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1 decline of episodic memory is detectable in preclinical Alzheimer's disease.
2 d as a useful population in whom to look for preclinical Alzheimer's disease.
3 y be sensitive to early neurodegeneration of preclinical Alzheimer's disease.
4 either of them was affected in patients with preclinical Alzheimer's disease.
5 ocalise progressive atrophy in patients with preclinical Alzheimer's disease.
6 ker for detecting neurofibrillary tangles in preclinical Alzheimer's disease.
7 nd Abeta42/40) were significantly changed in preclinical Alzheimer's disease.
8 first memory domains to decline in aging and preclinical Alzheimer's disease.
9 e a sensitive marker of cognitive changes in preclinical Alzheimer's disease.
10 o over a period of 240 weeks in persons with preclinical Alzheimer's disease.
11 tical tau pathology and cognitive decline in preclinical Alzheimer's disease.
12 d, in a phase 3 trial involving persons with preclinical Alzheimer's disease.
13 ritical region for rapid tau accumulation in preclinical Alzheimer's disease.
14 etween amyloid and fcMRI in individuals with preclinical Alzheimer's disease.
15 .5 cases, and it is proposed they represent "preclinical" Alzheimer's disease.
16 participants aged 70 years or older, 10% had preclinical Alzheimer's disease, 10.4% had prodromal Alz
17 als who would be categorised as stage 2 or 3 preclinical Alzheimer's disease (A+T+N-, A+T-N+, and A+T
18 effective, noninvasive screening methods for preclinical Alzheimer's disease (AD) and other neurocogn
19 igated the effects of top-down attention and preclinical Alzheimer's disease (AD) pathology on neural
20 ective cognitive decline in normal aging and preclinical Alzheimer's disease (AD) remains to be fully
21 sual short-term memory (VSTM) impairments in preclinical Alzheimer's disease (AD) remains unclear.
22 sized that amyloid-beta and tau pathology in preclinical Alzheimer's disease (AD) spread through func
23 e was to evaluate in normal older adults and preclinical Alzheimer's disease (AD) the impact of amylo
24 n cognitively healthy (CH) participants with preclinical Alzheimer's disease (AD), as classified by c
30 duction therapies, to slow the trajectory of preclinical Alzheimer's disease and delay or prevent the
31 ver, the specific impact of VEGF proteins in preclinical Alzheimer's disease and their relationships
32 g elevated amyloid-beta (Abeta) pathology in preclinical Alzheimer's disease are needed to facilitate
34 roportional hazards modelling indicated that preclinical Alzheimer's disease biomarker status, APOE e
36 However, few studies have evaluated whether preclinical Alzheimer's disease biomarkers predict Alzhe
37 d tau is detrimental to cognitive decline in preclinical Alzheimer's disease during late middle-age.
38 describe our lipidomic approach to detecting preclinical Alzheimer's disease in a group of cognitivel
39 older individuals and a lower prevalence of preclinical Alzheimer's disease in younger groups than p
42 omarkers among dementias and the spectrum of preclinical Alzheimer's disease, mild cognitive impairme
43 hirteen brain regions, three disease stages (preclinical Alzheimer's disease, mild cognitive impairme
44 aimed to characterise how typical ageing and preclinical Alzheimer's disease overlap in terms of beta
45 little is known about its relationships with preclinical Alzheimer's disease pathology and how memory
46 cise intensity and duration, the presence of preclinical Alzheimer's disease pathology, vascular and
51 active option, but none can currently detect preclinical Alzheimer's disease with the required sensit