ライフサイエンスコーパス: clinical dementia rating

1 e modified frontotemporal lobar degeneration clinical dementia rating.

2 eimer's Disease score, Braak stage score and clinical dementia rating.

3 te Examination and faster progression on the Clinical Dementia Ratings.

4 al CAMCOG, orientation and memory scores and clinical dementia ratings.

5 AD (DLB+AD n=23) and pure AD (n=89) who had Clinical Dementia Rating 0, 0.5 or 1 at their first visi

6 entia rating <1, n = 20) and presymptomatic (clinical dementia rating = 0, n = 15) stages of the dise

7 mong 207 older adults with normal cognition (Clinical Dementia Rating, 0).

8 .5; n = 69) and clinically manifest AD (AD; Clinical Dementia Rating = 1; n = 28).

9 211) as well as patients with very mild AD (Clinical Dementia Rating = .5; n = 69) and clinically ma

10 istructured assessments in order to assign a Clinical Dementia Rating and determine whether psychosis

11 period (average = 3.1 years), scores on the Clinical Dementia Rating and Global Deterioration Scale

12 followed over 6 years and assessed with the Clinical Dementia Rating and the Mini-Mental State Exami

13 There was no correlation between clinical dementia ratings and reduction of contrast sens

14 wer of attorney (96% scored 2 or less on the Clinical Dementia Rating, and 92% scored 5 or less on th

15 imaging Initiative (ADNI) and relying on the Clinical Dementia Rating as group-defining instrument, w

16 that ranged in AD severity from unaffected [clinical dementia rating (CDR) 0] to very mild (CDR 0.5)

17 ognitive function was investigated using the Clinical Dementia Rating (CDR) and the Informant Questio

18 0 individuals characterized according to the Clinical Dementia Rating (CDR) as cognitively unimpaired

19 omization, but 219 did not complete 18-month clinical dementia rating (CDR) assessments and thus were

20 Age, gender, Clinical Dementia Rating (CDR) Dementia Staging Instrume

21 timated years to symptom onset and who had a Clinical Dementia Rating (CDR) global score of 0 (cognit

22 der, lived independently, and had a baseline Clinical Dementia Rating (CDR) global score of 0.5 or le

23 The Clinical Dementia Rating (CDR) is a well-validated instr

24 on of CSF APOE with CSF Abeta(42) levels and clinical dementia rating (CDR) is not because of a rever

25 A total of 107 cases with a Clinical Dementia Rating (CDR) of > or = 1 met criteria

26 cteristic analyses in the PiB- sample with a clinical dementia rating (CDR) of 0.

27 ule that could be used as an addition to the Clinical Dementia Rating (CDR) plus National Alzheimer's

28 FDG hypometabolism was associated with worse Clinical Dementia Rating (CDR) plus National Alzheimer's

29 Secondary endpoints were Clinical Dementia Rating (CDR) plus National Alzheimer's

30 sed morphometry for image postprocessing and Clinical Dementia Rating (CDR) scale for cognitive asses

31 n of 7 years and assessed each time with the Clinical Dementia Rating (CDR) scale.

32 We studied 20 individuals who at death had a Clinical Dementia Rating (CDR) score of 0 (cognitively n

33 Twenty-seven patients had a clinical dementia rating (CDR) score of 0.5 (very mild d

34 In 109 subjects, the Clinical Dementia Rating (CDR) score was highly correlat

35 In this study clinical dementia rating (CDR) scores were used as a mea

36 s stages of clinical severity, as defined by clinical dementia rating (CDR) scores.

37 The two most commonly used measures, the Clinical Dementia Rating (CDR)+National Alzheimer's Dise

38 cognitive status had been assessed with the Clinical Dementia Rating (CDR), including 39 nondemented

39 d CR1 expression levels were associated with clinical dementia rating (CDR), with higher expression b

40 sociations with cognitive impairment (global Clinical Dementia Rating [CDR] >= 0.5) and rates of decl

41 lder adults who were cognitively normal (ie, Clinical Dementia Rating [CDR] global score of 0) at bas

42 part of a cohort study, cognitively normal (Clinical Dementia Rating [CDR] of 0) middle-aged researc

43 rticipants who were cognitively normal (CN) (Clinical Dementia Rating [CDR] score, 0) or had AD demen

44 ars from participants who were asymptomatic (Clinical Dementia Rating [CDR]=0) and annually for those

45 from patients with autopsy-confirmed AD and clinical dementia ratings (CDRs) before death.

