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1 ild Alzheimer's disease, 14 amyloid-positive mild cognitive impairment).
2 7%] were clinically normal and 537 [13%] had mild cognitive impairment).
3 articipants per arm in amyloid-beta-positive mild cognitive impairment).
4 rom a risk model developed for patients with mild cognitive impairment.
5 wareness and incident Alzheimer dementia and mild cognitive impairment.
6 nt of LLD participants met ADNI criteria for mild cognitive impairment.
7 phagocytosis by macrophages of patients with mild cognitive impairment.
8 an ND group that included participants with mild cognitive impairment.
9 ral cognitive function for older adults with mild cognitive impairment.
10 and psychosocial functioning in people with mild cognitive impairment.
11 ths, such as hippocampal subfield atrophy in mild cognitive impairment.
12 on spatially overlapped in the subjects with mild cognitive impairment.
13 grape juice are not exclusive to adults with mild cognitive impairment.
14 the preclinical stage, prior to the onset of mild cognitive impairment.
15 als with Alzheimer disease (AD) dementia and mild cognitive impairment.
16 depth in people with Alzheimer's Disease and Mild Cognitive Impairment.
17 impaired, and Ptau positive individuals with mild cognitive impairment.
18 ies, including hypertension, depression, and mild cognitive impairment.
19 paired (0.4 +/- 2.7%), amyloid-beta-negative mild cognitive impairment (-0.4 +/- 2.3%) or amyloid-bet
20 BP control significantly reduced the risk of mild cognitive impairment (14.6 vs 18.3 cases per 1000 p
22 imer's pathology (including amyloid-positive mild cognitive impairment), 19 patients with progressive
23 11 healthy controls, 223 patients with early mild cognitive impairment, 204 with late mild cognitive
25 signal was observed in amyloid-beta-positive mild cognitive impairment (3.0 +/- 5.3%) and Alzheimer's
27 mpaired individuals and 204 individuals with mild cognitive impairment (320 [53%] were female) were c
28 , 21% had normal cognitive function, 17% had mild cognitive impairment, 33% had moderate impairment,
29 and late-life hypotension had higher risk of mild cognitive impairment (37 affected individuals (odds
30 ulation norms, 37.2% of the participants had mild cognitive impairment, 43.7% had major cognitive imp
33 omparison with a matched archival dataset of mild cognitive impairment/Alzheimer's disease patients s
34 sonance imaging in 25 patients with amnestic mild cognitive impairment (aMCI) and 23 matched healthy
39 e longitudinal study of people with amnestic mild cognitive impairment (aMCI) we assessed three param
40 jects, including 10 probable AD, 15 amnestic mild cognitive impairment (aMCI), and 10 cognitively hea
42 nd the impaired group by clinical phenotype (mild cognitive impairment, amnestic dementia, and non-am
43 tively normal (n = 42), clinically-diagnosed mild cognitive impairment (amyloid positive, n = 47, and
44 Alzheimer's disease (AD), non-AD dementia or mild cognitive impairment and 20 age-matched and sex-mat
45 ively normal subjects, 97 clinically defined mild cognitive impairment and 48 possible or probable Al
46 d with Alzheimer's disease (n = 50 with late mild cognitive impairment and 71 with Alzheimer's dement
47 dary cognitive outcomes included adjudicated mild cognitive impairment and a composite outcome of mil
48 cortical (18)F T807 binding in patients with mild cognitive impairment and AD dementia compared to cl
49 omal F-actin levels in postmortem brain from mild cognitive impairment and AD patients compared with
50 ver, our findings propose a new way to fight mild cognitive impairment and aging-related cognitive de
51 etected AHN in aged adults and patients with mild cognitive impairment and Alzheimer's disease (AD),
52 commentary on this article.Individuals with mild cognitive impairment and Alzheimer's disease clinic
53 itudinal changes in microglial activation in mild cognitive impairment and Alzheimer's disease subjec
54 l) and was significantly elevated for Abeta+ mild cognitive impairment and Alzheimer's disease subjec
55 gorization of neuroanatomical alterations in mild cognitive impairment and Alzheimer's disease that c
56 tsburgh compound B was high in subjects with mild cognitive impairment and Alzheimer's disease, while
58 o pure LATE-NC and one pure ADNC) donors had mild cognitive impairment and another two donors with LA
60 erfusion has previously been associated with mild cognitive impairment and dementia in various cross-
61 ical data provide evidence that the risk for mild cognitive impairment and dementia is increased in i
67 myloid imaging specifically in subjects with mild cognitive impairment and in comparison with or in c
69 miologic data supporting previous studies on mild cognitive impairment and progression to AD are revi
70 wn to improve memory function in adults with mild cognitive impairment and reduce blood pressure in h
73 's dementia and n = 14 with amyloid-positive mild cognitive impairment) and 29 healthy control subjec
74 o completed the study (5 healthy controls, 6 mild cognitive impairment, and 10 AD) received 370 MBq o
77 nitively healthy controls, 197 patients with mild cognitive impairment, and 180 patients with AD with
78 er's disease (AD) patients, 40 subjects with mild cognitive impairment, and 40 controls with subjecti
79 nitively normal, 5 old cognitively normal, 5 mild cognitive impairment, and 5 Alzheimer disease (AD).
