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1 detection of Alzheimer's disease (AD) at the preclinical stage.
2 o subtle memory deficits observed during the preclinical stage.
3 or drug absorption and metabolism during the preclinical stage.
4 ected longitudinal changes, including at the preclinical stage.
5 ility of virus acquisition by insects at the preclinical stage.
6 indicate increased ADRD vulnerability at the preclinical stage.
7 ation of the development of new drugs in the preclinical stage.
8 pes in AD pathophysiology, starting from the preclinical stage.
9 een infants developing LOS and controls in a preclinical stage.
10 asis on the need for scientific rigor in the preclinical stage.
11  mitochondrial disorders are now at a mature preclinical stage.
12 ) PIB binding was observed during this early preclinical stage.
13 currently in clinical use or at the advanced preclinical stage.
14 ials have begun to target individuals at the preclinical stage.
15 d with metabolic disturbances already at the preclinical stage.
16 re cognitive symptoms emerge-during the long preclinical stage.
17 st clinical episode and, importantly, at the preclinical stage.
18 harbinger of Alzheimer disease (AD), even in preclinical stages.
19 lecular signature that emerges in very early preclinical stages.
20 ation of future disease was evaluated across preclinical stages.
21 ely phagocytose prions or PrPSc during early preclinical stages.
22 duals with early impaired kidney function at preclinical stages.
23 identify persons "at high risk" of AD in the preclinical stages.
24 sive due to rapid progression and absence of preclinical stages.
25 ndeed evaluating treatments at prodromal and preclinical stages.
26 le the survey of vascular pathologies during preclinical stages.
27 aptic dysfunction can be imaged beginning at preclinical stages.
28 anifestations of CTE, including clinical and preclinical stages.
29  hippocampal atrophy differ based on initial preclinical staging.
30 biomarkers, individuals were classified into preclinical stage 0 (Abeta-/ND-), 1 (Abeta+/ND-), or 2+
31  3) in patients 8 years of age or older with preclinical (stage 2) disease.
32 derate dementia from AD (AD(2)) and at their preclinical stage 3 to 8 yr earlier (AD(1)), with no dif
33 y are to evaluate the rate of progression of preclinical (Stage A and B) heart failure, identify asso
34 only about half of the compounds in advanced preclinical stages actually enter human trials.
35 nt, fully penetrant retinal dystrophy with a preclinical stage, an onset after the age of 30 years, a
36 ncreases in the whole AD continuum since the preclinical stage and represents a promising biomarker o
37  preselection and evaluation of drugs at the preclinical stage and the testing of putative neuroprote
38 rk deterioration on memory impairment in the preclinical stage, and a biphasic influence of the angul
39 tial dysbiosis in high-risk individuals at a preclinical stage, and therapeutically target pathogenic
40 ies are being developed and evaluated at the preclinical stage, and will lead to clinical trials in t
41 nt without metabolic consequences until late preclinical stages,and it remains unknown how early in t
42  Several promising therapeutic strategies in preclinical stages are identified.
43 but can emerge earlier in prodromal and even preclinical stages as part of mild behavioural impairmen
44 f CNS autoimmune demyelination including its preclinical stage at least in the primate MS model.
45 c co glycolic acid (PLGA) was chosen in this preclinical stage because it is readily translatable to
46          Autoimmune diseases often exhibit a preclinical stage before diagnosis.
47 s, especially if they can be identified in a preclinical stage by the development of antecedent bioma
48 in early childhood, can be identified in the preclinical stages by the detection of catecholamines in
49                     Brain alterations in the preclinical stage can be detected by structural MRI.
50 arly detection of brain abnormalities at the preclinical stage can be useful for developing preventiv
51 therapeutic index of a range of clinical and preclinical stage cancer chemotherapeutics.
52                 Alzheimer disease has a long preclinical stage characterized by beta-amyloid (Abeta)
53 liest solid tumor, is still incurable in the preclinical stages due to multifacet stroma, dense desmo
54               Testing IgE sensitization at a preclinical stage facilitates prediction of seasonal all
55 omise for precise diagnostics, especially at preclinical stages, facilitating personalized patient ma
56  0.838) in discriminating lung cancer at the preclinical stage from matched controls.