46 al traits (CERAD score, Braak staging score, Clinical Dementia Rating, cognitive function and clinica

47 i-Mental State Examination scores and higher Clinical Dementia Ratings compared to amyloid-beta negat

48 ences at initial NACC visit were examined on Clinical Dementia Rating Dementia Staging Instrument plu

49 The digital Electronic Clinical Dementia Rating (eCDR) can be remotely self-adm

50 d in a group of 10 mildly affected patients (clinical dementia rating equal to 0) using voxel-based m

51 Two global measures, the FTLD-modified Clinical Dementia Rating (FTLD-modified CDR) and the Cli

52 c Alzheimer's disease patients with the same Clinical Dementia Rating global score (mean UPDRS-III sc

53 Mutation carriers with a Clinical Dementia Rating global score of 2 exhibited mor

54 The main outcome measures were the Clinical Dementia Rating, Global Deterioration Scale for

55 riteria for early Alzheimer's disease with a Clinical Dementia Rating-Global Score of 0.5, a Mini-Men

56 ession to cognitive impairment measured by a Clinical Dementia Rating greater than 0.

57 rkers, 34.4% developed cognitive impairment (Clinical Dementia Rating > 0) as compared to 8.4% of tho

58 Symptomatic individuals (Clinical Dementia Rating > 0) demonstrated markedly incr

59 om amyloid onset to impairment onset (global clinical dementia rating >=1) in a subset of 595 ADNI pa

60 arriers and non-carriers in the preclinical (clinical dementia rating <1, n = 20) and presymptomatic

61 at baseline, cognitively normal at baseline (Clinical Dementia Rating of 0 and no impairment based on

62 the Mini-Mental State Examination, and had a Clinical Dementia Rating of 0 for the Anti-Amyloid Treat

63 icipants meeting criteria for PPA and with a Clinical Dementia Rating of 0 to 1 (in which scores rang

64 an, had APOE genotype information, and had a Clinical Dementia Rating of 0.

65 s, 557 amyloid-positive, cognitively normal (Clinical Dementia Rating of 0; aged 60-85 years) partici

66 ily living, or severe dementia (defined as a Clinical Dementia Rating of 3).

67 e more likely to receive lower scores on the Clinical Dementia Rating (P = .003).

68 <0.0001), despite similar progression on the clinical dementia rating (p>0.7), and CSF Abeta42 levels

69 ded 230 cognitively normal older adults (CN; Clinical Dementia Rating R [CDR] = 0) and 16 older adult

70 Participants underwent assessments with the Clinical Dementia Rating(R) (CDR(R)), neuropsychological

71 Disease progression was measured using Clinical Dementia Rating(R) Sum-of-Box scores.

72 nitive status was assessed longitudinally by Clinical Dementia Rating(R).

73 The patients with AD had clinical dementia ratings ranging from 0.5 to 3, corresp

74 r prevalence of deficits demonstrated on the Clinical Dementia Rating scale (45% vs 19%; P = .12).

75 gnition) and a positive association with the Clinical Dementia Rating Scale (a global functional asse

76 Patients were assessed by the Clinical Dementia Rating scale (CDR) to have no dementia

77 e 15-item Geriatric Depression Scale and the Clinical Dementia Rating Scale (CDR).

78 tis Dementia Rating Scale-2 (DRS-2), and the Clinical Dementia Rating Scale (CDR).

79 outcome of change in the sum of boxes of the Clinical Dementia Rating Scale (CDR-SB) score (range, 0-

80 gender, increased serum ACT correlated with Clinical Dementia Rating Scale (p = 0.0041) or Mattis De

81 tudy included 468 healthy older individuals (Clinical Dementia Rating scale [CDR] global scores of 0,

82 assessed annually for up to 4 years with the Clinical Dementia Rating scale and a battery of neuropsy

83 on (MMSE), Frontotemporal Lobar Degeneration-Clinical Dementia Rating scale and MRI.

84 d 133 clinically healthy older participants (Clinical Dementia Rating Scale global scores of 0) parti

85 ni-Mental State Examination and had a global Clinical Dementia Rating scale of 0.5, with a required m

86 quent decline in phonemic verbal fluency and Clinical Dementia Rating scale plus FTD modules.

87 change in Frontotemporal Lobar Degeneration-Clinical Dementia Rating scale score (b=-3.46 [SE 46.3];

88 other dementing disorders, the mean (+/-SD) Clinical Dementia Rating Scale score was 2.21 (+/-1.14),

89 The higher Clinical Dementia Rating Scale scores lacked correlation

90 Clinical Dementia Rating scale scores were significantly

91 er education level was associated with lower Clinical Dementia Rating Scale sum of boxes (beta = -0.1

92 neuritic plaques were associated with higher Clinical Dementia Rating Scale sum of boxes (beta = 1.64

93 med with neuropsychological measures and the Clinical Dementia Rating scale sum of boxes (CDRsb).

