ライフサイエンスコーパス: nondemented

1 re demented subjects from subjects alive and nondemented 10 years later and an AUROC of 0.75 for disc

2 We studied 515 nondemented (428 cognitively normal and 87 mild cognitiv

3 pitalization and 1-month post-discharge 1521 nondemented acute coronary syndrome survivors enrolled i

4 solute brain metabolite concentrations in 19 nondemented adults with Down's syndrome and 17 age- and

5 Older nondemented adults with Down's syndrome show normal rate

6 eight older (mean age = 50, SD = 7) healthy, nondemented adults with trisomy 21 Down's syndrome.

7 ons of the AD brain or in the hippocampus of nondemented age-matched controls show no such anomalies.

8 higher than the levels in the CSF taken from nondemented age-matched controls.

9 h AD, 14 with other types of dementia, and 9 nondemented aged volunteers; mean age +/- SD, 80.4 +/- 1

10 neurons distinguishes even very mild AD from nondemented aging.

11 Recent studies suggest that nondemented ALS patients can show selective cognitive im

12 Plasma of both nondemented and AD patients were found to contain autoan

13 These findings, across a continuum of nondemented and mildly impaired older adults, support th

14 In 4413 nondemented and stroke-free participants from the popula

15 Forty-two nondemented CAA patients, 50 HE subjects, and 43 AD/MCI

16 We found that as early as middle age, nondemented carriers of the varepsilon4 allele of the AP

17 Clinical Dementia Rating (CDR), including 39 nondemented cases (CDR = 0; age, 51-88 years), 15 very m

18 ide were higher than those of A(beta)x-40 in nondemented cases and remained higher throughout progres

19 Nondemented cases with high levels of AD-related patholo

20 e was also a substantial increase over other nondemented cases, both in the number of tangles and in

21 Tangles were found in all the nondemented cases, especially in hippocampal and parahip

22 structures characterized a further group of nondemented cases.

23 sorders clinic that included a predominantly nondemented cohort of 143 patients with PD.

24 e function, and brain morphology in a large, nondemented community-based cohort.

25 th elevated levels of glycated hemoglobin in nondemented community-dwelling elderly subjects.

26 Memory complaints of 364 nondemented, community-dwelling elderly individuals were

27 and hippocampal volumes were measured in 14 nondemented, community-dwelling older adults.

28 Nondemented control and AD plasmas demonstrated similar

29 In the temporalis muscles of the AD and nondemented control groups, the average values for Abeta

30 .05) at the basal state as compared with the nondemented control neurons.

31 otocol from patients with AD and age-matched nondemented control patients.

32 In the present study, AD and nondemented control plasma were analyzed for immunoreact

33 umber of superior temporal sulcus neurons in nondemented control subjects was stable across the sixth

34 uration ranging from 4 to 20 years, and nine nondemented control subjects with dense-core plaques.

35 oral sulcus of 34 individuals with AD and 17 nondemented control subjects, using statistically unbias

36 tively correlated with whole-brain volume in nondemented control subjects.

37 Autopsy specimens from nondemented controls (n = 3) and patients with AD (n = 5

38 nd to be significantly reduced compared with nondemented controls (p=0.018).

39 mbedded and frozen brain sections from three nondemented controls and five Alzheimer's disease (AD) p

40 stage AD dementia, but not in high pathology nondemented controls compared with age-matched normal co

41 D in a sample of 92 patients with AD and 166 nondemented controls from an inbred Israeli Arab communi

42 se issues, 12 early stage AD patients and 13 nondemented controls underwent fMRI while being exposed

43 rea 23) in 15 AD patients and 13 age-matched nondemented controls using quantitative cytochrome oxida

44 AD subjects was 4.2 times (P < 0.04) that in nondemented controls, suggesting up-regulated heme synth

45 a large sample of 1,544 LOAD cases and 1,642 nondemented controls.

46 heimer's disease (AD) and of her 47-year-old nondemented daughter.

47 synaptosomes of demented dogs compared with nondemented dogs.

48 In contrast, vessels from elderly nondemented donors are significantly (P<0.001) less leth

49 The subjects were 34 nondemented Down's syndrome adults (mean age=41.6 years,

50 ume of the hippocampus or amygdala among the nondemented Down's syndrome subjects and the comparison

51 Nondemented Down's syndrome subjects had significantly s

52 us of Alzheimer's disease (AD) compared with nondemented elderly (ND) patients, whereas complement co

53 episodes of Alzheimer's disease patients and nondemented elderly comparison subjects included similar

54 episodes of Alzheimer's disease patients and nondemented elderly comparison subjects, all support the

55 ts with probable Alzheimer's disease and 151 nondemented elderly comparison subjects.

56 the 2 AD proband groups and relatives of the nondemented elderly group.

57 of medial temporal lobe (MTL) regions in 32 nondemented elderly individuals with mild cognitive impa

58 ent replication data sets that included 4006 nondemented elderly individuals.

