ライフサイエンスコーパス: mild cognitive impairment

1 7%] were clinically normal and 537 [13%] had mild cognitive impairment).

2 sease dementia during follow-up (progressive mild cognitive impairment).

3 phagocytosis by macrophages of patients with mild cognitive impairment.

4 grape juice are not exclusive to adults with mild cognitive impairment.

5 the preclinical stage, prior to the onset of mild cognitive impairment.

6 r 227 healthy controls and 434 subjects with mild cognitive impairment.

7 pared to amyloid-beta negative patients with mild cognitive impairment.

8 s found only in patients with AD or amnestic mild cognitive impairment.

9 ogression over 36 months in 33 patients with mild cognitive impairment.

10 ividuals, and five individuals with amnestic mild cognitive impairment.

11 the rate of hippocampal atrophy in amnestic mild cognitive impairment.

12 e impairment (P < 0.05) compared with stable mild cognitive impairment.

13 ructural abnormalities on neural function in mild cognitive impairment.

14 =1.74, 95% CI=1.22-2.47) but not nonamnestic mild cognitive impairment.

15 lzheimer's disease and cognitively normal to mild cognitive impairment.

16 c mild cognitive impairment but not amnestic mild cognitive impairment.

17 ural MRI) in increasing the risk of incident mild cognitive impairment.

18 observed initially, increased risk for later mild cognitive impairment.

19 and psychosocial functioning in people with mild cognitive impairment.

20 ths, such as hippocampal subfield atrophy in mild cognitive impairment.

21 on spatially overlapped in the subjects with mild cognitive impairment.

22 imer's pathology (including amyloid-positive mild cognitive impairment), 19 patients with progressive

23 ty-five subjects (92 cognitively normal, 129 mild cognitive impairment, 64 Alzheimer's disease) were

24 h AD, 287 with prodromal AD, 399 with stable mild cognitive impairment, 99 with dementias other than

25 The overall effect on cognition in mild cognitive impairment across 17 trials was moderate

26 Mild cognitive impairment, AD dementia, and longitudinal

27 ects with normal cognition and patients with mild cognitive impairment, Alzheimer's disease dementia,

28 hout late-life depression (LLD) and amnestic mild cognitive impairment (aMCI) are unknown.

29 In 38 older human adults with amnestic mild cognitive impairment (aMCI) or normative cognition,

30 s that exhibited change in previous amnestic Mild Cognitive Impairment (aMCI) trials.

31 jects, including 10 probable AD, 15 amnestic mild cognitive impairment (aMCI), and 10 cognitively hea

32 brain connectivity in patients with amnestic mild cognitive impairment (aMCI).

33 tively normal (n = 42), clinically-diagnosed mild cognitive impairment (amyloid positive, n = 47, and

34 ntrols, 68 subjective memory complaints, 419 mild cognitive impairment and 121 Alzheimer's disease de

35 Alzheimer's disease (AD), non-AD dementia or mild cognitive impairment and 20 age-matched and sex-mat

36 cortical (18)F T807 binding in patients with mild cognitive impairment and AD dementia compared to cl

37 omal F-actin levels in postmortem brain from mild cognitive impairment and AD patients compared with

38 ver, our findings propose a new way to fight mild cognitive impairment and aging-related cognitive de

39 commentary on this article.Individuals with mild cognitive impairment and Alzheimer's disease clinic

40 itudinal changes in microglial activation in mild cognitive impairment and Alzheimer's disease subjec

41 l) and was significantly elevated for Abeta+ mild cognitive impairment and Alzheimer's disease subjec

42 gorization of neuroanatomical alterations in mild cognitive impairment and Alzheimer's disease that c

43 tsburgh compound B was high in subjects with mild cognitive impairment and Alzheimer's disease, while

44 REST is lost, however, in mild cognitive impairment and Alzheimer's disease.

45 ilar results in subgroup analyses within the mild cognitive impairment and cognitively normal cohorts

46 ower in the dementia group compared with the mild cognitive impairment and cognitively normal groups

47 pooled samples of patients with progressive mild cognitive impairment and corresponding healthy cont

48 erfusion has previously been associated with mild cognitive impairment and dementia in various cross-

49 fore the kindred's respective median ages at mild cognitive impairment and dementia onset.

