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1 te Examination and faster progression on the Clinical Dementia Ratings.
2 al CAMCOG, orientation and memory scores and clinical dementia ratings.
3 AD (DLB+AD n=23) and pure AD (n=89) who had Clinical Dementia Rating 0, 0.5 or 1 at their first visi
4 entia rating <1, n = 20) and presymptomatic (clinical dementia rating = 0, n = 15) stages of the dise
7 211) as well as patients with very mild AD (Clinical Dementia Rating = .5; n = 69) and clinically ma
8 istructured assessments in order to assign a Clinical Dementia Rating and determine whether psychosis
9 period (average = 3.1 years), scores on the Clinical Dementia Rating and Global Deterioration Scale
10 followed over 6 years and assessed with the Clinical Dementia Rating and the Mini-Mental State Exami
12 wer of attorney (96% scored 2 or less on the Clinical Dementia Rating, and 92% scored 5 or less on th
13 that ranged in AD severity from unaffected [clinical dementia rating (CDR) 0] to very mild (CDR 0.5)
14 ognitive function was investigated using the Clinical Dementia Rating (CDR) and the Informant Questio
15 on of CSF APOE with CSF Abeta(42) levels and clinical dementia rating (CDR) is not because of a rever
17 sed morphometry for image postprocessing and Clinical Dementia Rating (CDR) scale for cognitive asses
18 We studied 20 individuals who at death had a Clinical Dementia Rating (CDR) score of 0 (cognitively n
22 cognitive status had been assessed with the Clinical Dementia Rating (CDR), including 39 nondemented
23 d CR1 expression levels were associated with clinical dementia rating (CDR), with higher expression b
24 part of a cohort study, cognitively normal (Clinical Dementia Rating [CDR] of 0) middle-aged researc
25 rticipants who were cognitively normal (CN) (Clinical Dementia Rating [CDR] score, 0) or had AD demen
27 i-Mental State Examination scores and higher Clinical Dementia Ratings compared to amyloid-beta negat
28 d in a group of 10 mildly affected patients (clinical dementia rating equal to 0) using voxel-based m
32 arriers and non-carriers in the preclinical (clinical dementia rating <1, n = 20) and presymptomatic
36 r prevalence of deficits demonstrated on the Clinical Dementia Rating scale (45% vs 19%; P = .12).
37 gnition) and a positive association with the Clinical Dementia Rating Scale (a global functional asse
41 gender, increased serum ACT correlated with Clinical Dementia Rating Scale (p = 0.0041) or Mattis De
42 tudy included 468 healthy older individuals (Clinical Dementia Rating scale [CDR] global scores of 0,
43 assessed annually for up to 4 years with the Clinical Dementia Rating scale and a battery of neuropsy
44 d 133 clinically healthy older participants (Clinical Dementia Rating Scale global scores of 0) parti
45 other dementing disorders, the mean (+/-SD) Clinical Dementia Rating Scale score was 2.21 (+/-1.14),
48 er education level was associated with lower Clinical Dementia Rating Scale sum of boxes (beta = -0.1
49 neuritic plaques were associated with higher Clinical Dementia Rating Scale sum of boxes (beta = 1.64
50 med with neuropsychological measures and the Clinical Dementia Rating scale sum of boxes (CDRsb).
51 0% improvement in slope in rate of change of Clinical Dementia Rating Scale sum of boxes has 89% powe
52 n several standard clinical instruments: the Clinical Dementia Rating Scale sum of boxes, a verbal me
53 e on Folstein Mini-Mental State Examination, Clinical Dementia Rating Scale Sum of Boxes, Logical Mem
54 nation (range, 0-30, with 30 being best) and Clinical Dementia Rating scale sum-of-boxes scale (range
57 AS-Cog score, 1-step worsening on the global Clinical Dementia Rating scale, 15-point decline on the
58 ed at baseline and every 15 months using the Clinical Dementia Rating scale, a neurological evaluatio
59 P < 0.01) and greater worsening over time in Clinical Dementia Rating Scale, sum of boxes (P = 0.02).
60 by the Mini-Mental State Examination and the Clinical Dementia Rating scale, was detected 5 years bef
62 icant differences, with the exception of the Clinical Dementia Rating Scale, which suggested worsenin
68 of TS1 was significantly correlated with the Clinical Dementia Rating score (rho = 0.75, p = 2.2 x 10
69 ed States and Canada (91 participants with a Clinical Dementia Rating score of 0 and 150 individuals
70 rmal participants who progress from a global Clinical Dementia Rating score of 0 are significantly wo
71 al participants who are stable with a global Clinical Dementia Rating score of 0 at months 12, 24, an
75 isease Rating Scale Part III (UPDRS-III) and Clinical Dementia Rating scores and neuropsychological p
76 pe of Alzheimer disease accurately predicted clinical dementia rating scores in the other, further de
77 e in functional connectivity with increasing Clinical Dementia Rating scores were similar for both LO
78 onships between advancing dementia severity (Clinical Dementia Rating scores) and FMD and nitroglycer
80 and PSP were matched for severity using the clinical dementia rating sum of boxes (CDR-sb) scores.
82 ation (MMSE; 0 [worst] to 30 [best] points), Clinical Dementia Rating Sum of Boxes (CDR-Sum of Boxes;
83 APOE alleles on AD pathology and cognition (Clinical Dementia Rating Sum of Boxes and Mini-Mental St
84 totemporal dementia that had multiple serial Clinical Dementia Rating Sum of Boxes assessments (mean
85 The results showed the contributions of age, Clinical Dementia Rating Sum of Boxes composite test sco
87 se variables were associated with the actual Clinical Dementia Rating Sum of Boxes score estimated fo
88 in controls and rates of cognitive decline (Clinical Dementia Rating sum of boxes score: beta estima
89 th greater clinical impairment, based on the Clinical Dementia Rating Sum of Boxes, recruited a large
91 by a slowing of clinical decline measured by Clinical Dementia Rating-Sum of Boxes and Mini Mental St
93 ion of dementia (median annualized change in Clinical Dementia Rating-Sum of Boxes score, mutation ca
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