ライフサイエンスコーパス: MCI

1 MCI participants showed significantly decreased temporal

2 MCI was assessed with extensive cognitive tests.

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

4 total of 857 subjects from the AD (n = 213), MCI (n = 322), and control (CN, n = 322) groups, we used

5 rmal) and amyloid-beta (Abeta) PET (17 AD, 3 MCI, 2 cognitively normal) were available.

6 ognitive normal (CN, age = 83.8 +/- 6.9), 34 MCI (age = 83.9 +/- 6.6), and 22 AD (age = 84.1 +/- 6.1)

7 yes from 39 AD participants, 72 eyes from 37 MCI participants, and 254 eyes from 133 control particip

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

9 9; mild cognitive impairment (MCI) risk, 43; MCI, 6] and replication (CN,73; MCI, 45; AD, 20) cohorts

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

11 Methods: (18)F-FDG PET scans of 544 MCI patients were obtained from the Alzheimer Disease Ne

12 autopsy and for whom (18)F-FDG PET (30 AD, 6 MCI, 2 cognitively normal) and amyloid-beta (Abeta) PET

13 I) risk, 43; MCI, 6] and replication (CN,73; MCI, 45; AD, 20) cohorts.

14 prevalence of all-cause CI was 38.3% (27.8% MCI and 10.5% dementia) in 2015.

15 prevalence of all-cause CI was 30.5% (22.9% MCI and 7.6% dementia) in 2010.

16 as classified into MCI caused by AD (MCI-A), MCI caused by VaD (MCI-VD), and MCI caused by ODs (MCI-O

17 (MCI) was classified into MCI caused by AD (MCI-A), MCI caused by VaD (MCI-VD), and MCI caused by OD

18 kers were verified in comparison between AD, MCI and control, supporting the notion that AD and MCI a

19 independently for distinguishing between AD, MCI, and amyloid deposition.

20 NGF protein, but not mRNA, was higher in AD, MCI, and HA-NCI, while mature NGF was lower.

21 kers were included, and eligible data on AD, MCI and control were extracted.

22 and CVI may differ between patients with AD, MCI, and healthy cognition, whereas SFCT may not differ

23 Association of choroidal parameters with AD, MCI, or control subjects was assessed using multivariabl

24 In AD/MCI, lower CSF Abeta42 predicted Abeta deposition and Ab

25 en and CSF p-tau predicted MMSE scores in AD/MCI.

26 E contribution in PRS risk predictions of AD/MCI and amyloid deposition.

27 on-amnestic MCI (naMCI), MDD+naMCI, amnestic MCI (aMCI), and MDD+aMCI.

28 tia- remitted depression (MDD), non-amnestic MCI (naMCI), MDD+naMCI, amnestic MCI (aMCI), and MDD+aMC

29 th amnestic MCI (aMCI); 4% with non-amnestic MCI (naMCI).

30 rogression from normal cognition to amnestic MCI, suggesting that anxiety may be a neuropsychiatric s

31 win Study of Aging (VETSA): 7% with amnestic MCI (aMCI); 4% with non-amnestic MCI (naMCI).

32 Among MCI individuals with amyloid-positive status, we examine

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

34 in patients with AD (B = 1.68; p = .001) and MCI (B = 2.69; p < .001) compared with control subjects,

35 in patients with AD (B = 2.73; p = .001) and MCI (B = 4.38; p < .001) compared with control subjects.

36 probable dementia occurred in 325 (3.8%) and MCI in 640 (7.6%) participants.

37 SFCT was similar among patients with AD and MCI and control subjects on multivariable analysis (p >

38 d control, supporting the notion that AD and MCI are accompanied by inflammatory responses in both th

39 We found that AD and MCI are predicted by both APOE genotype and PRS (area un

40 ase in the frequency of AST errors in AD and MCI compared to the control group, as predicted.

41 the CNS tPA inhibitor, was higher in AD and MCI cortical samples.

42 nt results of inflammatory markers in AD and MCI quantitatively.

43 ate analysis of populations with pure AD and MCI revealed positive effects only in individuals with A

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

45 tive cognitively unimpaired older adults and MCI groups, to the highest concentrations in the amyloid

46 onship between alpha7-nAChR availability and MCI.

47 ffect of intensive treatment on dementia and MCI incidence.

48 with modestly increased odds of dementia and MCI later in life.