57 and mitigation of immunogenicity risk at the preclinical stage has the potential to reduce the incide
58 n insulin-resistant individuals at an early, preclinical stage, ie, well before the development of gl
59 g autoaggressive process beneficially at the preclinical stage, if produced at the correct location,
60 ary age-related tauopathy, likely already in preclinical stages in individuals with low Abeta patholo
61  nuclear antigen reactivity particularly, at preclinical stages/in at-risk subjects could be predicti
62 ibitors, along with a repertoire of clinical/preclinical stage kinase inhibitors that possess antivir
63  understanding of these relationships in the preclinical stage may advance our mechanistic understand
64                                           In preclinical stage mostly small molecule New Chemical Ent
65                    Amyloid deposition in the preclinical stage of AD appears to be associated with wo
66 ication, for identifying participants at the preclinical stage of AD who may be at risk for cognitive
67  suggest the presence of brain damage in the preclinical stage of AD.
68 as a noninvasive quantitative marker for the preclinical stage of AD.
69 med that plasma p-tau181 is increased at the preclinical stage of Alzheimer and further increases in
70 major growth in Abeta burden occurs during a preclinical stage of Alzheimer disease (AD), prior to th
71                        Given the decade-long preclinical stage of Alzheimer disease, these mechanisms
72 appears at the prodromal and possibly at the preclinical stage of Alzheimer's disease, and seems to p
73 nale for boosting TREM2 functions during the preclinical stage of Alzheimer's disease.
74 ions, most PROTACs do not make it beyond the preclinical stage of drug development.
75 ct subtle pathophysiological features in the preclinical stage of hypertension.
76             Other approaches, which are in a preclinical stage of investigation, include treatment wi
77 s and cortex of APP23 transgenic mice at the preclinical stage of the disease.
78 e estimates for clinical trials aimed at the preclinical stage of the disorder (HCs with evidence of
79 thus may provide protection against Abeta in preclinical stages of AD and other neurodegenerative pro
80     Conclusions and Relevance: More advanced preclinical stages of AD have greater longitudinal Abeta
81 fted to targeting at-risk populations in the preclinical stages of AD thus improved predictive marker
82 au217 levels were increased during the early preclinical stages of AD when insoluble tau aggregates w
83                                           In preclinical stages of AD, the cells of origin for the pe
84  the subtle VSTM impairments observed in the preclinical stages of AD.
85  tau are necessary for memory decline in the preclinical stages of AD.
86 lion cells may be affected very early at the preclinical stages of AD.
87 cal metrics of DTI tractography, even in the preclinical stages of AD.
88 r, accentuated early endosome enlargement at preclinical stages of AD.
89 which the hippocampus becomes hyperactive in preclinical stages of Alzheimer's disease (AD) have thus
90 efects and axonopathy are prominent in early preclinical stages of Alzheimer's disease (AD), often pr
91 -inositol and other metabolites occur in the preclinical stages of Alzheimer's disease associated wit
92 gm can detect metabolic abnormalities in the preclinical stages of Alzheimer's disease despite normal
93 sponse to amyloid-related neuronal injury in preclinical stages of Alzheimer's disease, but is relate
94 ting neuroinflammatory process is present at preclinical stages of Alzheimer's disease.
95 r evaluation may help identify people in the preclinical stages of Alzheimer's disease.
96 me therefore represents a model for studying preclinical stages of Alzheimer's disease.
97  comorbidities and their risk factors in the preclinical stages of chronic obstructive pulmonary dise
98 comorbid diseases were more prevalent in the preclinical stages of COPD and smokers without COPD.
99  placed on programs that reached clinical or preclinical stages of development.
100 t useful for vaccine candidates currently in preclinical stages of development.