50 s of daily living were pooled separately for mild cognitive impairment and dementia trials.

51 s (dementia), inferior parietal cortex (late mild cognitive impairment and dementia), and inferior te

52 and inferior temporal cortex (early and late mild cognitive impairment and dementia).

53 ontrols and greater volume reduction in late mild cognitive impairment and dementia.

54 ncluding patients with Alzheimer disease and mild cognitive impairment and healthy volunteers.

55 myloid imaging specifically in subjects with mild cognitive impairment and in comparison with or in c

56 As PD outcome variables, mild cognitive impairment and incident PDD were diagnose

57 iated with cognitive benefits in adults with mild cognitive impairment and neurodegenerative disease,

58 ntia, AD, and PD in all studies and incident mild cognitive impairment and progression of parkinsonia

59 miologic data supporting previous studies on mild cognitive impairment and progression to AD are revi

60 wn to improve memory function in adults with mild cognitive impairment and reduce blood pressure in h

61 A need exists for exploring mild cognitive impairment and risk of critical illness.

62 gTDP-25(+/0)), which at 6 months of age show mild cognitive impairments and no motor deficits.

63 ene cluster associated with delayed onset of mild-cognitive impairment and dementia.

64 nitively stable for at least 2 years (stable mild cognitive impairment) and those who progressed to A

65 o completed the study (5 healthy controls, 6 mild cognitive impairment, and 10 AD) received 370 MBq o

66 nitively healthy controls, 197 patients with mild cognitive impairment, and 180 patients with AD with

67 er's disease (AD) patients, 40 subjects with mild cognitive impairment, and 40 controls with subjecti

68 ent included 17.5% with dementia, 32.7% with mild cognitive impairment, and 49.5% cognitively normal.

69 nitively normal, 5 old cognitively normal, 5 mild cognitive impairment, and 5 Alzheimer disease (AD).

70 probable Alzheimer disease, 80 patients with mild cognitive impairment, and 59 healthy volunteers; an

71 ally characterized as PD, PDD, DLB, amnestic mild cognitive impairment, and AD.

72 spectrum of preclinical Alzheimer's disease, mild cognitive impairment, and Alzheimer's disease are d

73 s (n = 51), early (n = 66) and late (n = 41) mild cognitive impairment, and Alzheimer's disease with

74 A classification of normal cognitive aging, mild cognitive impairment, and dementia was adjudicated

75 ognitively normal controls, individuals with mild cognitive impairment, and individuals with AD to as

76 served as healthy controls, subjects who had mild cognitive impairment, and subjects who had Alzheime

77 d at baseline and follow-up in subjects with mild cognitive impairment, and this was compared with su

78 th a history of idiopathic falls, those with mild cognitive impairment, and those with Parkinson's di

79 me measures were as follows: 1) dementia and mild cognitive impairment; and 2) memory, speed of proce

80 ate that amyloid-beta positive patients with mild cognitive impairment are more likely on a path towa

81 rmal older participants and individuals with mild cognitive impairment assessed with baseline lumbar

82 fic commentary on this article.Subjects with mild cognitive impairment associated with cortical amylo

83 ls carrying this haplotype had a mean AAO of mild-cognitive impairment at 51.0 +/- 5.2 years compared

84 ent represents a major challenge in PD, with mild cognitive impairment being a prodromal stage of PD

85 pid cognitive decline among individuals with mild cognitive impairment both additively and multiplica

86 s were significant predictors of nonamnestic mild cognitive impairment but not amnestic mild cognitiv

87 In the CNS, mild cognitive impairment can be attributed to obesity-i

88 Twenty-six (62%) of 42 mild cognitive impairment cases showed a raised cortical

89 Twenty-two (85%) of the 26 amyloid-positive mild cognitive impairment cases showed clusters of incre

90 flammation in a majority of amyloid positive mild cognitive impairment cases, its cortical distributi

91 nd would be present in most amyloid-positive mild cognitive impairment cases.