49 Dementia and MCI were defined by hospitalization diagnosis codes (198

50 ith increased risk for probable dementia and MCI, independent of the intensity of hypertension treatm

51 urrence of adjudicated probable dementia and MCI.

52 r the prevalence of subtypes of dementia and MCI.

53 f preventing the development of dementia and MCI.

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

55 Moreover, GMNC and MCI associate differentially with the cell-cycle regulat

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

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

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

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

60 che assays in baseline subjects with SCD and MCI.

61 of AD dementia in cognitively unimpaired and MCI subjects.

62 AD (MCI-A), MCI caused by VaD (MCI-VD), and MCI caused by ODs (MCI-O).

63 More detailed study of CKD-associated MCI is needed to fully understand its clinical relevance

64 o have little or no effect on CKD-associated MCI, suggesting that the accumulation of uraemic neuroto

65 esis, may also be involved in CKD-associated MCI.

66 wareness was observed up to 1.6 years before MCI diagnosis, with memory awareness declining until the

67 xpanded to another medical diagnosis besides MCI.

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

69 re was no difference in SCP VD or PD between MCI and controls (P > 0.05).

70 Pervasive defects in both MCI and AD were found in select transcripts within these

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

72 these parameters, the cognitive status (both MCI and AD) was predicted with a receiver operating char

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

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

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

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

77 Relative risks (RR) of developing MCI when exposed to sleep characteristics were assessed

78 estions (a dialogue policy) that distinguish MCI from normal (NL) cognitive status.

79 y stable (CS), mild cognitive impairment-DS (MCI-DS), possible AD dementia, or definite AD dementia b

80 lobe in MCI participants (r = 0.43 for early MCI and r = 0.49 for late MCI).

81 aromaticity indices (NICS, ACID, HOMA, FLU, MCI).

82 D: adjusted OR, 1.30; 95% CI, 1.19-1.41; for MCI: adjusted OR, 2.00; 95% CI, 1.79-2.22; and for other

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

84 LK8 was a similarly strong discriminator for MCI (AUC=0.94) but slightly weaker for AD (AUC=0.83).

85 The cognitive function for MCI was evaluated using the questionnaires of the Korean

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

87 ults showed that 1) our prediction model for MCI conversion to AD yielded up to 75% accuracy (area un

88 3 m(2) was associated with a higher risk for MCI and a composite of dementia or MCI.

89 We identify an essential role for MCI in inducing deuterosome pathway components for the p

90 The lack of diagnostic specificity for MCI 'non-progressors' is a weakness inherent in framing

91 ogressors' is a weakness inherent in framing MCI primarily within a deterministic neurodegenerative p

92 mild CATD from normal cognition or CATD from MCI.

93 ormal cognition and distinguishing CATD from MCI.

94 ch single tool in predicting conversion from MCI to AD, underlining the incremental utility of (18)F-

95 complementary predictors of conversion from MCI to AD.

96 lic patterns associated with conversion from MCI to AD.

97 To predict conversion from MCI to probable AD, we applied a deep learning approach,

98 ired older adults (AUC=84.44%), but not from MCI (AUC=55.00%).

99 t cohort, and could predict progression from MCI to AD in a small preliminary test cohort of 11 parti

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

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

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

103 However, MCI is an aetiology-neutral description, which therefore

104 To identify MCI status at the earliest possible point, recent studie

105 t (MCI) precedes AD dementia and identifying MCI individuals at risk of progression is important for

106 lly relevant accuracy (~93%) for identifying MCI individuals who progress to AD within 3 years; ii) m

107 itively unimpaired, 42 cognitively impaired (MCI n = 16, Alzheimer's disease dementia n = 26), data o

108 itively unimpaired, 88 cognitively impaired (MCI n = 67, Alzheimer's disease dementia n = 21), data a

109 d controls (NCI), mild-cognitively impaired (MCI) and AD cases.

110 disease (AD) and mild cognitive impairment (MCI of the Alzheimer's type).

111 sed patients with mild cognitive impairment (MCI) (n = 178), AD dementia (n = 121), and other neurode

112 unimpaired (CU), mild cognitive impairment (MCI) and AD dementia patients characterized by Abeta PET

113 ples and CSF from mild cognitive impairment (MCI) and AD patients to analyse Abeta accumulation, cell

114 impairment (NCI), mild cognitive impairment (MCI) and AD.

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

116 ory disruption in mild cognitive impairment (MCI) and Alzheimer's disease (AD) is poorly understood,

117 in patients with mild cognitive impairment (MCI) and Alzheimer's disease (AD).

