carriers with the prote

207 Among the group that remained MCI until death, mixed AD neuropathologic changes (ADNC;

208 e, the main genetic risk factor for sporadic MCI/AD, display impaired cholinergic sprouting after EC

209 nosis of AD, conversion of MCI to AD, stable MCI, and SCD with good to excellent accuracy and AUC val

210 rogressive mild cognitive impairment, stable MCI and Normal Control participants).

211 entia group (1479 [1134-1842] pg/mL), stable MCI group (no progression to AD during follow-up; 1182 [

212 e AD dementia group compared with the stable MCI group (P = .01).

213 sis converted to AD versus those with stable MCI (AUC, 0.71; P > .05).

214 The MCI trials used attention controls more often than trial

215 The MCI-MI concentration was 100 ppm; the MI concentration i

216 peripheral inflammation occurs early at the MCI disease stages.

217 have cerebrovascular pathology and carry the MCI diagnosis for a longer interval.

218 Impaired sprouting during the MCI stage may contribute to the faster cognitive decline

219 In the MCI group, a higher CSF NFL concentration was associated

220 lation of 0.15 to predict progression in the MCI group.

221 t a short course of IVIG administered in the MCI stage of AD reduces brain atrophy, prevents cognitiv

222 Osteoporosis was evaluated using the MCI.

223 the intrinsic networks from normal aging to MCI to AD was inversely proportional to the conversion t

224 f this variant against risk of conversion to MCI or AD (p = 0.038) and against cognitive decline in i

225 with 35 reactions to MI only, 5 reactions to MCI-MI only, and 17 reactions to both.

226 ur Memory for Mild Cognitive Impairment (TYM-MCI) in the diagnosis of patients with amnestic mild cog

227 aMCI/AD scored poorly on their original TYM-MCI.

228 ant improvement analysis showed that the TYM-MCI added value to the conventional memory assessment.

229 The TYM-MCI correctly classified most patients who had equivocal

230 The TYM-MCI is a powerful short cognitive test that examines ver

231 As a single test, the TYM-MCI performed as well as the ACE-R in the distinction of

232 Patients completed the TYM-MCI, the Test Your Memory test (TYM), MMSE and revised A

233 96; P < .01), good performance for AD versus MCI (AUC, 0.89; P < .01), and poor performance for MCI v

234 abetes without cognitive impairment, 35 with MCI, and 35 with AD.

235 connectome of 170 patients with PD (54 with MCI, 116 without MCI) and 41 healthy control subjects wa

236 mostly computer based; those for adults with MCI were mostly held in group sessions.

237 ct dementia progression in older adults with MCI.

238 r adults that enrolled 112 older adults with MCI.

239 normal cognition and 5 enrolled adults with MCI.

240 pressants, or no treatment and compared with MCI patients without a history of depression.

241 Of the 874 individuals ever diagnosed with MCI, final clinical diagnoses were varied: 39.2% died wi

242 A majority (74%) of subjects who died with MCI were without "high"-level ADNC, Lewy body disease, o

243 learning and memory deficits in humans with MCI-AD and in mouse models.

244 prevalence of depression in individuals with MCI and identify reasons for heterogeneity in the report

245 A total of 469 individuals with MCI had data on neurodegeneration biomarkers; of these p

246 However, among participants with MCI, higher plasma total tau levels were associated with

247 Among participants with MCI, higher plasma total tau levels were not significant

248 Among 112 study participants with MCI, mean (SD) age was 76.6 (6.9) years, 55 were women (

249 age, 75.5 [6.7] years) and 522 patients with MCI (225 women and 297 men; mean [SD] age, 72.6 [7.8] ye

250 Plasma NFL was increased in patients with MCI (mean, 42.8 ng/L) and patients with AD dementia (mea

251 tients with PD (P < .001), and patients with MCI (P < .001), respectively, compared with those of you

252 a NFL was particularly high in patients with MCI and patients with AD dementia with Abeta pathologic

253 ished in English, (2) reported patients with MCI as a primary study group, (3) reported depression or

254 Initiative (ADNI) enrolled 928 patients with MCI at baseline and 249 selected variables available in

255 ia and any type of dementia in patients with MCI at the individual level.