92 roinflammation (microglial activation) in 42 mild cognitive impairment cases.

93 e and follow-up microglial activation in the mild cognitive impairment cohort compared to controls we

94 reduction of 18% in microglial activation in mild cognitive impairment cohort over 14 months, which w

95 ment due to Alzheimer's disease and a stable mild cognitive impairment cohort.

96 2, was down-regulated in persons with AD and mild cognitive impairment compared with controls.

97 dinally, amyloid-beta positive patients with mild cognitive impairment continued to show high levels

98 nths, patients with Parkinson's disease with mild cognitive impairment demonstrated more severe corti

99 aseline, cases with Parkinson's disease with mild cognitive impairment demonstrated widespread cortic

100 ian age of 44 years (95% CI, 43-45 years) at mild cognitive impairment diagnosis.

101 low the marker band already in patients with mild cognitive impairment due to AD.

102 d precursor protein (hAPP) and patients with mild cognitive impairment due to Alzheimer's disease (MC

103 yloid-positive patients meeting criteria for mild cognitive impairment due to Alzheimer's disease (n

104 Differentiation between cohorts with mild cognitive impairment due to Alzheimer's disease and

105 sease and a control cohort, or a cohort with mild cognitive impairment due to Alzheimer's disease and

106 We studied 12 human subjects diagnosed with mild cognitive impairment due to Alzheimer's disease, co

107 for probable Alzheimer's disease dementia or mild cognitive impairment due to Alzheimer's disease, pr

108 ore biomarkers were strongly associated with mild cognitive impairment due to Alzheimer's disease.

109 (4 controls, 3 with a history of TBI, 2 with mild cognitive impairment due to suspected Alzheimer dis

110 (4 controls, 3 with a history of TBI, 2 with mild cognitive impairment due to suspected Alzheimer dis

111 f locus coeruleus dysfunction reminiscent of mild cognitive impairment/early Alzheimer's disease.

112 Slopes for individuals who developed mild cognitive impairment (eg, neuroticism: beta = 0.00;

113 Thirty subjects (eight mild cognitive impairment, eight Alzheimer's disease and

114 ic interaction among brain regions for early mild cognitive impairment (eMCI) diagnosis.

115 compared with controls and those with stable mild cognitive impairment, even when stratifying for APO

116 erebrospinal fluid neurogranin levels in the mild cognitive impairment group correlated with longitud

117 Furthermore, within the progressive mild cognitive impairment group, elevated cerebrospinal

118 In the mild cognitive impairment group, high baseline cerebrosp

119 vanced clinical stage (Alzheimer's disease > mild cognitive impairment > older cognitively normal) an

120 However, previous studies in mild cognitive impairment have not included markers of a

121 studies using a memory task in patients with mild cognitive impairment have produced discordant resul

122 re also associated with an increased risk of mild cognitive impairment (hazard ratio, 2.9; 95% CI, 1.

123 By contrast, depression predicted amnestic mild cognitive impairment (hazard ratio=1.74, 95% CI=1.2

124 decline: hazard ratio [HR] = 0.57, p < 0.05; mild cognitive impairment: HR = 0.19, p < .01), indicati

125 n of preexisting cerebrovascular disease and mild cognitive impairment in 1 each).

