Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Amnestic mild cognitive impairment (aMCI) can be classified into single domain (S-aMCI) and multiple domain (M-aMCI) subtypes. However, there have been no studies that specifically investigate the structural differences that support this classification. In an attempt to compare regional cortical thickness in two subtypes of aMCI, we aimed to map the distribution of cortical thinning using a surface based cortical analysis of magnetic resonance imaging. The cortical thickness across the entire brain was measured in 9 patients with S-aMCI, 22 patients with M-aMCI, and 61 normal healthy subjects. Differences in the patterns of cortical thinning between S-aMCI and M-aMCI were assessed using ANCOVA on a vertex-by-vertex basis, and statistical maps of differences in cortical thickness between the groups were constructed using a surface model. Relative to controls, S-aMCI patients showed cortical thinning in the left medial temporal lobe, and M-aMCI patients showed cortical thinning in the left medial temporal lobe, precuneus, and anterior and inferior basal temporal, insular, and temporal association cortices. When the two MCI groups were directly compared, M-aMCI patients showed cortical thinning in left precuneus. Our studies suggest that M-aMCI is a transitional state between S-aMCI and Alzheimer's disease, and that the cortical thinning is evidence that the precuneus is responsible for the multiple cognitive impairments in M-aMCI.
 ...
PMID:Cortical thickness in single- versus multiple-domain amnestic mild cognitive impairment. 1745 30

The volume of parcellated cortical regions is a composite measure related to both thickness and surface area. It is not clear whether volumetric decreases in medial temporal lobe (MTL) cortical regions in aging and Alzheimer's disease (AD) are due to thinning, loss of surface area, or both, nor is it clear whether aging and AD differ in their effects on these properties. Participants included 28 Younger Normals, 47 Older Normals, and 29 patients with mild AD. T1-weighted MRI data were analyzed using a novel semi-automated protocol (presented in a companion article) to delineate the boundaries of entorhinal (ERC), perirhinal (PRC), and posterior parahippocampal (PPHC) cortical regions and calculate their mean thickness, surface area, and volume. Compared to Younger Normals, Older Normals demonstrated moderately reduced ERC and PPHC volumes, which were due primarily to reduced surface area. In contrast, the expected AD-related reduction in ERC volume was produced by a large reduction in thickness with minimal additional effect (beyond that of aging) on surface area. PRC and PPHC also showed large AD-related reductions in thickness. Of all these MTL morphometric measures, ERC and PRC thinning were the best predictors of poorer episodic memory performance in AD. Although the volumes of MTL cortical regions may decrease with both aging and AD, thickness is relatively preserved in normal aging, while even in its mild clinical stage, AD is associated with a large degree of thinning of MTL cortex. These differential morphometric effects of aging and AD may reflect distinct biologic processes and ultimately may provide insights into the anatomic substrates of change in memory-related functions of MTL cortex.
 ...
PMID:Differential effects of aging and Alzheimer's disease on medial temporal lobe cortical thickness and surface area. 1786 84

Amyloid-beta peptide (A beta) is considered a triggering agent of Alzheimer's disease. In relation to a therapeutic treatment of the disease, the interaction of A beta with the cell membrane has to be elucidated at the molecular level to understand its mechanism of action. In previous works, we had ascertained by neutron diffraction on stacked lipid multilayers that a toxic fragment of A beta is able to penetrate and perturb the lipid bilayer. Here, the influence of A beta(1-42), the most abundant A beta form in senile plaques, on unilamellar lipid vesicles of phospholipids is investigated by small-angle neutron scattering. We have used the recently proposed separated form factor method to fit the data and to obtain information about the vesicle diameter and structure of the lipid bilayer and its change upon peptide administration. The lipid membrane parameters were obtained with different models of the bilayer profile. As a result, we obtained an increase in the vesicle radii, indicating vesicle fusion. This effect was particularly enhanced at pH 7.0 and at a high peptide/lipid ratio. At the same time, a thinning of the lipid bilayer occurred. A fusogenic activity of the peptide may have very important consequences and may contribute to cytotoxicity by destabilizing the cell membrane. The perturbation of the bilayer structure suggests a strong interaction and/or insertion of the peptide into the membrane, although its localization remains beyond the limit of the experimental resolution.
 ...
PMID:Membrane fusogenic activity of the Alzheimer's peptide A beta(1-42) demonstrated by small-angle neutron scattering. 1816 13

