ライフサイエンスコーパス: dement

1 act, 31% as cognitively impaired, and 33% as demented.

2 d in body mass index, and no participant was demented.

3 acrophages, not all patients with HIV become demented.

4 ad minor cognitive/motor disorder, and 1 was demented.

5 ior to death; 7 were demented and 8 were not demented.

6 tegories: Mild, moderate, very mild, and non-demented.

7 ividuals, ranging from cognitively normal to demented.

8 athology for comorbid AD, of whom 89.5% were demented.

9 as dementia (<7); cognitive impairment, not demented (7-11) 7<=Cogtot27<12; and normal (>=12)-was al

10 We have retested non-demented 80-year-olds who were participants in the Scott

11 rgic deficits are characteristic of severely demented AD patients, in this study, cholinergic deficit

12 Early identification of younger, non-demented adults at elevated risk for Alzheimer's disease

13 disease in a general population of older non-demented adults.

14 reveals that, in contrast to brains from non-demented age-matched individuals and control mice, the m

15 Participants were non-demented, aged 70 years or older, and community-dwelling

16 Twenty-eight non-demented ALS patients were compared with 18 healthy cont

17 athological analysis of 27 patients with non-demented ALS who had undergone cognitive testing (Edinbu

18 a valid predictor of TDP-43 pathology in non-demented ALS.

19 of cognitive impairment in patients with non-demented ALS.

20 with PET, is within normal limits in mildly demented Alzheimer patients but fails with worsening dem

21 d-beta plaques and tangles to those found in demented Alzheimer's cases without experiencing dementia

22 s of Alzheimer's changes ('mismatches'), and demented Alzheimer's cases.

23 Compared to controls, all non-demented Alzheimer's disease individuals had increased r

24 cerebral blood flow differences between non-demented amyloid-positive (n = 87) and amyloid-negative

25 mpared to diffuse plaques and plaques in non-demented, amyloid positive individuals (n = 5).

26 ed plaque, was observed in AD but not in non-demented, amyloid positive patients.

27 e cognitive impairment revealed in some non- demented amyotrophic lateral sclerosis (ALS) patients is

28 erformed diffusion tensor imaging (DTI) on 2 demented and 21 subjects at-risk for inheriting an FAD m

29 sing antemortem T1-weighted MRI scans of 423 demented and 361 control participants from National Alzh

30 Matching brain sections from 2 demented and 4 nondemented subjects were processed for t

31 ollowed prospectively prior to death; 7 were demented and 8 were not demented.

32 and in the glial response that discriminated demented and non-demented individuals with high loads of

33 no significant difference between brains of demented and nondemented patients.

34 Based on antemortem diagnoses, demented and nondemented subjects were examined together

35 This same patient also became transiently demented and psychotic.

36 ely normal, 97 mild cognitive impairment, 30 demented and seven unclassified); from Alzheimer's Disea

37 Participants were determined to be non-demented and without any medical or psychiatric conditio

38 ) individuals that were determined to be non-demented and without any medical or psychiatric conditio

39 atched for cognitive status (demented or non-demented) and age (+/- 3 years).

40 determined from the biomarker values of non-demented apparently healthy control (AHC) cases.

41 iduals aged 72 years and older, who were not demented at baseline, were followed longitudinally from

42 er's disease was strongest in those who were demented at time of blood draw (OR = 1.25, 95%CI = 1.02-

43 ion to a full-length (L) isoform in aged non-demented brains, we found a short isoform (S) lacking a

44 ong IDE isoform transcripts was found in non-demented brains.

45 As non-demented carriers approached the expected age of dementi

46 metabolism of the basal forebrain in 167 non-demented carriers of the Colombian PSEN1 E280A mutation

47 (CDR = 0; age, 51-88 years), 15 very mildly demented cases (CDR = 0.5), and 8 severely demented (CDR

48 Demented cases also had significantly more Alzheimer neu

49 s into the synaptic compartment was noted in demented cases compared with controls but not in mismatc

50 al geometry compared to demented cases; (ii) demented cases had significantly higher burdens of fibri

51 mpanying amyloid-beta and tau pathologies in demented cases was remarkably reduced in mismatches.

