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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  with progression to Abeta positivity in 292 nondemented, Abeta-negative ADNI participants.
4 pitalization and 1-month post-discharge 1521 nondemented acute coronary syndrome survivors enrolled i
5 solute brain metabolite concentrations in 19 nondemented adults with Down's syndrome and 17 age- and
6                                        Older nondemented adults with Down's syndrome show normal rate
7 eight older (mean age = 50, SD = 7) healthy, nondemented adults with trisomy 21 Down's syndrome.
8 ons of the AD brain or in the hippocampus of nondemented age-matched controls show no such anomalies.
9 higher than the levels in the CSF taken from nondemented age-matched controls.
10 h AD, 14 with other types of dementia, and 9 nondemented aged volunteers; mean age +/- SD, 80.4 +/- 1
11 neurons distinguishes even very mild AD from nondemented aging.
12                  Recent studies suggest that nondemented ALS patients can show selective cognitive im
13                               Plasma of both nondemented and AD patients were found to contain autoan
14        These findings, across a continuum of nondemented and mildly impaired older adults, support th
15                                      In 4413 nondemented and stroke-free participants from the popula
16  averaged 90 years at death, two-thirds were nondemented, and 60% evidenced pathologic Alzheimer's di
17                                    Forty-two nondemented CAA patients, 50 HE subjects, and 43 AD/MCI
18        We found that as early as middle age, nondemented carriers of the varepsilon4 allele of the AP
19 Clinical Dementia Rating (CDR), including 39 nondemented cases (CDR = 0; age, 51-88 years), 15 very m
20 ide were higher than those of A(beta)x-40 in nondemented cases and remained higher throughout progres
21                                              Nondemented cases with high levels of AD-related patholo
22 e was also a substantial increase over other nondemented cases, both in the number of tangles and in
23                Tangles were found in all the nondemented cases, especially in hippocampal and parahip
24  structures characterized a further group of nondemented cases.
25 sorders clinic that included a predominantly nondemented cohort of 143 patients with PD.
26 e function, and brain morphology in a large, nondemented community-based cohort.
27 th elevated levels of glycated hemoglobin in nondemented community-dwelling elderly subjects.
28                     Memory complaints of 364 nondemented, community-dwelling elderly individuals were
29  and hippocampal volumes were measured in 14 nondemented, community-dwelling older adults.
30                                              Nondemented control and AD plasmas demonstrated similar
31      In the temporalis muscles of the AD and nondemented control groups, the average values for Abeta
32 .05) at the basal state as compared with the nondemented control neurons.
33 otocol from patients with AD and age-matched nondemented control patients.
34                 In the present study, AD and nondemented control plasma were analyzed for immunoreact
35 umber of superior temporal sulcus neurons in nondemented control subjects was stable across the sixth
36 uration ranging from 4 to 20 years, and nine nondemented control subjects with dense-core plaques.
37 tive at reducing Abeta in human neurons from nondemented control subjects, as well as subjects with f
38 oral sulcus of 34 individuals with AD and 17 nondemented control subjects, using statistically unbias
39 tively correlated with whole-brain volume in nondemented control subjects.
40                       Autopsy specimens from nondemented controls (n = 3) and patients with AD (n = 5
41 nd to be significantly reduced compared with nondemented controls (p=0.018).
42 mbedded and frozen brain sections from three nondemented controls and five Alzheimer's disease (AD) p
43 stage AD dementia, but not in high pathology nondemented controls compared with age-matched normal co
44 D in a sample of 92 patients with AD and 166 nondemented controls from an inbred Israeli Arab communi
45 se issues, 12 early stage AD patients and 13 nondemented controls underwent fMRI while being exposed
46 rea 23) in 15 AD patients and 13 age-matched nondemented controls using quantitative cytochrome oxida
47 AD subjects was 4.2 times (P < 0.04) that in nondemented controls, suggesting up-regulated heme synth
48 a large sample of 1,544 LOAD cases and 1,642 nondemented controls.
49 heimer's disease (AD) and of her 47-year-old nondemented daughter.