118 e pathogenesis of mild cognitive impairment (MCI) and Alzheimer's disease (AD).

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

120 decline (SCD) or mild cognitive impairment (MCI) can serve to predict progression to AD dementia.

121 d KLK8 for AD and mild cognitive impairment (MCI) due to AD.

122 descriptive term mild cognitive impairment (MCI) for those with cognitive difficulties not impairing

123 luded people with mild cognitive impairment (MCI) from single-centre and multicentre cohorts in Europ

124 rly biomarkers of mild cognitive impairment (MCI) has been central to the Alzheimer's Disease (AD) an

125 racteristics with mild cognitive impairment (MCI) have been examined in cross-sectional, but rarely i

126 e of dementia and mild cognitive impairment (MCI) in 9361 participants in the randomized Systolic Blo

127 S) could identify mild cognitive impairment (MCI) in adults who were only in their 50s.

128 Mild cognitive impairment (MCI) is an intermediate stage between cognitively normal

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

130 LOAD) preceded by mild cognitive impairment (MCI) is the most common type of dementia.

131 dent dementia and mild cognitive impairment (MCI) later in life.

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

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

134 ly to progress to mild cognitive impairment (MCI) or dementia in Cox proportional hazards analyses ad

135 individuals with mild cognitive impairment (MCI) or dementia, elevated brain iron together with beta

136 ical diagnosis of mild cognitive impairment (MCI) or early AD when compared to ApoE4(-/-) subjects.

137 , and a cohort of mild cognitive impairment (MCI) patients with four-year clinical follow-up.

138 hy controls (HC), mild cognitive impairment (MCI) patients, and AD patients, and explore how cerebral

139 rodromal state of mild cognitive impairment (MCI) precedes AD dementia and identifying MCI individual

140 tmortem brains of mild cognitive impairment (MCI) rather than symptomatic AD patients reveal a remark

141 normal (CN), 19; mild cognitive impairment (MCI) risk, 43; MCI, 6] and replication (CN,73; MCI, 45;

142 g conversion from mild cognitive impairment (MCI) to Alzheimer dementia (AD) is currently under debat

143 e conversion from mild cognitive impairment (MCI) to Alzheimer disease (AD).

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

145 Mild cognitive impairment (MCI) was classified into MCI caused by AD (MCI-A), MCI c

146 inical AD (pAD) + mild cognitive impairment (MCI) without SCeVD (pAD/MCI without SCeVD, n = 22), and

147 14 patients with mild cognitive impairment (MCI), a prodromal stage to dementia, and 17 cognitively

148 and patients with mild cognitive impairment (MCI), AD dementia and non-AD neurodegenerative diseases.

149 participants with mild cognitive impairment (MCI), Alzheimer's disease, and frontotemporal dementia.

150 197 patients with mild cognitive impairment (MCI), and 180 patients with AD dementia from the Alzheim

151 normal (CN), 160 mild cognitive impairment (MCI), and 73 AD subjects who were further classified bas

152 n accuracy of AD, mild cognitive impairment (MCI), and amyloid deposition risks with PRS, including a

153 r's disease (AD), mild cognitive impairment (MCI), and cognitively intact controls using OCT angiogra

154 d analysis of AD, mild cognitive impairment (MCI), and healthy subjects.

155 le dementia (SD), mild cognitive impairment (MCI), and other neurodegenerative diseases.

156 r's disease (AD), mild cognitive impairment (MCI), FCD and healthy controls.

157 who progressed to mild cognitive impairment (MCI), heightened memory awareness was observed up to 1.6

158 eimer's dementia, Mild Cognitive Impairment (MCI), or no cognitive impairment with high (HA-NCI) and

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

160 gnosed with AD or mild cognitive impairment (MCI), SNPs within the BACE2 locus are associated with ce

161 and its prodrome, mild cognitive impairment (MCI), which are characterized by deficits in executive f

162 (AD) dementia or mild cognitive impairment (MCI).

163 nt of dementia or mild cognitive impairment (MCI).

164 rmal cognition or mild cognitive impairment (MCI).

165 of patients with mild cognitive impairment (MCI).

166 ue to AD; 65 with mild cognitive impairment (MCI); 95 control participants).