126 ohort study to estimate the risk of incident mild cognitive impairment in cognitively normal elderly

127 Mild cognitive impairment in Parkinson's disease (PD) is

128 uld be a biomarker in therapeutic studies of mild cognitive impairment in Parkinson's disease for pro

129 Mild cognitive impairment in Parkinson's disease is asso

130 Clinical factors associated with baseline mild cognitive impairment included age, male gender, str

131 sought to determine whether the presence of mild cognitive impairment independently increases the ri

132 ls with persistent depression, children with mild cognitive impairment, individuals matched on childh

133 is could reflect that activated microglia in mild cognitive impairment initially may adopt a protecti

134 In patients with mild cognitive impairment, intraneuronal Abeta immunorea

135 Mild cognitive impairment is a common disorder affecting

136 The presence of mild cognitive impairment is independently associated wi

137 ults with remitted major depression (36 with mild cognitive impairment (LLD+MCI) and 44 with normal c

138 ver 3 years), and from cognitively normal to mild cognitive impairment (maximum balanced accuracy of

139 As mild cognitive impairment may be a contributor to poorer

140 on [MMSE] score, 28 [0.3]), 61 patients with mild cognitive impairment (MCI) (mean [SE] age, 68 [1] y

141 An additional 65 patients with mild cognitive impairment (MCI) (mean age, 76.2 years +/

142 in a cohort of patients with AD (n = 95) or mild cognitive impairment (MCI) (n = 192) and in cogniti

143 hy controls (HC), 33 patients with diagnosed mild cognitive impairment (MCI) and 30 patients with Alz

144 al (CN) controls, 52 with recently diagnosed mild cognitive impairment (MCI) and 31 with probable Alz

145 human trials as a candidate therapeutic for mild cognitive impairment (MCI) and AD, and therefore it

146 ssociations between FDG metabolism and IR in mild cognitive impairment (MCI) and AD, as well as MCI c

147 dy normal participants and 2 patient groups: mild cognitive impairment (MCI) and AD.

148 Monocyte/macrophages of patients with mild cognitive impairment (MCI) and Alzheimer disease (A

149 F, in a cohort of controls and patients with mild cognitive impairment (MCI) and Alzheimer disease (A

150 ngles) using a postmortem sample of healthy, mild cognitive impairment (MCI) and Alzheimer's individu

151 clinically classified healthy controls (HC), mild cognitive impairment (MCI) and Alzheimer's particip

152 an men, and the sex-dependent association of mild cognitive impairment (MCI) and APOE has not been es

153 t study was conducted among individuals with mild cognitive impairment (MCI) and cognitively normal i

154 al tau level, cognitive decline, and risk of mild cognitive impairment (MCI) and dementia; (2) whethe

155 cose metabolism occur in patients exhibiting Mild Cognitive Impairment (MCI) and glucose hypometaboli

156 in patients with Parkinson disease (PD) and mild cognitive impairment (MCI) and in patients with PD

157 Depression is common in individuals with mild cognitive impairment (MCI) and may confer a higher

158 lar risk factors with the risk of developing mild cognitive impairment (MCI) and MCI progression to d

159 of patients with Alzheimer disease (AD) and mild cognitive impairment (MCI) and subjects with subjec

160 is) of patients with Alzheimer's disease and mild cognitive impairment (MCI) are defective in amyloid

161 Patients with Parkinson disease (PD) and mild cognitive impairment (MCI) are vulnerable to dement

162 The introduction of mild cognitive impairment (MCI) as a diagnostic category

163 ver, it has to be acknowledged that treating mild cognitive impairment (MCI) as a prodrome for AD has

164 eta) imaging with (18)F-florbetaben (FBB) in mild cognitive impairment (MCI) by evaluating its progno

165 newly developed Alzheimer's disease (AD) and mild cognitive impairment (MCI) criteria.

166 g early help seeking have increased rates of mild cognitive impairment (MCI) diagnosis in Western cou

167 ) on brain atrophy and cognitive function in mild cognitive impairment (MCI) due to Alzheimer's disea

168 It differentiates subjects with mild cognitive impairment (MCI) from healthy controls.

169 2) discriminates patients with diabetes with mild cognitive impairment (MCI) from those with normal c

170 es and biomarker data from 562 subjects with mild cognitive impairment (MCI) from two national studie

171 oved predictive accuracy, especially for the Mild Cognitive Impairment (MCI) group.

172 clinical and subclinical hypothyroidism with mild cognitive impairment (MCI) has not been established

173 olipoprotein E epsilon4 (APOE-e4) allele and mild cognitive impairment (MCI) in elderly subjects.