50  synaptosomes of demented dogs compared with nondemented dogs.
51            In contrast, vessels from elderly nondemented donors are significantly (P<0.001) less leth
52                         The subjects were 34 nondemented Down's syndrome adults (mean age=41.6 years,
53 ume of the hippocampus or amygdala among the nondemented Down's syndrome subjects and the comparison
54                                              Nondemented Down's syndrome subjects had significantly s
55 us of Alzheimer's disease (AD) compared with nondemented elderly (ND) patients, whereas complement co
56 episodes of Alzheimer's disease patients and nondemented elderly comparison subjects included similar
57 episodes of Alzheimer's disease patients and nondemented elderly comparison subjects, all support the
58 ts with probable Alzheimer's disease and 151 nondemented elderly comparison subjects.
59 the 2 AD proband groups and relatives of the nondemented elderly group.
60 similar sets of fibril polymorphs develop in nondemented elderly individuals and AD patients but with
61 tructures of AB fibrils from brain tissue of nondemented elderly individuals with high amyloid loads
62  of medial temporal lobe (MTL) regions in 32 nondemented elderly individuals with mild cognitive impa
63 atients are observed in brain tissue of some nondemented elderly individuals.
64 egeneration using longitudinal biomarkers in nondemented elderly individuals.
65 ent replication data sets that included 4006 nondemented elderly individuals.
66 egeneration using longitudinal biomarkers in nondemented elderly individuals.
67 ease (AD) pathophysiology and cognition in a nondemented elderly population.
68 bands, and 7646 parents and siblings of 1493 nondemented elderly probands.
69 obands (P<.001), but not in the relatives of nondemented elderly probands.
70 ophy is greater in association with APOE4 in nondemented elderly subjects, subjects with MCI, and tho
71 0 years and 85% PiB positivity in the APOE*4 nondemented elderly subjects.
72 ility for this disease relative to less-aged nondemented elderly.
73                         Subjects included 45 nondemented, elderly depressed patients who achieved rem
74 hippocampal formation in 240 community-based nondemented elders (mean age, 79.7 years) who received a
75 and a wide age range (18 to 92 years old) of nondemented human brains (n = 25).
76 rons in brains from AD, Down's syndrome, and nondemented humans.
77 tsburgh compound B twice 2 years apart in 81 nondemented individuals 83 years and older.
78 etic, and neuroimaging parameters from 2,710 nondemented individuals age 60 or older, examined betwee
79  prevalence of depressive disorders in 4,559 nondemented individuals aged 65 to 100 years.
80  that Abeta deposition increases with age in nondemented individuals and that arterial stiffness is s
81 evant to treatments targeting brain Abeta in nondemented individuals at risk for AD and suggest that
82             A total of 2,258 community-based nondemented individuals in New York were prospectively e
83               Human brains from age-matched, nondemented individuals rarely displayed either CCR1 or
84 eep and next-morning learning ability in 107 nondemented individuals who were between 55 and 84 years
85 ng offers the potential for predicting which nondemented individuals will eventually develop Alzheime
86 the disease course and were apparent even in nondemented individuals with AD pathology (low ptau181,
87 ty in subjects with normal cognition, but in nondemented individuals with cognitive impairment, memor
88                            The subjects were nondemented individuals with nonpsychotic major depressi
89 reconstructed the white matter network of 55 nondemented individuals with type 2 diabetes (mean age,
90        In this community-based population of nondemented individuals, higher concurrent choline intak
91 ally diagnosed Alzheimer disease (AD) and of nondemented individuals.
92 nts, compared to early-onset AD patients and nondemented individuals.
93 essure and measures of arterial stiffness in nondemented individuals.
94 Olmsted County, Minnesota, that included 480 nondemented Mayo Clinic Study of Aging participants who
95 ated with the transition of individuals from nondemented MCI to AD.
96 d using Affymetrix Exon Array microarrays on nondemented, MCI, and AD patients.
97 e of clinical progression in a sample of 393 nondemented memory clinic patients.