94 0% improvement in slope in rate of change of Clinical Dementia Rating Scale sum of boxes has 89% powe

95 by the mini-mental state examination and the clinical dementia rating scale sum of boxes scores.

96 n several standard clinical instruments: the Clinical Dementia Rating Scale sum of boxes, a verbal me

97 e on Folstein Mini-Mental State Examination, Clinical Dementia Rating Scale Sum of Boxes, Logical Mem

98 nation (range, 0-30, with 30 being best) and Clinical Dementia Rating scale sum-of-boxes scale (range

99 impairment as measured with the MMSE and the Clinical Dementia Rating scale sum-of-boxes score.

100 Secondary outcome measures included the Clinical Dementia Rating scale sum-of-boxes, the Neurops

101 tive functioning (Mini-Mental State Exam and Clinical Dementia Rating Scale), emotional/behaviour sym

102 AS-Cog score, 1-step worsening on the global Clinical Dementia Rating scale, 15-point decline on the

103 ed at baseline and every 15 months using the Clinical Dementia Rating scale, a neurological evaluatio

104 P < 0.01) and greater worsening over time in Clinical Dementia Rating Scale, sum of boxes (P = 0.02).

105 by the Mini-Mental State Examination and the Clinical Dementia Rating scale, was detected 5 years bef

106 Neuropsychological evaluation, including the Clinical Dementia Rating scale, was performed.

107 icant differences, with the exception of the Clinical Dementia Rating Scale, which suggested worsenin

108 Primary outcome was the Clinical Dementia Rating scale-global score (CDR-global)

109 n changes from baseline to post-treatment in Clinical Dementia Rating scale-Sum of Boxes (CDR-SB) and

110 utcomes included the change in scores on the Clinical Dementia Rating Scale-Sum of Boxes (CDR-SB), th

111 rom baseline to week 104 in the score on the Clinical Dementia Rating Scale-Sum of Boxes (CDR-SB; sco

112 essment Scale-Cognitive Subscale [ADAS-Cog], Clinical Dementia Rating scale-sum of boxes [CDR-SB], an

113 lation presented a stable performance of the Clinical Dementia Rating Scale-Sum of Boxes score, where

114 The Clinical Dementia Rating Scale-Sum of Boxes was selected

115 B PET, estimated years to symptom onset and Clinical Dementia Rating Scale-Sum of Boxes.

116 nd completed a neuropsychological battery or clinical dementia rating scale.

117 functional abilities were examined with the Clinical Dementia Rating Scale.

118 er clinical impairments as assessed with the clinical dementia rating scale.

119 the Mini-Mental State Examination (MMSE) and Clinical Dementia Rating scale.

120 unction of dementia severity measured by the Clinical Dementia Rating Scale.

121 subjects for dementia severity by using the Clinical Dementia Rating Scale.

122 f these cases was also done by employing the Clinical Dementia Rating Scale.

123 CASP-19; DEMQOL); cognition and functioning (Clinical Dementia Rating Scale; S-MMSE); capability (ICE

124 easured by Mini-Mental State Examination and Clinical Dementia Rating scales.

125 of TS1 was significantly correlated with the Clinical Dementia Rating score (rho = 0.75, p = 2.2 x 10

126 e modified frontotemporal lobar degeneration clinical dementia rating score and CSF neuronal biomarke

127 Persons 65 to 85 years of age with a global Clinical Dementia Rating score of 0 (range, 0 to 3, with

128 ed States and Canada (91 participants with a Clinical Dementia Rating score of 0 and 150 individuals

129 rmal participants who progress from a global Clinical Dementia Rating score of 0 are significantly wo

130 cipants with healthy cognition, defined as a Clinical Dementia Rating score of 0 at baseline and subs

131 al participants who are stable with a global Clinical Dementia Rating score of 0 at months 12, 24, an

132 were identified as clinically normal (per a Clinical Dementia Rating score of 0) and cognitively uni

133 cognitive impairment (MCI), identified by a Clinical Dementia Rating score of 0.5 or greater in Knig

134 Rating score of 0 and 150 individuals with a Clinical Dementia Rating score of 0.5).

135 nation score of 18 points or higher and/or a Clinical Dementia Rating score of less than 2 points.

136 vior, corrected for age, education, sex, and clinical dementia rating score.

137 ctivities, a comorbidity index, and baseline Clinical Dementia Rating score.

138 related to dementia state as measured by the clinical dementia rating score.