256 sulted in good performance for patients with MCI diagnosis converted to AD versus subjects with SCD (

257 .01) and fair performance for patients with MCI diagnosis converted to AD versus those with stable M

258 A total of 525 patients with MCI from the Amsterdam Dementia Cohort (longitudinal coh

259 ved omega-3 supplementation in patients with MCI have shown polarization of Apoepsilon3/epsilon3 pati

260 he prevalence of depression in patients with MCI in community-based samples was 25% (95% CI, 19-30) a

261 Results: Among the 928 patients with MCI in the ADNI database, 94 had 224 of the required var

262 he prevalence of depression in patients with MCI is high.

263 per year; P < .05) but not in patients with MCI or AD.

264 their Abeta+ counterparts, all patients with MCI SNAP subtypes displayed better preservation of tempo

265 in discriminating between the patients with MCI vs. early AD was achieved with the volumetric measur

266 in discriminating between the patients with MCI vs. early AD.

267 ed prevalence of depression in patients with MCI was 32% (95% CI, 27-37), with significant heterogene

268 criminating between HC and the patients with MCI was achieved with the volumetric measurement of the

269 ll prevalence of depression in patients with MCI was pooled using a random-effects model.

270 Patients with MCI with APOEepsilon4, abnormal CSF tau level, hippocamp

271 a+N+, 32.6%) were also seen in patients with MCI with SNAP subtypes compared with their Abeta+ counte

272 patients with probable AD; 60 patients with MCI, of whom 12 remained stable, 12 were converted to a

273 he prevalence of depression in patients with MCI, reported as a percentage with 95% CIs.

274 ation of future AD dementia in patients with MCI.

275 ed with executive functions in patients with MCI.

276 emerging cognitive effects in patients with MCI.

277 ne male and seven female human patients with MCI.

278 -derived, omega-3-supplemented patients with MCI.

279 ies, and follow-up planning in patients with MCI.

280 ta phagocytosis by Mvarphis of patients with MCI.

281 ith progression to dementia in patients with MCI.

282 visual memory consolidation in patients with MCI.

283 he prevalence of depression in patients with MCI.

284 In persons with MCI, cholinesterase inhibitors did not reduce dementia r

285 Results for populations with MCI suggested no effect of training on performance (low-

286 (mean age, 67 years +/- 8), 34 subjects with MCI (mean age, 72 years +/- 5), and 44 patients with PD

287 atients with PD (P = .007) and subjects with MCI (P < .001), respectively, and B0 shim changes were 1

288 ubjects, patients with PD, and subjects with MCI demonstrated 1.5, 2, and 2.5 times stronger head mov

289 hree patients with PD and four subjects with MCI were excluded because of excessive head motion (ie,

290 ubjects, patients with PD, and subjects with MCI, 6%, 35%, 38%, and 51%, respectively, moved more tha

291 alence estimates of depression in those with MCI are required to guide both clinical decisions and pu

292 persons with normal cognition and those with MCI, these pharmacologic treatments neither improved nor

293 0 patients with PD (54 with MCI, 116 without MCI) and 41 healthy control subjects was obtained by usi

294 iabetes mellitus or the MetS with or without MCI is a promising approach in early interventions to pr

295 ontrol subjects and patients with PD without MCI (range, P = .004 to P = .048).

296 ontrol subjects and patients with PD without MCI with fair to good accuracy (cross-validated area und

297 When compared with patients with PD without MCI, those with PD and MCI had a network with decreased

298 with PD and MCI and patients with PD without MCI.

299 irment (MCI) and in patients with PD without MCI.

300 rations relative to patients with PD without MCI.