98 explored this question using data from 1,917 nondemented men and women (average age = 76 years) in th
99 was to ascertain whether, among nondiabetic, nondemented middle-aged and elderly individuals, poorer
100 erm effect of pomegranate juice on memory in nondemented middle-aged and older adults.
101 he changes that underlie the transition from nondemented mild cognitive impairment (MCI) to AD, are m
102  with AD and VaD (separately) in a cohort of nondemented, nondepressed older adults.
103 lity (standard deviation)) in a subset of 48 nondemented older adults (24 males; mean age=81 years) d
104 magnetic resonance imaging (MRI) scans of 92 nondemented older adults (age 59-85 years at baseline) i
105          Similarly, WMH are detected in many nondemented older adults and there is a body of evidence
106                  These findings suggest that nondemented older adults exhibit increased stride length
107 al volume, in the MEMENTO clinical cohort of nondemented older adults with isolated memory complaint
108   Amyloid deposition is present in 20-50% of nondemented older adults yet the functional consequences
109 flow (CBF), as well as relative CBF (R1), in nondemented older adults.
110 ocampal subfield volumes and chronic pain in nondemented older adults.
111      We investigated this relationship in 34 nondemented older humans (CN, N = 18; MCI, N = 16).
112 raphy to quantify brain amyloid burden in 57 nondemented older individuals (mean age 78.5 years) in t
113                              We examined 241 nondemented older individuals from research centers acro
114                    For the current study, 48 nondemented older individuals with T2DM (mean age 70.3 +
115                                           In nondemented older individuals, Abeta-associated volume l
116 en rs3818361 and brain amyloid deposition in nondemented older individuals.
117 phy, and apolipoprotein E epsilon4 status in nondemented, older individuals.
118 mptomatic AD) and 483 controls (who remained nondemented) on each of 15 cognitive measures were trans
119                      Longitudinal studies in nondemented Parkinson disease (PD) subjects offer an opp
120                                              Nondemented Parkinson's disease (PD) patients report pro
121 ic acetylcholine receptors were imaged in 10 nondemented Parkinson's disease patients and 15 age-matc
122                              A total of 1111 nondemented participants (mean [SD] age, 75.0 [5.9] year
123                                   Fifty-five nondemented participants (mean age, 78.5 y) in the Balti
124                         Three hundred thirty nondemented participants aged 90 years and older at base
125                       We studied a sample of nondemented participants from the population-based Mayo
126            The control group consisted of 29 nondemented participants of similar age and sex.
127 creased prevalence of OAG (17.5% vs 4.5% for nondemented participants, p = 0.003).
128                     Participants included 20 nondemented patients (10 LPD, 10 RPD) and 11 normal cont
129 t this relationship was weaker in those from nondemented patients (r = 0.30) despite equivalent Abeta
130 region of the BACE gene in these same AD and nondemented patients and performed allelic association a
131                                All long-stay nondemented patients in two U.K. hospitals scheduled for
132 opsychological tests, the authors studied 15 nondemented patients who had Parkinson's disease without
133 ents with dementia of the Alzheimer type and nondemented patients with Abeta plaque pathology.
134                                 We treated 4 nondemented patients with advanced PD, 2 with severe bra
135          It involved consecutively referred, nondemented patients with mild cognitive symptoms (origi
136                        Participants were 128 nondemented patients with new-onset parkinsonism (104 wi
137 tive plaques also were seen in the brains of nondemented patients with numerous A beta deposits.
138 al head and eye movements was examined in 13 nondemented patients with Parkinson's disease (PD) of mi
139                         Amnesic patients and nondemented patients with Parkinson's disease were given
140 e for cognitive dysfunction and dysphoria in nondemented patients with Parkinson's disease.
141 underlie cognitive and dysphoric symptoms in nondemented patients with Parkinson's disease.
142      After administration of (11)C-MeNER, 15 nondemented patients with PD and 10 healthy subjects und
143 een "sequence" and "random" conditions in 12 nondemented patients with PD and education- and gender-m
144 ue density fully distinguished demented from nondemented patients, with no overlap between groups in
145 ing 5/5 patients with HIV-1 dementia and 4/5 nondemented patients.
