Diffusion Tensor Imaging of Normal-Appearing White Matter in Mild Cognitive Impairment and Early Alzheimer Disease: Preliminary Evidence of Axonal Degeneration in the Temporal Lobe

Huang, Juebin; Friedland, Robert P.; Auchus, Alexander P.

doi:10.3174/ajnr.a0700

Cited by 204 publications

(156 citation statements)

References 50 publications

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“…The involvement of this tract as well as the CC, fornix, perforant path, and temporal WM is consistent with previous findings from DTI studies that reported diffusivity increases or anisotropy decreases in the same set of WM areas (Fellgiebel et al, 2004;Medina et al, 2006;Xie et al, 2006;Huang et al, 2007;Teipel et al, 2007;Zhang et al, 2007). Atrophy of the CC and perforant path have also already been highlighted in previous VBM studies of AD (Chaim et al, 2007) and MCI (Stoub et al, 2006), respectively.…”

Section: Discussionsupporting

confidence: 79%

Relationships between Hippocampal Atrophy, White Matter Disruption, and Gray Matter Hypometabolism in Alzheimer's Disease

Villain¹,

Desgranges²,

Viader³

et al. 2008

Journal of Neuroscience

338

243

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In early Alzheimer's disease (AD), the hippocampal region is the area most severely affected by cellular and structural alterations, yet glucose hypometabolism predominates in the posterior association cortex and posterior cingulate gyrus. One prevalent hypothesis to account for this discrepancy is that posterior cingulate hypometabolism results from disconnection from the hippocampus through disruption of the cingulum bundle. However, only partial and indirect evidence currently supports this hypothesis. Thus, using structural magnetic resonance imaging and 2-[ 18 F]fluoro-2-deoxy-D-glucose positron emission tomography in 18 patients with early AD, we assessed the relationships between hippocampal atrophy, white matter integrity, and gray matter metabolism by means of a whole-brain voxel-based correlative approach. We found that hippocampal atrophy is specifically related to cingulum bundle disruption, which is in turn highly correlated to hypometabolism of the posterior cingulate cortex but also of the middle cingulate gyrus, thalamus, mammillary bodies, parahippocampal gyrus, and hippocampus (all part of Papez's circuit), as well as the right temporoparietal associative cortex. These results provide the first direct evidence supporting the disconnection hypothesis as a major factor contributing to the early posterior hypometabolism in AD. Disruption of the cingulum bundle also appears to relate to hypometabolism in a large connected network over and above the posterior cingulate cortex, encompassing the whole memory circuit of Papez (consistent with the key location of this white matter tract within this loop) and also, but indirectly, the right posterior association cortex.

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Section: Discussionsupporting

confidence: 79%

Relationships between Hippocampal Atrophy, White Matter Disruption, and Gray Matter Hypometabolism in Alzheimer's Disease

Villain¹,

Desgranges²,

Viader³

et al. 2008

Journal of Neuroscience

338

243

View full text Add to dashboard Cite

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“…It has been shown to be susceptible to atrophy in AD, mainly as a correlate of wallerian degeneration of commissural nerve fibers of the neocortex. 25,27 It is generally assumed that there is a topographic arrangement of axons within the CC, according to their origin, that could justify its texture differences in healthy controls and patients with AD, whose callosal atrophy might be restricted just to axons proceeding from atrophic temporal structures, for example, as shown in a diffusion tensor study by Huang et al 35 In fact, our study found significant differences among the 3 groups for the CC (Table 1), in 6/44 texture parametersnamely, the contrast (for distances 1 and 2) and difference variance (for all distances) parameters. It is better to have fewer significant parameters because in an ideal situation, we would like to have a unique descriptor extracted from the images that could indicate the presence or absence of tissue alterations.…”

Section: Discussionmentioning

confidence: 99%

MR Imaging Texture Analysis of the Corpus Callosum and Thalamus in Amnestic Mild Cognitive Impairment and Mild Alzheimer Disease

Oliveira¹,

Balthazar²,

D’Abreu³

et al. 2010

AJNR Am J Neuroradiol

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BACKGROUND AND PURPOSE:TA is a branch of image processing that seeks to reduce image information by extracting texture descriptors from the image. TA of MR images of anatomic structures in mild AD and aMCI is not well-studied. Our objective was to attempt to find differences among patients with aMCI and mild AD and normal-aging subjects, by using TA applied to the MR images of the CC and the thalami of these groups of subjects.

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“…Abnormal DT derived indices have also been demonstrated in frontal region, and specifically in the cingulum posterior, corpus callosum, fasciculus longitudinalis superior, and fasciculus uncinatus [193][194][195].…”

Section: Diffusion Tensor Imagingmentioning

confidence: 99%

Perspective on future role of biological markers in clinical therapy trials of Alzheimer's disease: A long-range point of view beyond 2020

Hampel

Lista

Teipel

et al. 2014

Biochemical Pharmacology

105

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Recent advances in understanding the molecular mechanisms underlying various paths toward the pathogenesis of Alzheimer's disease (AD) has begun to provide new insight for interventions to modify disease progression. The evolving knowledge gained from multidisciplinary basic research has begun to identify new concepts for treatments and distinct classes of therapeutic targets; as well as putative disease-modifying compounds that are now being tested in clinical trials. There is a mounting consensus that such disease modifying compounds and/or interventions are more likely to be effectively administered as early as possible in the cascade of pathogenic processes preceding and underlying the clinical expression of AD. The budding sentiment is that "treatments" need to be applied before various molecular mechanisms converge into an irreversible pathway leading to morphological, metabolic and functional alterations that characterize the pathophysiology of AD. In light of this, biological indicators of pathophysiological mechanisms are desired to chart and detect AD throughout the asymptomatic early molecular stages into the prodromal and early dementia phase. A major conceptual development in the clinical AD research field was the recent proposal of new diagnostic criteria, which specifically incorporate the use of biomarkers as defining criteria for preclinical stages of AD. This paradigm shift in AD definition, conceptualization, operationalization, detection and diagnosis represents novel fundamental opportunities for the modification of interventional trial designs. This perspective summarizes not only present knowledge regarding biological markers but also unresolved questions on the status of surrogate indicators for detection of the disease in asymptomatic people and diagnosis of AD

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Diffusion Tensor Imaging of Normal-Appearing White Matter in Mild Cognitive Impairment and Early Alzheimer Disease: Preliminary Evidence of Axonal Degeneration in the Temporal Lobe

Cited by 204 publications

References 50 publications

Relationships between Hippocampal Atrophy, White Matter Disruption, and Gray Matter Hypometabolism in Alzheimer's Disease

Relationships between Hippocampal Atrophy, White Matter Disruption, and Gray Matter Hypometabolism in Alzheimer's Disease

MR Imaging Texture Analysis of the Corpus Callosum and Thalamus in Amnestic Mild Cognitive Impairment and Mild Alzheimer Disease

Perspective on future role of biological markers in clinical therapy trials of Alzheimer's disease: A long-range point of view beyond 2020

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