59 ease (AD) pathophysiology and cognition in a nondemented elderly population.

60 bands, and 7646 parents and siblings of 1493 nondemented elderly probands.

61 obands (P<.001), but not in the relatives of nondemented elderly probands.

62 ophy is greater in association with APOE4 in nondemented elderly subjects, subjects with MCI, and tho

63 0 years and 85% PiB positivity in the APOE*4 nondemented elderly subjects.

64 ility for this disease relative to less-aged nondemented elderly.

65 Subjects included 45 nondemented, elderly depressed patients who achieved rem

66 hippocampal formation in 240 community-based nondemented elders (mean age, 79.7 years) who received a

67 and a wide age range (18 to 92 years old) of nondemented human brains (n = 25).

68 rons in brains from AD, Down's syndrome, and nondemented humans.

69 tsburgh compound B twice 2 years apart in 81 nondemented individuals 83 years and older.

70 prevalence of depressive disorders in 4,559 nondemented individuals aged 65 to 100 years.

71 that Abeta deposition increases with age in nondemented individuals and that arterial stiffness is s

72 evant to treatments targeting brain Abeta in nondemented individuals at risk for AD and suggest that

73 A total of 2,258 community-based nondemented individuals in New York were prospectively e

74 Human brains from age-matched, nondemented individuals rarely displayed either CCR1 or

75 eep and next-morning learning ability in 107 nondemented individuals who were between 55 and 84 years

76 ng offers the potential for predicting which nondemented individuals will eventually develop Alzheime

77 the disease course and were apparent even in nondemented individuals with AD pathology (low ptau181,

78 ty in subjects with normal cognition, but in nondemented individuals with cognitive impairment, memor

79 The subjects were nondemented individuals with nonpsychotic major depressi

80 reconstructed the white matter network of 55 nondemented individuals with type 2 diabetes (mean age,

81 In this community-based population of nondemented individuals, higher concurrent choline intak

82 ally diagnosed Alzheimer disease (AD) and of nondemented individuals.

83 essure and measures of arterial stiffness in nondemented individuals.

84 ated with the transition of individuals from nondemented MCI to AD.

85 d using Affymetrix Exon Array microarrays on nondemented, MCI, and AD patients.

86 e of clinical progression in a sample of 393 nondemented memory clinic patients.

87 explored this question using data from 1,917 nondemented men and women (average age = 76 years) in th

88 was to ascertain whether, among nondiabetic, nondemented middle-aged and elderly individuals, poorer

89 he changes that underlie the transition from nondemented mild cognitive impairment (MCI) to AD, are m

90 lity (standard deviation)) in a subset of 48 nondemented older adults (24 males; mean age=81 years) d

91 magnetic resonance imaging (MRI) scans of 92 nondemented older adults (age 59-85 years at baseline) i

92 Similarly, WMH are detected in many nondemented older adults and there is a body of evidence

93 These findings suggest that nondemented older adults exhibit increased stride length

94 Amyloid deposition is present in 20-50% of nondemented older adults yet the functional consequences

95 flow (CBF), as well as relative CBF (R1), in nondemented older adults.

96 ocampal subfield volumes and chronic pain in nondemented older adults.

97 We investigated this relationship in 34 nondemented older humans (CN, N = 18; MCI, N = 16).

98 raphy to quantify brain amyloid burden in 57 nondemented older individuals (mean age 78.5 years) in t

99 We examined 241 nondemented older individuals from research centers acro

100 For the current study, 48 nondemented older individuals with T2DM (mean age 70.3 +

101 In nondemented older individuals, Abeta-associated volume l

102 en rs3818361 and brain amyloid deposition in nondemented older individuals.

103 phy, and apolipoprotein E epsilon4 status in nondemented, older individuals.

104 mptomatic AD) and 483 controls (who remained nondemented) on each of 15 cognitive measures were trans

105 Longitudinal studies in nondemented Parkinson disease (PD) subjects offer an opp

106 Nondemented Parkinson's disease (PD) patients report pro

107 ic acetylcholine receptors were imaged in 10 nondemented Parkinson's disease patients and 15 age-matc

108 A total of 1111 nondemented participants (mean [SD] age, 75.0 [5.9] year

109 Fifty-five nondemented participants (mean age, 78.5 y) in the Balti

110 Three hundred thirty nondemented participants aged 90 years and older at base

111 We studied a sample of nondemented participants from the population-based Mayo

112 The control group consisted of 29 nondemented participants of similar age and sex.

113 creased prevalence of OAG (17.5% vs 4.5% for nondemented participants, p = 0.003).

114 Participants included 20 nondemented patients (10 LPD, 10 RPD) and 11 normal cont

115 t this relationship was weaker in those from nondemented patients (r = 0.30) despite equivalent Abeta

116 region of the BACE gene in these same AD and nondemented patients and performed allelic association a

117 All long-stay nondemented patients in two U.K. hospitals scheduled for

118 opsychological tests, the authors studied 15 nondemented patients who had Parkinson's disease without

119 ents with dementia of the Alzheimer type and nondemented patients with Abeta plaque pathology.