52 on obtained from male AD and age-matched non-demented cases were examined for amyloid plaques and Dkk

53 gnificant differences between mismatches and demented cases.

54 ptic markers and axonal geometry compared to demented cases; (ii) demented cases had significantly hi

55 y demented cases (CDR = 0.5), and 8 severely demented (CDR = 3) cases.

56 ased by >2-fold in subjects with post-stroke demented compared to post-stroke non-demented subjects (

57 ss and ventricular expansion were greater in demented compared with nondemented subjects.

58 important neurodevelopmental component to a dementing condition that has been predominantly consider

59 In contrast with more common dementing conditions that typically develop over years,

60 Several familial dementing conditions with atypical features have been ch

61 airments resemble those seen in degenerative dementing conditions.

62 ll autopsy or genetically confirmed; and non-demented control (AHC) patients N = 27.

63 noprecipitation of tau from human AD and non-demented control brains to identify novel interactions b

64 ssue, temporal neocortex of 27 AD and 21 non-demented control brains was examined to assess mRNA leve

65 ease, prodromal Alzheimer's disease, and non-demented control cases.

66 er's disease (termed sAD1, sAD2) and two non-demented control individuals into iPSC lines.

67 tients with Alzheimer's disease and five non-demented control subjects and found that synapse loss ar

68 ears (Braak V-VI) and 5 age-matched male non-demented control subjects were i) stained with a modifie

69 poradic Alzheimer's disease cases and 33 non-demented control subjects.

70 As compared to age-matched, non-demented 'control' brain tissues, highly significant inc

71 eimer's disease was elevated compared to non-demented controls (P < 0.0001).

72 neurodegenerative diseases, age-matched, non-demented controls and healthy younger individuals via im

73 ents with Alzheimer-type dementia and 14 non-demented controls matched for age and sex.

74 nts (P < 0.0001), and not different from non-demented controls.

75 zheimer's disease, and eight age-matched non-demented controls.

76 ated in human AD brains as compared with non-demented controls.

77 er's disease (AD) patients compared with non-demented controls.

78 nosis at different stages of the more common dementing diseases and in the assessment of disease prog

79 or comorbidities typical to several types of dementing diseases are usually not taken into account in

80 agnosed in only 9% of the patients and other dementing diseases were diagnosed in only 4% of the pati

81 group of healthy subjects and patients with dementing diseases.

82 syndrome) followed by a neuropsychiatric and dementing disorder owing to cerebral perivascular demyel

83 f neurodegeneration and synapse loss in this dementing disorder that is associated with oxidative str

84 ase (AD) is a complex and slowly progressing dementing disorder that results in neuronal and synaptic

85 hippocampus of subjects with AD or a related dementing disorder, dementia with Lewy bodies (DLB).

86 anisms involved in neurodegeneration in this dementing disorder.

87 quality of life of persons with this severe dementing disorder.

88 Alzheimer disease and other dementing disorders are major sources of morbidity and m

89 ome 17 (FTDP-17), a major class of inherited dementing disorders whose genetic basis is unknown.

90 strategies to delay onset or reduce risk for dementing disorders would be greatly beneficial.

91 thology is also central to a number of other dementing disorders, such as Pick's disease, progressive

92 g a neuropathologic diagnosis of AD or other dementing disorders, the mean (+/-SD) Clinical Dementia

93 arge-scale neurocognitive networks (NCNs) in dementing disorders.

94 or memory, which is a major component of the dementing disorders.

95 correlation with neuropathologic evidence of dementing disorders.

96 ocused on (18)F-FDG PET/MR neurodegenerative dementing disorders.

97 and anterior temporal brain disease and for dementing disorders.

98 f hyperphosphorylated tau in synaptosomes of demented dogs compared with nondemented dogs.

99 Most demented dogs displayed senile plaques, mainly in the fr

100 al dominant AD linked to PSEN1 mutations, in demented Down syndrome individuals and in sporadic AD su

101 ocampus and the amygdala were smaller in the demented Down's syndrome subjects than in their comparis

102 Of 180 patients, 52 (28.9%) became demented during a mean follow-up period of 3.6 +/- 2.2 y

103 A broader spectrum of non-demented elderly control subjects from previous studies

104 those with late-onset AD (LOAD), and in non-demented elderly controls.