167 emory-predominant mild cognitive impairment (MCI; n = 75), or neurologically normal control subjects

168 individuals with mild cognitive impairment (MCI; women, 38%; 76.9 [7.3] years) from the Harvard Agin

169 fare, and mild cognitive decline/impairment (MCI) can further develop into Dementia/Alzheimer's disea

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

171 ficant dysregulation of a mosaic of genes in MCI and AD that were not previously appreciated in terms

172 Plasminogen protein was higher in MCI and AD brain tissue, with plasminogen mRNA not likew

173 stage of Alzheimer and further increases in MCI and AD dementia.

174 au deposition in the medial temporal lobe in MCI participants (r = 0.43 for early MCI and r = 0.49 fo

175 haemodynamic factors or lipid metabolism in MCI pathogenesis.

176 rting higher availability of alpha7-nAChR in MCI.

177 s: Higher (18)F-ASEM binding was observed in MCI patients than in controls across all regions, suppor

178 MMP9), which degrades NGF, was overactive in MCI and AD.

179 ns in cerebrospinal fluid (CSF) or plasma in MCI Abeta+ and AD Abeta+.

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

181 sTREM2 (0.695, p<0.05) in CSF, were shown in MCI compared with the control.

182 ifferential expression of key transcripts in MCI and AD compared to NCI that underlie signaling defec

183 volume changes after donepezil treatment in MCI, which is a prodromal phase of AD, using voxel-based

184 Incident MCI and sleep characteristics were assessed in 1,890 par

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

186 40, 0.94-2.08) were associated with incident MCI.

187 lated by the mitochondrial complexity index (MCI) providing quantitative and morphological informatio

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

189 gnitive impairment (MCI) was classified into MCI caused by AD (MCI-A), MCI caused by VaD (MCI-VD), an

190 r = 0.43 for early MCI and r = 0.49 for late MCI).

191 e of infarcts across diagnostic groups (CS < MCI-DS < possible AD dementia < definite AD dementia).

192 have implicated the nuclear protein MCIDAS (MCI), in the transcriptional regulation of MCC specifica

193 ith participants 15+ years younger than most MCI samples, these findings are promising with regard to

194 olling for non-independence of twins and non-MCI factors that can affect cognition, higher PRSs were

195 used by VaD (MCI-VD), and MCI caused by ODs (MCI-O).

196 a under the curve (AUC)=0.89) and in case of MCI (AUC=0.97) even superior to CSF Abeta42.

197 lusion criteria were a baseline diagnosis of MCI, at least 6 months of follow-up, and availability of

198 generation, and transition to a diagnosis of MCI/AD.

199 cognitive resilience) for identification of MCI individuals who progress to AD within 3 years.

200 cerebrospinal fluid (CSF) miR-195 levels of MCI subjects are positively correlated with cognitive pe

201 hich is 20 years prior to estimated onset of MCI among mutation carriers.

202 well as understanding of the pathogenesis of MCI in connection with brain morphometric change.

203 and ineffective sometimes, the prevention of MCI by identifying modifiable risk factors is a compleme

204 Consequently, a proportion of MCI cases are due to non-neurodegenerative processes, in

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

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

207 For time in bed, the risk of MCI was increased for <= 5 hours (RR = 2.86, 1.24-6.60,

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

209 In a subset of MCI participants who progressed to dementia, awareness w

210 nts or caregivers addressed the treatment of MCI or mild to moderate dementia.

211 istinguish between participants in the AD or MCI groups and those in the FCD or healthy control group

212 ne over time in PD subjects but not in AD or MCI subjects.

213 ggesting SCeVD appear at the pre-clinical or MCI stage of AD and therapeutic lowering of neurotoxic p

214 dementia in adults with normal cognition or MCI.

215 ng adjudicated outcomes, odds of dementia or MCI were higher among participants with restrictive (mul

216 ere not associated with probable dementia or MCI, nor did the urinary ACR modify the effect of intens

217 l disease may be associated with dementia or MCI, though results were inconsistent across studies and

218 risk for MCI and a composite of dementia or MCI.

219 l/min per 1.73 m(2) and risk for dementia or MCI.