174 ects (mean age, 79.9 years; 40% female) with mild cognitive impairment (MCI) in the ADNI database and

175 Because mild cognitive impairment (MCI) is a prodromal stage for

176 Mild cognitive impairment (MCI) is common in early Parki

177 Mild cognitive impairment (MCI) is defined as the sympto

178 tem of patients with Alzheimer's disease and mild cognitive impairment (MCI) is deregulated with high

179 linical classification of early dementia and mild cognitive impairment (MCI) is imprecise.

180 es ranging from normal aging to AD-including mild cognitive impairment (MCI) not converting or conver

181 individuals with high risk of progression to mild cognitive impairment (MCI) or AD.

182 increase the opportunity to delay or prevent mild cognitive impairment (MCI) or Alzheimer disease (AD

183 ting activities and decreased odds of having mild cognitive impairment (MCI) or Alzheimer disease hav

184 eveloped risk estimates for the incidence of mild cognitive impairment (MCI) or dementia among cognit

185 d DLB and AD, as well as in their prodromal, mild cognitive impairment (MCI) phases.

186 People with mild cognitive impairment (MCI) show a high risk to deve

187 protein [hAPP]) and patients in the earlier mild cognitive impairment (MCI) stage of AD in their res

188 miRNAs in serum samples from AD patients and Mild cognitive impairment (MCI) subjects relative to hea

189 brospinal fluid (CSF) biomarker criteria and mild cognitive impairment (MCI) symptoms.

190 : To optimize prediction of progression from mild cognitive impairment (MCI) to AD dementia by combin

191 tment on CSF biomarkers and progression from mild cognitive impairment (MCI) to Alzheimer's dementia.

192 factors for predicting the progression from mild cognitive impairment (MCI) to Alzheimer's disease (

193 mal cognition through the prodromal stage of mild cognitive impairment (MCI) to clinical dementia.

194 ed as a clinical marker for progression from mild cognitive impairment (MCI) to dementia.

195 osis and for predicting the progression from mild cognitive impairment (MCI) to dementia.

196 470 patients (138 with AD, 332 with mild cognitive impairment (MCI)) were selected from the

197 ulation method during sleep in patients with mild cognitive impairment (MCI), a precursor of AD, and

198 In the presence of fornix damage in mild cognitive impairment (MCI), a recognized prodrome o

199 nts with subjective cognitive decline (SCD), mild cognitive impairment (MCI), Alzheimer's disease (AD

200 imer disease (AD) patients, 11 patients with mild cognitive impairment (MCI), and 11 healthy controls

201 nitively healthy controls, 197 patients with mild cognitive impairment (MCI), and 180 patients with A

202 on between PACAP biomarkers and preclinical, mild cognitive impairment (MCI), and dementia stages of

203 n asymptomatic subjects and individuals with mild cognitive impairment (MCI), but their cognitive pro

204 e Alzheimer dementia (pAD), in patients with mild cognitive impairment (MCI), in cognitively normal c

205 tions to prevent or delay cognitive decline, mild cognitive impairment (MCI), or dementia are uncerta

206 tment to prevent or delay cognitive decline, mild cognitive impairment (MCI), or dementia is uncertai

207 (MR) spectroscopic imaging in subjects with mild cognitive impairment (MCI), patients with Parkinson

208 Mild cognitive impairment (MCI), which often precedes AD

209 outcomes for adults with normal cognition or mild cognitive impairment (MCI).

210 related neuronal structures in patients with mild cognitive impairment (MCI).

211 f hypometabolism and atrophy in persons with mild cognitive impairment (MCI).

212 a biomarker for AD and its prodromal stage, mild cognitive impairment (MCI).

213 g, clinical, and paraclinical data in AD and mild cognitive impairment (MCI).

214 nic obstructive pulmonary disease (COPD) and mild cognitive impairment (MCI).

215 for clinicians, especially in patients with mild cognitive impairment (MCI).

216 gy, which is already evident at the stage of mild cognitive impairment (MCI).