80 teral ventricular SUVR across the Alzheimer, mild cognitive impairment, and healthy control groups (P
81 ognitively normal controls, individuals with mild cognitive impairment, and individuals with AD to as
82 lthy control participants, participants with mild cognitive impairment, and participants with AD deme
83 d at baseline and follow-up in subjects with mild cognitive impairment, and this was compared with su
84 th a history of idiopathic falls, those with mild cognitive impairment, and those with Parkinson's di
85 number of DCX(+)PCNA(+) cells is reduced in mild cognitive impairments, and higher numbers of neurob
86 risk predictions of dementia in people with mild cognitive impairment are highly relevant for care p
87 fic commentary on this article.Subjects with mild cognitive impairment associated with cortical amylo
88 r's Coordinating Center on participants with mild cognitive impairment at baseline and either no neur
89 igation task can differentiate patients with mild cognitive impairment at low and high risk of develo
91 participants with a global CDR of 0.5 (i.e. mild cognitive impairment) at baseline, 126 with primary
92 ent represents a major challenge in PD, with mild cognitive impairment being a prodromal stage of PD
93 sure significantly reduced the occurrence of mild cognitive impairment, but not probable dementia.
94 ending Alzheimer dementia and its precursor, mild cognitive impairment, but prior studies have not sy
97 Twenty-two (85%) of the 26 amyloid-positive mild cognitive impairment cases showed clusters of incre
98 flammation in a majority of amyloid positive mild cognitive impairment cases, its cortical distributi
101 e and follow-up microglial activation in the mild cognitive impairment cohort compared to controls we
102 reduction of 18% in microglial activation in mild cognitive impairment cohort over 14 months, which w
104 renia, bipolar disorder, multiple sclerosis, mild cognitive impairment, dementia, and Parkinson's dis
105 re characterized as cognitively stable (CS), mild cognitive impairment-DS (MCI-DS), possible AD demen
106 d precursor protein (hAPP) and patients with mild cognitive impairment due to Alzheimer's disease (MC
107 yloid-positive patients meeting criteria for mild cognitive impairment due to Alzheimer's disease (n
108 for probable Alzheimer's disease dementia or mild cognitive impairment due to Alzheimer's disease, pr
109 ore biomarkers were strongly associated with mild cognitive impairment due to Alzheimer's disease.
110 (4 controls, 3 with a history of TBI, 2 with mild cognitive impairment due to suspected Alzheimer dis
111 (4 controls, 3 with a history of TBI, 2 with mild cognitive impairment due to suspected Alzheimer dis
112 f locus coeruleus dysfunction reminiscent of mild cognitive impairment/early Alzheimer's disease.
116 l diagnostic groups: cognitively unimpaired, mild cognitive impairment, frontotemporal dementia, prob
117 s glucose for energy, but in AD and amnestic mild cognitive impairment glucose metabolism is dramatic
118 were the most severe impaired domains in the mild cognitive impairment group, attention and visuospat
119 vanced clinical stage (Alzheimer's disease > mild cognitive impairment > older cognitively normal) an
120 re also associated with an increased risk of mild cognitive impairment (hazard ratio, 2.9; 95% CI, 1.
