Cerebrospinal fluid tau/beta-amyloid(42) ratio as a prediction of cognitive decline in nondemented older adults.

By Anne M. Fagan, C. Roe, C. Xiong, Mark A. Mintun, John C. Morris, D. Holtzman. Archives of Neurology, 2007

947 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Physiology, Psychiatry and Mental health

View Paper: https://www.semanticscholar.org/paper/c4b562733c411c5d484eb3b943e272253f42e920

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Citations in the corpus

Human apoE isoforms differentially regulate brain amyloid-β peptide clearance (2011, neutral): “Several groups have now validated molecular and neuroimaging biomarkers of the neuropathological hallmarks of AD (15-19).”
PET Imaging of Tau Deposition in the Aging Human Brain (2016, neutral): “We also found that global Ab was related to retrospective longitudinal decline in global cognition, consistent with findings from a series of studies using CSF and PET measures of Ab in relation to cognitive performance (Fagan et al., 2007; Landau et al., 2012; Villemagne et al., 2013).”
In Vivo Imaging of Amyloid Deposition in Alzheimer’s Disease using the Novel Radioligand [18F]AV-45 (Florbetapir F 18) (2010, background): “Although cerebrospinal fluid Ab levels are reliably decreased in AD (6), cerebrospinal fluid studies are inevitably indirect markers.”
Brain imaging in Alzheimer disease. (2012, background): “…in CSF Ab42 appear to occur early (at least as early as changes in amyloid PET) and precipitously— achieving its final level very early in the course of the pathophysiological spectrum of AD— probably presymptomatically (Blennow and Hampel 2003; Hansson et al. 2006; Fagan et al. 2007, 2009).”
Alzheimer’s Disease: The Challenge of the Second Century (2011, background): “Support that these biomarker changes are clinically relevant comes from data showing that, in cognitively normal elderly individuals, a high ratio of CSF tau/Ab42 and a high level of cerebral Ab burden as shown by amyloid radiotracers both predict conversion to MCI (208) or to very mild dementia ove”
Multi-modal techniques for diagnosis and prognosis of Alzheimer’s disease (2009, background): “In several longitudinal studies, especially when combined with information about the levels of tau or phosphorylated tau in the cerebrospinal fluid, cerebrospinal-fluid Aβ 42 has shown a capacity to predict progression from cognitive normalcy to mild cognitive impairment or dementia of the Alzheime”
Toward defining the preclinical stages of Alzheimer's disease: Recommendations from the National Institute on Aging-Alzheimer's Association workgroups on diagnostic guidelines for Alzheimer's disease (2011, background): “A few early studies have reported that Aβ positivity in clinically normal older individuals is associated with an increased rate of atrophy [55] and an increased risk of cognitive decline and progression to dementia [56–62].”
The evolution of preclinical Alzheimer’s disease: Implications for prevention trials (2014, neutral): “Existing CSF tau measures have been quite valuable in the prediction of cognitive decline among Ab+ CN (Desikan et al., 2012; Fagan et al., 2007), and increases in CSF tau do correlate with Tau pathologic burden at postmortem overall (Tapiola et al.”
Cerebrospinal fluid levels of β-amyloid 1-42, but not of tau, are fully changed already 5 to 10 years before the onset of Alzheimer dementia. (2012, background): “Thus, A 42 levels probably decrease very early during the pathogenesis of AD and reach plateau levels long before dementia develops, maybe even during presymptomatic stages, that is, before any cognitive symptoms are recognized by the affected individual.(30,31) In contrast, the finding that late co”