146 nt difference between brains of demented and nondemented patients.
147 e measures did not distinguish demented from nondemented patients.
148  a decrease in PDK1 expression compared with nondemented patients.
149 rated that posterior cortical dysfunction in nondemented PD patients precedes cognitive decline and t
150                                      In 5171 nondemented people (age 45-99 years) from the population
151                                           In nondemented people, there is only a marginal joint effec
152 ects with other late-life dementias, and 113 nondemented people.
153 inguishable profiles compared to age-matched nondemented people.
154 emission tomography in middle-aged and older nondemented persons with normal memory performance.
155                  These results show that, in nondemented persons, TMEM106B influences the volume of t
156 er these genes jointly affect cognition in a nondemented population and improve prediction of AD.
157 ability in the cognitive performance in this nondemented population.
158 mains equivocal regarding whether amyloid in nondemented populations is deleterious to cognition.
159      This prospective observational study in nondemented postmenopausal women aged 50-89 from the Bal
160  effect of estrogen on cognitive function in nondemented postmenopausal women.
161  of AD may be more highly concentrated among nondemented probands aged >/=90 years and their relative
162 nts in 6,660 first-degree relatives of 1,049 nondemented probands aged 60-102 years.
163  dementia (9/16) than in the CSF from either nondemented seropositive (2/11) or seronegative (0/11) c
164 d 23 were married and living with a healthy, nondemented spouse.
165 e outcome (clinical onset of AD vs continued nondemented status) within a prospective community-based
166 ittee and with informed written consent, 106 nondemented subjects (62 men, 44 women) aged 78-79 years
167 vealed a 55% prevalence of PiB positivity in nondemented subjects age >80 years and 85% PiB positivit
168 mined amyloid-beta (Abeta) deposition in 190 nondemented subjects aged >/=82 years to determine the p
169 t (MAP) are longitudinal studies that enroll nondemented subjects and include annual clinical evaluat
170 ompared specific cortical PiB retention in 6 nondemented subjects diagnosed with probable CAA with 15
171                                   For the 20 nondemented subjects followed longitudinally, memory per
172  is a population-based longitudinal study of nondemented subjects in Olmsted County, Minnesota.
173  Based on antemortem diagnoses, demented and nondemented subjects were examined together and separate
174 atching brain sections from 2 demented and 4 nondemented subjects were processed for the demonstratio
175           Functional MRI was performed on 25 nondemented subjects with probable CAA (mean +/- standar
176 tmortem brain tissues from LOAD patients and nondemented subjects, and we demonstrate that LOAD recon
177 rain tissue specimens from two ADs and three nondemented subjects.
178  at autopsy from AD patients and age-matched nondemented subjects.
179 ignificant after restricting the analysis to nondemented subjects.
180 y significant for either the demented or the nondemented subjects.
181  cortex of 40 AD patients and 32 age-matched nondemented subjects.
182 +) astrocytes and MHC2(+) microglia than the nondemented subjects.
183 nsion were greater in demented compared with nondemented subjects.
184     We show that T2 in brain white matter of nondemented volunteers follows a U-shaped trajectory wit
185 o cognitive deficits (strictly defined) in a nondemented, well characterized PD sample, and into the
186 tia has been challenged by the emergence of "nondemented with Alzheimer's neuropathology" (NDAN) indi
187 ndemented with negligible AD-type pathology, nondemented with incipient AD pathology, mild cognitive
188 ses were separated into four groups: elderly nondemented with negligible AD-type pathology, nondement
189 rum sex hormone binding globulin levels than nondemented women (86.4 vs 56.6 nmol/L, p = 0.02), but s
190 l homocysteine were assayed in 700 disabled, nondemented women aged 65 years and over living in the c
191  beneficial effect on verbal memory in older nondemented women.
192                        Cohort B included 105 nondemented younger individuals (aged 20-34 years) with

 
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