2016
DOI: 10.2174/1567205013666151218150534
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Structural MRI Biomarkers of Mild Cognitive Impairment from Young Elders to Centenarians

Abstract: Structural MRI distinguishes aMCI, but not naMCI, from CN in elderly individuals. The structures that best distinguish aMCI from CN differ in those <85 from those ≥85, suggesting different neuropathological underpinnings of cognitive impairment in the very old.

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Cited by 13 publications
(13 citation statements)
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“…18 Yang and colleagues found reduced regional temporal and frontal volume reductions among others when comparing patients with aMCI to healthy controls, whereas no significant volumetric differences could be detected between non-aMCI patients and controls. 29 In line with our results and existing PET data, this suggests that brain structure changes in patients with aMCI are less localized than it could be assumed given the characteristic memory impairment.…”
Section: Discussionsupporting
confidence: 91%
“…18 Yang and colleagues found reduced regional temporal and frontal volume reductions among others when comparing patients with aMCI to healthy controls, whereas no significant volumetric differences could be detected between non-aMCI patients and controls. 29 In line with our results and existing PET data, this suggests that brain structure changes in patients with aMCI are less localized than it could be assumed given the characteristic memory impairment.…”
Section: Discussionsupporting
confidence: 91%
“…Cerebrospinal fluid and plasma biomarkers, as well as amyloid imaging markers, can offer information about neuropathological symptoms of AD, when no evidence markers for hippocampal volume loss can be accurately exported from MRI scanning [ 49 ]. Especially structrural MRI biomarkers conclude to major variations among young and elderly populations, associating different neuropathological underpinnings of cognitive impairment in the very old populations [ 50 ].…”
Section: Discussionmentioning
confidence: 99%
“…According to BN theory, if we assume a directed graph G with N nodes, each node n ∈ N has a number of paternal nodes pa(n) that may be linked with “child” nodes and the joint distribution for such a network given as follows: leftPfalse(Nfalse)=nNpfalse(n|pafalse(nfalse)false). By taking into consideration the latest calculations for the relative probabilities of AD progression due to certain brain lesions (Table 2) (Christen, 2000; de la Torre, 2002; Praticò et al, 2002; Modrego and Ferrández, 2004; Hooper et al, 2007; Cheung et al, 2008; Stone, 2008; Schuff et al, 2009; Snider et al, 2009; Wang et al, 2009; Israeli-Korn et al, 2010; Barnes and Yaffe, 2011; Nazem and Mansoori, 2011; Serrano-Pozo et al, 2011; Bird, 2012; Alzheimer's Association, 2015; Chakrabarty et al, 2015) and the majority of the published AD biomarkers (Albert et al, 2010, 2011; Besson et al, 2015; Cabezas-Opazo et al, 2015; Dong et al, 2015; Duce et al, 2015; Eskildsen et al, 2015; Jansen et al, 2015; Madeira et al, 2015; Michel, 2015; Nakanishi et al, 2015; Ossenkoppele et al, 2015; Østergaard et al, 2015; Quiroz et al, 2015; Ringman et al, 2015; Risacher et al, 2015; Sastre et al, 2015; Schindler and Fagan, 2015; Sutphen et al, 2015; Thordardottir et al, 2015; Cauwenberghe et al, 2016; Counts et al, 2016; Gaël et al, 2016; Yang et al, 2016) or calculating indirectly the relative probabilities, we designed a Bayesian model for the prediction of AD based on the abnormal testing of one or more biomarkers. The described probabilities were exported through major clinical trials globally and are continuously subject to updating and redefinition.…”
Section: Methodsmentioning
confidence: 99%