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

221 ne specimens from individuals who had SCD or MCI revealed that NT1 tau, but not tau measured using Qu

222 prospectively followed patients with SCD or MCI who remained cognitively stable, converted to AD dem

223 Overall, MCI patients presented an intermediate gyrification patt

224 eVD (pAD/MCI without SCeVD, n = 22), and pAD/MCI with SCeVD (n = 16) for ELISA quantification of carg

225 spho-181T-tau were higher in both CN and pAD/MCI with SCeVD groups than in the corresponding controls

226 ficantly higher in the CN with SCeVD and pAD/MCI with SCeVD groups than their corresponding control g

227 ognitive impairment (MCI) without SCeVD (pAD/MCI without SCeVD, n = 22), and pAD/MCI with SCeVD (n =

228 Abeta42 were significantly higher in the pAD/MCI with SCeVD group but not in the CN with SCeVD group

229 longitudinal study with older participants, MCI risk was increased in persons with poor sleep qualit

230 PD-MCI was classified using Movement Disorders Society Task

231 cipants reverted to normal cognition from PD-MCI.

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

233 concentrations in the amyloid beta-positive MCI and Alzheimer's disease groups (p<0.001, Alzheimer's

234 coma patients may have increased odds of SD, MCI, and other neurodegenerative diseases.

235 associated with verbal memory in this small MCI sample.

236 have better responses to rTMS and tDCS than MCI.

237 preclinical AD and further increased at the MCI and dementia stages.

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

239 red to detect a 30% or greater change in the MCI and dementia groups.

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

241 Altogether, we demonstrated that the MCI is a valuable quantitative morphological parameter t

242 id-beta may identify participants closest to MCI for secondary prevention trials.

243 e, asthma, marital status also contribute to MCI risk, which is less exploited previously.

244 importance of various factors contributed to MCI and predicted cognitive declined.

245 s declining until the time of progression to MCI (-0.08 discrepant-points/yr).

246 gs will be useful for screening and tracking MCI, as well as understanding of the pathogenesis of MCI

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

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

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

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

251 MCI caused by AD (MCI-A), MCI caused by VaD (MCI-VD), and MCI caused by ODs (MCI-O).

252 s (maximum effect size of 1.10 for CN versus MCI and 1.39 for CN versus AD, p < 0.0001).

253 udy efficacy and patient outcomes by viewing MCI as a descriptive term with a wide differential diagn

254 including 98 patients with mild AD, 21 with MCI due to AD and 118 controls were collected.

255 rtile range, 71-80]; 50.9% women; 60.5% with MCI).

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

257 normal cognition and 5 enrolled adults with MCI.

258 Among Medicare beneficiaries with MCI or dementia of uncertain etiology evaluated by demen

259 l management for Medicare beneficiaries with MCI or dementia.

260 r VD, PD, and GC-IPL thickness compared with MCI and controls.

261 nferonasal (P = 0.025) sectors compared with MCI and significantly decreased GC-IPL thickness over th

262 in the 6-mm circle (P = 0.047) compared with MCI and significantly decreased SCP VD and PD in the 3-m

263 05) levels were observed in AD compared with MCI.

264 gnificant numbers of patients diagnosed with MCI do not 'convert' to dementia.

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

266 2 eyes) with AD, 74 patients (143 eyes) with MCI, and 137 (248 eyes) control subjects.

267 urther progression to AD of individuals with MCI and amyloid-positive status is predicted by PRS over

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

269 We included all 2611 individuals with MCI in the four cohorts, 1007 (39%) of whom progressed t

270 ppocampal volume results in individuals with MCI, and help research and clinical settings to prepare

271 ial matrix was possible in mitochondria with MCI >= 7.

272 vel of adaptive control in participants with MCI or AD dementia.

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

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

275 results were positive in 3817 patients with MCI (55.3%) and 3154 patients with dementia (70.1%).

276 point changed in 4159 of 6905 patients with MCI (60.2% [95% CI, 59.1%-61.4%]) and 2859 of 4504 patie

277 CVI was significantly lower in patients with MCI (B = -0.58; p = .002) compared with control subjects

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

279 ethods: The study included 319 patients with MCI from the Alzheimer Disease Neuroimaging Initiative d

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

281 he average scores of K-MMSE in patients with MCI improved by 8% after donepezil treatment.

282 ompared with healthy controls, patients with MCI showed significantly lower GM volumes in the hippoca

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

284 Patients with MCI underwent the magnetic resonance imaging (MRI) befor

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

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

287 Patients with MCI were identified with a sensitivity of 80%.

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

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

290 ta phagocytosis by Mvarphis of patients with MCI.

291 ith progression to dementia in patients with MCI.

292 eening and monitoring tool for patients with MCI.

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

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

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

296 0 patients with PD (54 with MCI, 116 without MCI) and 41 healthy control subjects was obtained by usi

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

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

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

300 rations relative to patients with PD without MCI.