ライフサイエンスコーパス: dement

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

2 ividuals, ranging from cognitively normal to 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 athology for comorbid AD, of whom 89.5% were demented.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

24 This same patient also became transiently demented and psychotic.

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

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

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

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

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

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

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

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

33 Demented cases also had significantly more Alzheimer neu

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

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

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

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

38 gnificant differences between mismatches and demented cases.

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

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

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

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

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

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

45 Several familial dementing conditions with atypical features have been ch

46 airments resemble those seen in degenerative dementing conditions.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

64 group of healthy subjects and patients with dementing diseases.

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

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

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

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

69 anisms involved in neurodegeneration in this dementing disorder.

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

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

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

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

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

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

76 correlation with neuropathologic evidence of dementing disorders.

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

78 and anterior temporal brain disease and for dementing disorders.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

104 eimer disease is a complex neurodegenerative dementing illness.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

122 Other dementing neurodegenerative disorders are also uncommon.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

150 34 amyloid-negative healthy controls and 20 demented patients with a high probability of Alzheimer's

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

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

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

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

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

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

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

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

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

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

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

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

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

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

165 and behavioral disturbances in nondepressed, demented patients.

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

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

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

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

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

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

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

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

174 e acute cognitive dysfunction in elderly and demented populations.

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

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

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

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

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

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

181 tive or other biologic pathways connected to dementing processes.

182 genetic influences on cognitive function and dementing processes.

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

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

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

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

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

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

189 1989 and 17 June 1993, we assessed OH in non-demented, stroke-free participants of the population-bas

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

191 Moderately demented subjects exhibited a range of disturbances of t

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

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

194 Mildly demented subjects had daily activity rhythms comparable

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

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

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

198 Demented subjects tended to exhibit marginally greater n

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

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

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

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

203 Cognition Examination scores in post-stroke demented subjects.

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

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

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

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

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

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

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

211 Demented women had higher mean serum sex hormone binding