217 estigate the nature of olfactory deficits in mild cognitive impairment (MCI).

218 l outcomes following a clinical diagnosis of mild cognitive impairment (MCI).

219 on in conversion risk (from healthy aging to mild cognitive impairment (MCI)/AD or from MCI to AD) an

220 e clinical BDNF data in patients with AD and mild cognitive impairment (MCI, a prodromal stage of AD)

221 s of non-cognitively impaired (NCI; n = 23), mild cognitive impairment (MCI; n = 21), and mild to mod

222 oses of cognitively normal ([CN] n = 570) or mild cognitive impairment ([MCI] n = 131) were included.

223 valuated 798 subjects (225 control, 388 with mild cognitive impairment [MCI], and 185 with AD) from t

224 = 70; subjective cognitive concerns: n = 74; mild cognitive impairment [MCI]: n = 29, AD dementia: n

225 Forty-five patients with mild cognitive impairment (mean age +/- SD, 72.69 +/- 6.

226 ognitively normal subjects, 95 subjects with mild cognitive impairment (Mini-Mental State Examination

227 ic ADAD participants (n = 21), patients with mild cognitive impairment (n = 11) and sporadic AD (n =

228 ages 45-86, 17 male) and normal cognition or mild cognitive impairment (n = 13), and 21 cognitively n

229 individuals with normal cognition (n = 90), mild cognitive impairment (n = 130), and AD (n = 59) and

230 Subjects with mild cognitive impairment (n = 1607), 766 of whom had bo

231 omprising AD patients (n = 8), patients with mild cognitive impairment (n = 17), and healthy controls

232 lzheimer's disease with dementia (n = 95) or mild cognitive impairment (n = 173), as well as in cogni

233 thers were clinically normal (n = 33) or had mild cognitive impairment (n = 38).

234 sease subjects into Parkinson's disease with mild cognitive impairment (n = 39) and Parkinson's disea

235 6 new subjects with brain tumors (n = 12) or mild cognitive impairment (n = 4) who underwent CT and P

236 anatomical differences between subjects with mild cognitive impairment (n = 530) and Alzheimer's dise

237 The cohort was followed to incident mild cognitive impairment (N=365) or censoring variables

238 d relative risk for functional limitation or mild cognitive impairment of 1.10 to 1.29 could offset t

239 human subjects and age-matched subjects with mild cognitive impairment or Alzheimer's disease (n=15 e

240 predicted phenoconversion to either amnestic mild cognitive impairment or Alzheimer's disease within

241 ere classified into those with conversion to mild cognitive impairment or dementia during the study (

242 >50 years: 1) cases with a firm diagnosis of mild cognitive impairment or dementia of any type or sev

243 al change in personality before the onset of mild cognitive impairment or dementia was identified.

244 diagnosis of cognitive impairment (combined mild cognitive impairment or dementia) at 2 years as out

245 ates of progression to clinically classified mild cognitive impairment or dementia, little research h

246 ontrolled trials of CCT in older adults with mild cognitive impairment or dementia.

247 personality traits occur before the onset of mild cognitive impairment or dementia.

248 rs (15 of 39 [38.5%]; P = .04) progressed to mild cognitive impairment or dementia.

249 ative pathology, resulting in mixed forms of mild cognitive impairment or dementia.

250 own about the efficacy of CCT in people with mild cognitive impairment or dementia.

251 ontrolled trials of CCT in older adults with mild cognitive impairment or dementia.

252 on from normal cognition to symptom onset of mild cognitive impairment or dementia: Paired Associates

253 and management options for older adults with mild cognitive impairment or early dementia and their ca

254 l individuals, and symptomatic patients with mild cognitive impairment or mild AD dementia.