105 the nucleus basalis of Meynert (NBM) of non-demented elderly humans.

106 ural integrity in the corpus callosum of non-demented elderly individuals, and this may partially exp

107 s targeting several lifestyle factors in non-demented elderly patients and moderately positive interi

108 Sixteen moderately to severely demented elderly patients with aggressive behavioral dis

109 ncognitive signs and symptoms of dementia in demented elderly patients.

110 Among non-demented elderly, amyloid load correlated with a topogra

111 t predicts conversion in iRBD to more severe/dementing forms of synucleinopathy.

112 levels to plaque density fully distinguished demented from nondemented patients, with no overlap betw

113 beta and plaque measures did not distinguish demented from nondemented patients.

114 te matter that would distinguish post-stroke demented from post-stroke non-demented subjects.

115 s (64% female; 89 mean age at death; 62% non-demented) from the Rush Memory and Aging Project complet

116 e values in a relatively large sample of non-demented, generally healthy adults (UK Biobank).

117 Within the moderately demented group, however, the degree of circadian disrupt

118 l deficits being most common amongst the non-demented group.

119 imer's disease (n = 33) relative to both non-demented groups, but no cerebral blood flow differences

120 n the brains of ADC patients compared to non-demented HIV patients.

121 Alzheimer's disease (AD) is a major dementing illness characterized by regional concentratio

122 burden of disease from cognitive decline and dementing illness is rising.

123 Alzheimer's disease (AD) is the most common dementing illness of the elderly and is a mounting publi

124 er's disease (AD) is the world's most common dementing illness, affecting over 150 million patients.

125 corticobasal degeneration, for example as a dementing illness, and the syndromes that look like it b

126 play an increasing role in the management of dementing illness.

127 eimer disease is a complex neurodegenerative dementing illness.

128 ure for what is perceived as the most common dementing illness: Alzheimer disease (AD).

129 s such as Alzheimer's disease (AD) and other dementing illnesses in humans.

130 the human brain in the course of age-related dementing illnesses may have appeared only recently duri

131 ed attention to cognition, especially to the dementing illnesses that occur in old age.

132 this new architectural feature in two common dementing illnesses, Alzheimer disease and dementia with

133 ose cognitive function ranges from intact to demented, including those with mild cognitive impairment

134 Judicial evaluations of criminality in the demented individual might require different criteria tha

135 edictor of progression to AD dementia in non-demented individuals (hazard ratio = 2.11).

136 y to result from poorer dietary habits among demented individuals (reverse causality) because meat co

137 ts of amyloid beta peptides in the brains of demented individuals are a defining feature of the disea

138 Furthermore, three non-demented individuals at risk of familial Alzheimer's dis

139 ee of substantial Alzheimer's pathology, non-demented individuals before death but whose post-mortem

140 d biochemical assessments on brains from non-demented individuals before death whose brains were free

141 ampal/medial temporal memory function in non-demented individuals depends on the presence of amyloid

142 and neuropathological assessment, and 75 non-demented individuals underwent brain amyloid imaging.

143 In order to avoid diagnosing non-demented individuals with Abeta abnormality, finding add

144 response that discriminated demented and non-demented individuals with high loads of Alzheimer's path

145 , single-centre cohort consisting of 277 non-demented individuals with SVD was conducted.

146 urofilament light were determined in 159 non-demented individuals, 123 patients with Alzheimer's dise

147 heimer neurofibrillary changes (Ch) from non-demented individuals, and controls (C) were labeled with

148 nt after testing additional affected and non-demented individuals.

149 mulation, brain atrophy and cognition in non-demented individuals.

150 This study employs the DEMENT model of microbial decomposition, along with empi

151 sm of the cholinergic basal forebrain in non-demented mutation carriers for autosomal dominant Alzhei

152 nitive impairment (MCI) due to AD, and a non-demented (ND) control group.

153 gic study performed to identify AD and other dementing neurodegenerative diseases in elderly patients

154 Seven other types of dementing neurodegenerative diseases were examined, and

155 Other dementing neurodegenerative disorders are also uncommon.

156 Alzheimer's disease (AD) includes a group of dementing neurodegenerative disorders that have diverse

157 PD subjects who did not become demented (non-PDD), compared with controls, had reduced

158 In this study, 780 non-demented older adults completed a battery of neuropsycho

159 ning and information processing speed in non-demented older adults from the CHARGE (Cohorts for Heart

160 predicted greater regional atrophy among non-demented older adults who were amyloid-negative.