139 rs, P < 0.001) and had more severe dementia (Clinical Dementia Rating score: active = 2.36, remote =

140 with basal ganglia amyloid-beta deposition, Clinical Dementia Rating scores and estimated years to s

141 isease Rating Scale Part III (UPDRS-III) and Clinical Dementia Rating scores and neuropsychological p

142 pe of Alzheimer disease accurately predicted clinical dementia rating scores in the other, further de

143 e in functional connectivity with increasing Clinical Dementia Rating scores were similar for both LO

144 onships between advancing dementia severity (Clinical Dementia Rating scores) and FMD and nitroglycer

145 or AD (N = 5) based on clinical history and Clinical Dementia Rating scores.

146 with the progression of AD, as reflected by Clinical Dementia Rating scores.

147 es and was stratified by participant sex and Clinical Dementia Rating severity score.

148 s gamma tACS groups were significant for the Clinical Dementia Rating sum of boxes (0.35; 95% CI, 0.1

149 oncentration prior to death or prior to last Clinical Dementia Rating Sum of Boxes (CDR-SB) assessmen

150 Clinical progression was assessed with the Clinical Dementia Rating Sum of Boxes (CDR-SB) score.

151 and PSP were matched for severity using the clinical dementia rating sum of boxes (CDR-sb) scores.

152 separate models to assess associations with Clinical Dementia Rating Sum of Boxes (CDR-SB), Mini-Men

153 nal disease severity was evaluated using the Clinical Dementia Rating Sum of Boxes (CDR-SB).

154 es of daily living scale (ADCS-ADL), and the clinical dementia rating sum of boxes (CDR-sb).

155 ation (MMSE; 0 [worst] to 30 [best] points), Clinical Dementia Rating Sum of Boxes (CDR-Sum of Boxes;

156 assessed by longitudinal measurements of the Clinical Dementia Rating Sum of Boxes (p < .001) and Min

157 Clinical assessment (Clinical Dementia Rating Sum of Boxes [CDR-SB]) and tau

158 APOE alleles on AD pathology and cognition (Clinical Dementia Rating Sum of Boxes and Mini-Mental St

159 totemporal dementia that had multiple serial Clinical Dementia Rating Sum of Boxes assessments (mean

160 The results showed the contributions of age, Clinical Dementia Rating Sum of Boxes composite test sco

161 ate of functional decline as measured by the Clinical Dementia Rating Sum of Boxes scale.

162 se variables were associated with the actual Clinical Dementia Rating Sum of Boxes score estimated fo

163 deterioration in bvFTD (1.86-point change in Clinical Dementia Rating Sum of Boxes score per bvFTD at

164 in controls and rates of cognitive decline (Clinical Dementia Rating sum of boxes score: beta estima

165 te (assessed by longitudinal measurements of Clinical Dementia Rating Sum of Boxes).

166 ormance on Mini-Mental State Examination and Clinical Dementia Rating Sum of Boxes, a result that was

167 th greater clinical impairment, based on the Clinical Dementia Rating Sum of Boxes, recruited a large

168 by calculating the annualized change in the Clinical Dementia Rating Sum-of-Boxes (CDR-SB) scores fr

169 clinical progression was assessed using the Clinical Dementia Rating (Sum of Boxes).

170 5% confidence interval, CI -2.5 to -0.2) and Clinical Dementia Rating-Sum of Boxes (1.15 point/pathol

171 he change from baseline up to Week 96 in the Clinical Dementia Rating-Sum of Boxes (CDR-SB) score.

172 come was change from baseline to week 105 in Clinical Dementia Rating-Sum of Boxes (CDR-SB) score.

173 Alzheimer's Disease Rating Scale (iADRS) and Clinical Dementia Rating-Sum of Boxes (CDR-SB) scores.

174 rval: -3.13 to 1.97; unadjusted P = 0.65) or Clinical Dementia Rating-Sum of Boxes (CDR-SoB) (-0.06;

175 th the Mini-Mental State Examination and the Clinical Dementia Rating-Sum of Boxes (rho >= 0.45, P <

176 by a slowing of clinical decline measured by Clinical Dementia Rating-Sum of Boxes and Mini Mental St

177 ni-Mental State Examination items, and all 6 Clinical Dementia Rating-Sum of Boxes items.

178 ry outcomes were change from baseline on the Clinical Dementia Rating-Sum of Boxes score from baselin

179 [55.7%]), similar increases were seen on the Clinical Dementia Rating-Sum of Boxes score in the place

180 ion of dementia (median annualized change in Clinical Dementia Rating-Sum of Boxes score, mutation ca

181 e (relative difference in adjusted means for Clinical Dementia Rating-Sum of Boxes was -9% in pooled

182 using the Mini-Mental State Examination, the Clinical Dementia Rating-Sum of Boxes, clinical diagnosi

183 s also shed light on the crucial role of the Clinical Dementia Rating tool in predicting AD.

184 e modified frontotemporal lobar degeneration clinical dementia rating was obtained as a measure of di