121 (HR = 3.03), olfactory deficit (HR = 2.62), mild cognitive impairment (HR = 1.91-2.37), erectile dys
122 was also associated with increased risk for mild cognitive impairment (HR, 1.47 [CI, 1.20 to 1.81];
123 decline: hazard ratio [HR] = 0.57, p < 0.05; mild cognitive impairment: HR = 0.19, p < .01), indicati
125 nimpaired participants and 100 patients with mild cognitive impairment in the Swedish BioFINDER study
126 Clinical factors associated with baseline mild cognitive impairment included age, male gender, str
127 Initiative (17 with AD dementia and 199 with mild cognitive impairment), including (18)F-florbetapir
128 sought to determine whether the presence of mild cognitive impairment independently increases the ri
129 is could reflect that activated microglia in mild cognitive impairment initially may adopt a protecti
130 between ST6GAL1 mutations and conversion of mild cognitive impairment into clinical Alzheimer's dise
131 healthy people and patients exhibiting late mild cognitive impairment leading to Alzheimer disease.
134 ing early-stage Alzheimer's disease (AD) and mild cognitive impairment (MCI of the Alzheimer's type).
135 301) and clinically diagnosed patients with mild cognitive impairment (MCI) (n = 178), AD dementia (
136 hy controls (HC), 33 patients with diagnosed mild cognitive impairment (MCI) and 30 patients with Alz
137 DNI), including cognitively unimpaired (CU), mild cognitive impairment (MCI) and AD dementia patients
138 d choroid plexus tissue samples and CSF from mild cognitive impairment (MCI) and AD patients to analy
141 plays a crucial role in the pathogenesis of mild cognitive impairment (MCI) and Alzheimer's disease
143 g the cognitive performance in patients with mild cognitive impairment (MCI) and Alzheimer's disease
144 clinically classified healthy controls (HC), mild cognitive impairment (MCI) and Alzheimer's particip
145 an men, and the sex-dependent association of mild cognitive impairment (MCI) and APOE has not been es
146 t study was conducted among individuals with mild cognitive impairment (MCI) and cognitively normal i
147 al tau level, cognitive decline, and risk of mild cognitive impairment (MCI) and dementia; (2) whethe
148 in patients with Parkinson disease (PD) and mild cognitive impairment (MCI) and in patients with PD
149 Depression is common in individuals with mild cognitive impairment (MCI) and may confer a higher
150 lar risk factors with the risk of developing mild cognitive impairment (MCI) and MCI progression to d
151 of patients with Alzheimer disease (AD) and mild cognitive impairment (MCI) and subjects with subjec
152 is) of patients with Alzheimer's disease and mild cognitive impairment (MCI) are defective in amyloid
154 s with subjective cognitive decline (SCD) or mild cognitive impairment (MCI) can serve to predict pro
156 ) on brain atrophy and cognitive function in mild cognitive impairment (MCI) due to Alzheimer's disea
157 ngs make liberal use of the descriptive term mild cognitive impairment (MCI) for those with cognitive
158 his modelling study, we included people with mild cognitive impairment (MCI) from single-centre and m
159 2) discriminates patients with diabetes with mild cognitive impairment (MCI) from those with normal c
160 es and biomarker data from 562 subjects with mild cognitive impairment (MCI) from two national studie
163 Associations of sleep characteristics with mild cognitive impairment (MCI) have been examined in cr
164 nsion treatment on incidence of dementia and mild cognitive impairment (MCI) in 9361 participants in
165 AD polygenic risk score (PRS) could identify mild cognitive impairment (MCI) in adults who were only
166 olipoprotein E epsilon4 (APOE-e4) allele and mild cognitive impairment (MCI) in elderly subjects.