161 burden with cognitive functioning in 47 non-demented older adults with type-2 diabetes from the Isra

162 ribute to lower cognitive functioning in non-demented older adults with type-2 diabetes, supporting a

163 dings show that among community-dwelling non-demented older adults, history of TBI is common but may

164 We aimed to investigate if non-demented older individuals with increased amyloid burden

165 of cognitive and clinical decline in 632 non-demented older individuals, even after controlling for A

166 gy is commonly observed in the brains of non-demented older individuals.

167 early to middle stages of their disease, not demented or depressed, and were tested 'on' dopaminergic

168 tors, who were matched for cognitive status (demented or non-demented) and age (+/- 3 years).

169 not statistically significant for either the demented or the nondemented subjects.

170 2-1.53), but an effect existed among the non-demented (OR = 1.05, 95% CI = 1.01-1.10).

171 Thirty-one non-demented Parkinson's disease patients (16 LPD, 15 RPD) a

172 roscopy ((31)P-MRS) was performed in 10 non- demented Parkinson's disease patients and nine age-match

173 right and P = 0.014 left cortex) for the non-demented Parkinson's disease patients compared with cont

174 etal cortical hypometabolism was seen in non-demented Parkinson's disease patients with both (31)P-MR

175 ortical and subcortical volume occurs in non-demented Parkinson's disease, our longitudinal analyses

176 les and clinical data obtained from 4444 non-demented participants in the Rotterdam study at baseline

177 population-based cohort included 43,1834 non-demented participants with spirometry from the UK Bioban

178 (beta = -0.31, P = 0.007), including in non-demented patients (beta = -0.28, P = 0.05).

179 Ten non-demented patients (eight females/two males; age 73.9 +/-

180 ed long-term global cognitive decline in non-demented patients [F(1, 110) = 9.72, P = 0.002], remarka

181 es of amyloid senile plaques in the brain of demented patients and patients with early memory symptom

182 Alternative options for feeding elderly demented patients are available for family members consi

183 acrostructural and microstructural damage in demented patients compared with controls.

184 xpression reflects pain as well or better in demented patients compared with normals.

185 ve performance and the social functioning of demented patients for 6 months to 1 year.

186 Concerns have existed about whether demented patients produce diagnostically meaningful faci

187 suscitate goals, decreased the time terminal demented patients remained in the intensive care unit, a

188 considered, and we believe that for severely demented patients the practice should be discouraged on

189 34 amyloid-negative healthy controls and 20 demented patients with a high probability of Alzheimer's

190 heterogeneity of cognitive impairment in non-demented patients with ALS.

191 Seventeen non-demented patients with clinically definite or probable A

192 al decline and conversion to dementia in non-demented patients with cognitive symptoms.

193 Many non-demented patients with PD have cognitive impairment espe

194 Our study included 70 non-demented patients with probable CAA, 70 age-matched heal

195 eighted magnetic resonance imaging in 38 non-demented patients with probable cerebral amyloid angiopa

196 sk related to the APOE epsilon4 allele among demented patients with stroke was 41% overall, 33% among

197 arkinson's disease, we hypothesized that non-demented patients with this illness would show blunted r

198 However, Abeta oligomer concentrations in demented patients' lysates were tightly correlated with

199 al decline and conversion to dementia in non-demented patients, and may support AD diagnosis in clini

200 mplementary DNA, brain biopsy specimens from demented patients, and postmortem samples of frontal neo

201 DG studies detect metabolic abnormalities in demented patients, but with limited specificity.

202 of daily living, which occur in even mildly demented patients, may be related to attentional deficit

203 In the mildly demented patients, rCMRglc responses were within 2 SDs o

204 ate the importance of extending the study to demented patients.

205 anagement of sleep patterns in home-dwelling demented patients.

206 d reached nearly 50% among the most severely demented patients.

207 ficantly lowered CSF levels of A beta in non-demented patients.

208 and behavioral disturbances in nondepressed, demented patients.