255 ) in the diagnosis of patients with amnestic mild cognitive impairment or mild Alzheimer's disease (a

256 The study included 262 patients with mild cognitive impairment or subjective cognitive declin

257 h a clinical diagnosis of Alzheimer disease, mild cognitive impairment, or normal cognition underwent

258 malignant phenotype were more likely to have mild cognitive impairment, orthostatic hypotension, and

259 s recommended to screen patients with PD for mild cognitive impairment, orthostatic hypotension, and

260 's disease dementia (P < 0.001), progressive mild cognitive impairment (P < 0.001) and stable mild co

261 cognitive impairment (P < 0.001) and stable mild cognitive impairment (P < 0.05) compared with contr

262 disease dementia (P < 0.01) and progressive mild cognitive impairment (P < 0.05) compared with stabl

263 P = 2.06 x 10(-7)) and cognitively normal to mild cognitive impairment (P = 0.033).

264 We prospectively recruited a pool of 117 mild cognitive impairment patients (45 amnestic type and

265 phage polarization and improved cognition in mild cognitive impairment patients on omega-3 supplement

266 dies indicated greater tau binding in AD and mild cognitive impairment patients than in controls in a

267 found was based on orthostatic hypotension, mild cognitive impairment, rapid eye movement sleep beha

268 Nine subjects (5 with AD, 4 with mild cognitive impairment) received a 90-min dynamic (S)

269 een those with normal cognitive function and mild cognitive impairment regarding baseline health and

270 ariables of baseline health, the presence of mild cognitive impairment remained a significant predict

271 aseline, amyloid-beta positive patients with mild cognitive impairment showed increased hippocampal a

272 lyses revealed that Parkinson's disease with mild cognitive impairment shows more extensive atrophy a

273 ing Initiative cohort, including progressive mild cognitive impairment, stable MCI and Normal Control

274 and prognosis of Alzheimer's disease at the mild cognitive impairment stage according to these crite

275 of subjects with Alzheimer's disease at the mild cognitive impairment stage and progression to Alzhe

276 teria to identify Alzheimer's disease at the mild cognitive impairment stage.

277 VT was greater in mild cognitive impairment subjects than controls in the

278 clinically diagnosed Alzheimer's disease or mild cognitive impairment subjects.

279 mmation is increased relative to controls in mild cognitive impairment than it is for dementia, and t

280 and dentate gyrus subdivisions worsened with mild cognitive impairment that correlated with injury to

281 osis of Alzheimer's disease in subjects with mild cognitive impairment: the International Working Gro

282 APOE2 also reduced the risk of mild cognitive impairment to AD conversion by half.

283 curacy of 99%), and predicts conversion from mild cognitive impairment to Alzheimer's disease (maximu

284 ificant risk factor for conversion from both mild cognitive impairment to Alzheimer's disease (P = 2.

285 eimer's disease, and predict conversion from mild cognitive impairment to Alzheimer's disease and cog

286 G carriers were more likely to progress from mild cognitive impairment to Alzheimer's disease and exh

287 ease progression, from cognitively normal to mild cognitive impairment to Alzheimer's disease.

288 s we subsequently study the progression from mild cognitive impairment to dementia, demonstrating tha

289 es the full range of cognitive deficits from mild cognitive impairment to dementia.

290 ort cognitive test: the Test Your Memory for Mild Cognitive Impairment (TYM-MCI) in the diagnosis of

291 to Alzheimer's disease and those with stable mild cognitive impairment was also strong (average ratio

292 During 24569 person-years, mild cognitive impairment was diagnosed in 104 (5.1%) in

293 An increased incidence of mild cognitive impairment was observed in community-dwel

294 Patients with mild cognitive impairment were grouped into those that r

295 otal of 374 participants diagnosed as having mild cognitive impairment were included.

296 .+/-6.7, 55-87 years) with dementia prodrome mild cognitive impairment were recruited in the SMART (S

297 n postmortem brain tissue from subjects with mild cognitive impairment, when Abeta trimers are abunda

298 on in microglial activation in subjects with mild cognitive impairment, while subjects with Alzheimer

299 to Alzheimer's disease and those with stable mild cognitive impairment who had a follow-up time of at

300 normal individuals and 277 individuals with mild cognitive impairment) who completed intellectual li