170 tem of patients with Alzheimer's disease and mild cognitive impairment (MCI) is deregulated with high
171 e-onset Alzheimer disease (LOAD) preceded by mild cognitive impairment (MCI) is the most common type
173 es ranging from normal aging to AD-including mild cognitive impairment (MCI) not converting or conver
175 increase the opportunity to delay or prevent mild cognitive impairment (MCI) or Alzheimer disease (AD
176 ting activities and decreased odds of having mild cognitive impairment (MCI) or Alzheimer disease hav
177 eveloped risk estimates for the incidence of mild cognitive impairment (MCI) or dementia among cognit
178 west tertile were more likely to progress to mild cognitive impairment (MCI) or dementia in Cox propo
180 oE4(+/-) patients with clinical diagnosis of mild cognitive impairment (MCI) or early AD when compare
181 ealthy control participants, and a cohort of mild cognitive impairment (MCI) patients with four-year
182 n differences between healthy controls (HC), mild cognitive impairment (MCI) patients, and AD patient
184 sease (AD) continuum, the prodromal state of mild cognitive impairment (MCI) precedes AD dementia and
186 dent discovery [cognitively normal (CN), 19; mild cognitive impairment (MCI) risk, 43; MCI, 6] and re
187 miRNAs in serum samples from AD patients and Mild cognitive impairment (MCI) subjects relative to hea
188 : To optimize prediction of progression from mild cognitive impairment (MCI) to AD dementia by combin
189 (18)F-FDG PET for predicting conversion from mild cognitive impairment (MCI) to Alzheimer dementia (A
190 id deposition related to the conversion from mild cognitive impairment (MCI) to Alzheimer disease (AD
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 (
195 with SCeVD (n = 22), preclinical AD (pAD) + mild cognitive impairment (MCI) without SCeVD (pAD/MCI w
197 ulation method during sleep in patients with mild cognitive impairment (MCI), a precursor of AD, and
198 this cross-sectional study, 14 patients with mild cognitive impairment (MCI), a prodromal stage to de
199 ly unimpaired participants and patients with mild cognitive impairment (MCI), AD dementia and non-AD
200 nts with subjective cognitive decline (SCD), mild cognitive impairment (MCI), Alzheimer's disease (AD
201 ts (mean age 63-69 years), participants with mild cognitive impairment (MCI), Alzheimer's disease, an
202 nitively healthy controls, 197 patients with mild cognitive impairment (MCI), and 180 patients with A
203 udy included 83 cognitively normal (CN), 160 mild cognitive impairment (MCI), and 73 AD subjects who
204 dy, we tested the prediction accuracy of AD, mild cognitive impairment (MCI), and amyloid deposition
205 ry plexus (SCP) in Alzheimer's disease (AD), mild cognitive impairment (MCI), and cognitively intact
206 RI with hippocampal subfield analysis of AD, mild cognitive impairment (MCI), and healthy subjects.
207 ascular dementia (VD), senile dementia (SD), mild cognitive impairment (MCI), and other neurodegenera
208 ch of four groups: Alzheimer's disease (AD), mild cognitive impairment (MCI), FCD and healthy control
209 subset of CN participants who progressed to mild cognitive impairment (MCI), heightened memory aware
210 tions to prevent or delay cognitive decline, mild cognitive impairment (MCI), or dementia are uncerta
211 tment to prevent or delay cognitive decline, mild cognitive impairment (MCI), or dementia is uncertai
212 from individuals with Alzheimer's dementia, Mild Cognitive Impairment (MCI), or no cognitive impairm
213 (MR) spectroscopic imaging in subjects with mild cognitive impairment (MCI), patients with Parkinson
214 n epsilon4 non-carriers diagnosed with AD or mild cognitive impairment (MCI), SNPs within the BACE2 l
215 pulation) of both dementia and its prodrome, mild cognitive impairment (MCI), which are characterized
226 cipants (42 with dementia due to AD; 65 with mild cognitive impairment (MCI); 95 control participants
227 e clinical BDNF data in patients with AD and mild cognitive impairment (MCI, a prodromal stage of AD)
228 er disease (AD; n = 300), memory-predominant mild cognitive impairment (MCI; n = 75), or neurological
229 %; 73.8 [8.5] years) and 55 individuals with mild cognitive impairment (MCI; women, 38%; 76.9 [7.3] y
230 = 70; subjective cognitive concerns: n = 74; mild cognitive impairment [MCI]: n = 29, AD dementia: n
232 ognitively normal subjects, 95 subjects with mild cognitive impairment (Mini-Mental State Examination
233 s and 767 cognitively impaired participants (mild cognitive impairment n = 420, Alzheimer's disease d
234 ively unimpaired (n = 153), or patients with mild cognitive impairment (n = 139) or Alzheimer's disea
235 individuals with normal cognition (n = 180), mild cognitive impairment (n = 148), or AD dementia (n =
236 omprising AD patients (n = 8), patients with mild cognitive impairment (n = 17), and healthy controls
237 Lewy bodies (n = 1), Parkinson disease with mild cognitive impairment (n = 2), corticobasal syndrome
238 anatomical differences between subjects with mild cognitive impairment (n = 530) and Alzheimer's dise
239 n = 62) and prodromal (amyloid-beta-positive mild cognitive impairment, n = 49) Alzheimer's disease h
240 (22 years before the estimated median age at mild cognitive impairment onset of 44 years), although t
241 ) and 20 amyloid-beta-positive patients with mild cognitive impairment or Alzheimer's disease dementi
242 4 clinical variables from 1909 patients with Mild Cognitive Impairment or Alzheimer's Disease to trai
243 onship with age, beta-amyloid pathology, and mild cognitive impairment or clinical AD diagnostic stat
244 ere classified into those with conversion to mild cognitive impairment or dementia during the study (
245 al change in personality before the onset of mild cognitive impairment or dementia was identified.