120 We treated 4 nondemented patients with advanced PD, 2 with severe bra

121 It involved consecutively referred, nondemented patients with mild cognitive symptoms (origi

122 Participants were 128 nondemented patients with new-onset parkinsonism (104 wi

123 tive plaques also were seen in the brains of nondemented patients with numerous A beta deposits.

124 al head and eye movements was examined in 13 nondemented patients with Parkinson's disease (PD) of mi

125 Amnesic patients and nondemented patients with Parkinson's disease were given

126 e for cognitive dysfunction and dysphoria in nondemented patients with Parkinson's disease.

127 underlie cognitive and dysphoric symptoms in nondemented patients with Parkinson's disease.

128 After administration of (11)C-MeNER, 15 nondemented patients with PD and 10 healthy subjects und

129 een "sequence" and "random" conditions in 12 nondemented patients with PD and education- and gender-m

130 ue density fully distinguished demented from nondemented patients, with no overlap between groups in

131 ing 5/5 patients with HIV-1 dementia and 4/5 nondemented patients.

132 nt difference between brains of demented and nondemented patients.

133 e measures did not distinguish demented from nondemented patients.

134 a decrease in PDK1 expression compared with nondemented patients.

135 rated that posterior cortical dysfunction in nondemented PD patients precedes cognitive decline and t

136 In 5171 nondemented people (age 45-99 years) from the population

137 In nondemented people, there is only a marginal joint effec

138 ects with other late-life dementias, and 113 nondemented people.

139 inguishable profiles compared to age-matched nondemented people.

140 emission tomography in middle-aged and older nondemented persons with normal memory performance.

141 These results show that, in nondemented persons, TMEM106B influences the volume of t

142 er these genes jointly affect cognition in a nondemented population and improve prediction of AD.

143 ability in the cognitive performance in this nondemented population.

144 mains equivocal regarding whether amyloid in nondemented populations is deleterious to cognition.

145 This prospective observational study in nondemented postmenopausal women aged 50-89 from the Bal

146 effect of estrogen on cognitive function in nondemented postmenopausal women.

147 of AD may be more highly concentrated among nondemented probands aged >/=90 years and their relative

148 nts in 6,660 first-degree relatives of 1,049 nondemented probands aged 60-102 years.

149 dementia (9/16) than in the CSF from either nondemented seropositive (2/11) or seronegative (0/11) c

150 d 23 were married and living with a healthy, nondemented spouse.

151 e outcome (clinical onset of AD vs continued nondemented status) within a prospective community-based

152 ittee and with informed written consent, 106 nondemented subjects (62 men, 44 women) aged 78-79 years

153 vealed a 55% prevalence of PiB positivity in nondemented subjects age >80 years and 85% PiB positivit

154 mined amyloid-beta (Abeta) deposition in 190 nondemented subjects aged >/=82 years to determine the p

155 t (MAP) are longitudinal studies that enroll nondemented subjects and include annual clinical evaluat

156 ompared specific cortical PiB retention in 6 nondemented subjects diagnosed with probable CAA with 15

157 For the 20 nondemented subjects followed longitudinally, memory per

158 is a population-based longitudinal study of nondemented subjects in Olmsted County, Minnesota.

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

160 atching brain sections from 2 demented and 4 nondemented subjects were processed for the demonstratio

161 Functional MRI was performed on 25 nondemented subjects with probable CAA (mean +/- standar

162 tmortem brain tissues from LOAD patients and nondemented subjects, and we demonstrate that LOAD recon

163 at autopsy from AD patients and age-matched nondemented subjects.

164 ignificant after restricting the analysis to nondemented subjects.

165 y significant for either the demented or the nondemented subjects.

166 cortex of 40 AD patients and 32 age-matched nondemented subjects.

167 +) astrocytes and MHC2(+) microglia than the nondemented subjects.

168 nsion were greater in demented compared with nondemented subjects.

169 rain tissue specimens from two ADs and three nondemented subjects.

170 We show that T2 in brain white matter of nondemented volunteers follows a U-shaped trajectory wit

171 o cognitive deficits (strictly defined) in a nondemented, well characterized PD sample, and into the

172 ndemented with negligible AD-type pathology, nondemented with incipient AD pathology, mild cognitive

173 ses were separated into four groups: elderly nondemented with negligible AD-type pathology, nondement

174 rum sex hormone binding globulin levels than nondemented women (86.4 vs 56.6 nmol/L, p = 0.02), but s

175 l homocysteine were assayed in 700 disabled, nondemented women aged 65 years and over living in the c

176 beneficial effect on verbal memory in older nondemented women.

177 Cohort B included 105 nondemented younger individuals (aged 20-34 years) with