101                                           In preclinical stages of diagnostic or therapeutic developm
102 use models of RA and investigations into the preclinical stages of disease also support the hypothesi
103 trullinated protein antibodies (ACPA) during preclinical stages of disease and accumulation of hyperc
104  and in turn prevent overt IDDM at different preclinical stages of disease development.
105 linical trials in at-risk individuals during preclinical stages of disease progression.
106  NOD female mice representing early and late preclinical stages of disease were treated with mouse an
107 ent in pyramidal neurons of the neocortex at preclinical stages of disease when Alzheimer-like neurop
108 seline CRP (i.e., levels manifest during the preclinical stages of disease).
109  therapeutic trials by shifting focus to the preclinical stages of disease.
110 hnology can have critical roles in different preclinical stages of drug development and highlight the
111 alternative guide for drug therapy at early, preclinical stages of graft rejection and for evaluating
112 iabetes in NOD mice treated at early or late preclinical stages of IDDM.
113 n changes in aging may provide insights into preclinical stages of neurodegenerative diseases.
114 eviously found to contribute to the earliest preclinical stages of pancreatic beta cell destruction.
115 munity and which appear to be present in the preclinical stages of RA.
116 shift in functional microglial phenotypes in preclinical stages of superoxide dismutase 1 (SOD1)-muta
117 he neurovascular alterations observed in the preclinical stages of tauopathies.
118 fective, this therapy should be given in the preclinical stages of the disease, which are assessed mo
119 hypertension, but its role as a biomarker of preclinical stages of this disease has not been investig
120 velopment may permit recognition of early or preclinical stages of vascular contributions to cognitiv
121 s the field begins to test the concept of a "preclinical" stage of neurodegenerative disease, when th
122 ly detection of autoimmunity, potentially at preclinical stages, offers a window of opportunity for t
123 cal and neuropathological changes during the preclinical stages (onset approximately 24-30 months of
124 beta and their receptors was examined at the preclinical stage, onset, peak, and recovery by RT-PCR a
125 nt of multiple ZIKV vaccines that are at the preclinical stage or in early-stage clinical trials.
126   We found that these cells are sensitive to preclinical stage pharmacological inhibitors of N-myrist
127 s the brain's functional architecture in the preclinical stage, possibly contributing to pathology pr
128 lzheimer disease (AD) pathophysiology at the preclinical stage, prior to the onset of mild cognitive
129  larger cardiac tissue constructs remains in preclinical stages, progress has been achieved in the de
130 e show that (a) sera from FS patients in the preclinical stage recognized epitopes on the COOH-termin
131 from childhood, but the determinants of this preclinical stage remain uncertain.
132                                     The long preclinical stage represents a therapeutic window before
133                                        Later preclinical stages (stages 1 and 2+) had elevated Abeta
134                             We suggest a new preclinical staging system featuring clinical, seeding a
135 ished to give developers of new drugs in the preclinical stage the opportunity to test the metabolism
136 mined cross-sectional associations across AD preclinical stages, those with all biomarkers normal, an
137  drug development pipeline, from 2.0% at the preclinical stage to 8.2% among mechanisms for approved
138  biological continuum, from its asymptomatic preclinical stage to its clinically overt dementia stage
139 anslating these promising therapies from the preclinical stage to the clinic, especially for genome e
140 urred in microglial activity during the late preclinical stage, transitioning from PrPSc uptake to es
141 icancer activity are often developed through preclinical stages using response criteria observed in c
142 stand their relationship during the earliest preclinical stages, we investigated baseline CSF markers
143                    Alzheimer's disease has a preclinical stage when cerebral amyloid-B deposition occ
144  and tissue engineering could be used at the preclinical stage where attrition rates are high.
145 to market involves many steps, including the preclinical stage, where various properties of the drug
146 of immediate free recall/new learning at the preclinical stage, which is mediated by progressive atro
147 romote specific CD4+ T-cell responses in the preclinical stage, while in MCI it may be important to t
148 novel antigens, adjuvants and vectors in the preclinical stage with computational analyses of clinica
149 ed by UAAs impact the progress of analogs in preclinical stages with an emphasis on the role played b

 
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