246 a combined group of participants with either mild cognitive impairment or dementia with Alzheimer's c
247 diagnosis of cognitive impairment (combined mild cognitive impairment or dementia) at 2 years as out
253 on from normal cognition to symptom onset of mild cognitive impairment or dementia: Paired Associates
254 e conducted (11)C-UCB-J PET on patients with mild cognitive impairment or early Alzheimer disease (AD
256 ) in the diagnosis of patients with amnestic mild cognitive impairment or mild Alzheimer's disease (a
257 95% CI, 0.69-0.95) and the combined rate of mild cognitive impairment or probable dementia (20.2 vs
261 e final diagnosis of Alzheimer disease (AD), mild cognitive impairment, or neither at fluorine 18 ((1
262 h a clinical diagnosis of Alzheimer disease, mild cognitive impairment, or normal cognition underwent
263 We prospectively recruited a pool of 117 mild cognitive impairment patients (45 amnestic type and
264 ed effects models) and amyloid-beta-negative mild cognitive impairment patients (beta = 0.67, P < 0.0
265 ) had accelerated p-tau217 compared to other mild cognitive impairment patients (beta = 0.79, P < 0.0
266 phage polarization and improved cognition in mild cognitive impairment patients on omega-3 supplement
267 dies indicated greater tau binding in AD and mild cognitive impairment patients than in controls in a
270 een those with normal cognitive function and mild cognitive impairment regarding baseline health and
271 ariables of baseline health, the presence of mild cognitive impairment remained a significant predict
274 ing Initiative cohort, including progressive mild cognitive impairment, stable MCI and Normal Control
276 l HE subjects, 4 AD subjects, and 2 amnestic mild cognitive impairment subjects after a bolus injecti
279 ween groups of Alzheimer's disease patients, mild cognitive impairment subjects, and normal controls.
282 mmation is increased relative to controls in mild cognitive impairment than it is for dementia, and t
284 ), followed by those modelling prediction of mild cognitive impairment to Alzheimer's disease (n=15),
285 s we subsequently study the progression from mild cognitive impairment to dementia, demonstrating tha
287 ort cognitive test: the Test Your Memory for Mild Cognitive Impairment (TYM-MCI) in the diagnosis of
288 eimer's disease kindred, who did not develop mild cognitive impairment until her seventies, three dec
290 mer disease (AD), and subjects with amnestic mild cognitive impairment were characterized in a study
291 estionnaire, incident Alzheimer dementia and mild cognitive impairment were documented in detailed an
292 .+/-6.7, 55-87 years) with dementia prodrome mild cognitive impairment were recruited in the SMART (S
293 n postmortem brain tissue from subjects with mild cognitive impairment, when Abeta trimers are abunda
294 on in microglial activation in subjects with mild cognitive impairment, while subjects with Alzheimer
295 a-negative participants, or in patients with mild cognitive impairment who did not convert to Alzheim
296 to Alzheimer's disease and those with stable mild cognitive impairment who had a follow-up time of at
297 that Abeta34 is elevated in individuals with mild cognitive impairment who later progressed to dement
298 controls, but also between individuals with Mild Cognitive Impairment who were later diagnosed with
299 s) with clinical diagnosis of probable AD or mild cognitive impairment with positive PET biomarker fo
300 hout a loss of muscle mass) in patients with mild cognitive impairment, with progression of cognitive