209 orrelated with each other and were higher in demented patients.

210 ectable CSF MIP-1alpha, levels were lower in demented patients.

211 r shape is observed in human cerebellum from demented patients.

212 ropathological diagnosis was observed in the demented patients: 71% had more than one pathology, but

213 ergic and cholinergic function is present in demented PD and, on occasion, amyloid deposits can be de

214 The vast majority of demented PD patients show widespread neurofibrillary tan

215 d only in parietal and occipital cortex, but demented PD subjects had extensive cortical binding decr

216 Six subjects became demented (PDD), with a mean time of 3.8 +/- 1.7 y (range

217 ission tomography was carried out in 101 non-demented people with Parkinson's (76.24% male, mean age

218 We excluded actively psychotic or demented people, those with both suicidal ideation and c

219 Participants were 420 non-demented persons from the Memory and Aging Project, a lo

220 ess the risk of developing dementia in a non-demented population.

221 e acute cognitive dysfunction in elderly and demented populations.

222 isease, the neural mechanisms underlying the dementing process and its associated cognitive deficits

223 gement may already have been modified by the dementing process and may be associated with prodromal d

224 Our work suggests that the dementing process in Parkinson's disease is predictable

225 nction in early PD and demonstrates that the dementing process in this illness is heralded by both po

226 th childhood-onset schizophrenia is due to a dementing process or simply failure to acquire new infor

227 gy is a downstream but essential part of the dementing process.

228 tive or other biologic pathways connected to dementing processes.

229 genetic influences on cognitive function and dementing processes.

230 using the Staff Experiences of Working with Demented Residents questionnaire (SEWDR) and perceived c

231 genotypes were 5 times more likely to become demented (RR = 4.7; 95% CI = 1.2, 17.9).

232 sk of placement for patients who were mildly demented (RR, 0.18; 95% CI, 0.04 to 0.77) or moderately

233 R, 0.18; 95% CI, 0.04 to 0.77) or moderately demented (RR, 0.38; 95% CI, 0.17 to 0.82).

234 atter hyperintensities in an independent non-demented sample).

235 ngs suggested that remarkably >/= 75% of the demented stroke survivors met the current criteria for v

236 1989 and 17 June 1993, we assessed OH in non-demented, stroke-free participants of the population-bas

237 study to date investigating LOAD-PGR and non-demented structural brain MRI and cognition phenotypes.

238 -stroke demented compared to post-stroke non-demented subjects (P = 0.026) and by 11-fold in older co

239 Moderately demented subjects exhibited a range of disturbances of t

240 d an AUROC of 0.75 for discriminating future demented subjects from all other subjects (including dec

241 ve (AUROC) of 0.81 for discriminating future demented subjects from subjects alive and nondemented 10

242 Mildly demented subjects had daily activity rhythms comparable

243 levels tended to be higher in the moderately demented subjects in the afternoon, but this effect was

244 ic inflammation in a community sample of non-demented subjects older than seventy years of age are as

245 We evaluated non-demented subjects over age 50 years in the Mayo Clinic S

246 In contrast, brains from age-matched, non-demented subjects showed only occasional staining for Zn

247 Demented subjects tended to exhibit marginally greater n

248 Fifty-nine non-demented subjects were assessed annually with the Dement

249 In a multivariate analysis, demented subjects were more likely to have detectable CS

250 One hundred and five non-demented subjects with newly diagnosed idiopathic Parkin

251 In this population-based study of non-demented subjects, most of the associations between biom

252 roblem compared with 13% among more severely demented subjects.

253 post-stroke demented versus post-stroke non-demented subjects.

254 Cognition Examination scores in post-stroke demented subjects.

255 sh post-stroke demented from post-stroke non-demented subjects.

256 y and Lewy bodies and microinfarcts than non-demented survivors.

257 ex and cognitive function in 88 healthy, non-demented, unmedicated men aged 65-70 years.

258 white matter were not greater in post-stroke demented versus post-stroke non-demented subjects.

259 he same extent of neuropathology, one may be demented while the other remains cognitively intact.

260 mer's disease (AD), which we refer to as Non-Demented with Alzheimer's disease Neuropathology (NDAN).

261 Demented women had higher mean serum sex hormone binding