In vivo measurement of cortical thickness is a sensitive representation of pathology in neurodegenerative disorders which primarily target the gray mantle. In this study we used magnetic resonance images to describe the patterns of cortical thinning in 11 frontotemporal dementia (FTD), 38 Alzheimer's disease (AD) and 34 healthy elderly (H(E)) subjects. AD and FTD displayed significant thinning of the cortical mantle compared to the H(E) group, but with distinctive distributions. AD subjects had significantly thinner cortex in all lobes whereas FTD compared to H(E) showed significant differences only in specific regions of frontal and temporal lobes. When compared to AD, the FTD subjects had a trend of thinner cortex in the anterior cingulate region and in selective regions of anterior frontal and temporal regions. In conclusion, the cortical thinning in dementia when compared to H(E), is disease specific whereby FTD subjects display a pattern distinct than that seen in Alzheimer's disease.
 ...
PMID:Patterns of cortical thinning in Alzheimer's disease and frontotemporal dementia. 1826 28

Previous magnetic resonance imaging (MRI) studies have used volumetric methods to investigate cerebral atrophy and showed its linear pattern with the measure of dementia severity in Alzheimer's disease (AD). This study analyzed the phase- and region-specific changes in cortical thickness with dementia severity. In 43 normal controls and 60 AD patients with clinical dementia rating (CDR) (0.5, n=21; 1, n=28; 2, n=11), the cortical thickness was measured using automated surface-based analysis of MRI data. Statistical analyses were performed to investigate overall the hemispheric mean thicknesses as well as the topography of cortical atrophy based on vertices in the groups. No significant difference in cortical thickness was observed for the mild (from CDR=0.5 to 1) stage of dementia. In contrast, a significant reduction of cortical thickness occurred from CDR=1 to 2. Topographic analysis of cortical atrophy showed that the significant cortical thinning in CDR=0.5 relative to normal was found in most association cortices, with this being more extensive than previously reported. There were significant cortical atrophies between CDR=1 and 2 in the frontal, inferolateral temporal, inferior parietal lobule, medial occipital, and posterior-cingulated regions. Our results confirm and extend previous findings, suggesting that widespread cortical thinning occurs before the onset of dementia (from normal to CDR=0.5), and that once dementia starts, cortical atrophy in association cortices accelerates in moderate AD (from CDR=1 to 2).
 ...
PMID:Variations in cortical thickness with dementia severity in Alzheimer's disease. 1840 Mar 96

Alzheimer's disease (AD) is associated with neurodegeneration in vulnerable limbic and heteromodal regions of the cerebral cortex, detectable in vivo using magnetic resonance imaging. It is not clear whether abnormalities of cortical anatomy in AD can be reliably measured across different subject samples, how closely they track symptoms, and whether they are detectable prior to symptoms. An exploratory map of cortical thinning in mild AD was used to define regions of interest that were applied in a hypothesis-driven fashion to other subject samples. Results demonstrate a reliably quantifiable in vivo signature of abnormal cortical anatomy in AD, which parallels known regional vulnerability to AD neuropathology. Thinning in vulnerable cortical regions relates to symptom severity even in the earliest stages of clinical symptoms. Furthermore, subtle thinning is present in asymptomatic older controls with brain amyloid binding as detected with amyloid imaging. The reliability and clinical validity of AD-related cortical thinning suggests potential utility as an imaging biomarker. This "disease signature" approach to cortical morphometry, in which disease effects are mapped across the cortical mantle and then used to define ROIs for hypothesis-driven analyses, may provide a powerful methodological framework for studies of neuropsychiatric diseases.
 ...
PMID:The cortical signature of Alzheimer's disease: regionally specific cortical thinning relates to symptom severity in very mild to mild AD dementia and is detectable in asymptomatic amyloid-positive individuals. 1863 39

The goal of this project was to utilize an information theoretic formalism for medical image analysis initially proposed in [Young et al. (2005): Phys Rev Lett 94:098701-1] to detect and quantify subtle global and regional differences in spatial patterns in patients suffering from Alzheimer's disease (AD) and frontotemporal dementia (FTD) by estimating the structural complexity of anatomical brain MRI. The sensitivity and specificity of the results are compared with those of a recent analysis, currently considered state of the art for MR studies of neurodegeneration. The previous study used regional estimates of cortical thinning and/or volume loss to differentiate between normal aging, AD, and FTD. The analysis illustrates that the structural complexity estimation method, a general multivariate approach to the study of variation in brain structure which does not depend on highly specialized volumetric and thickness estimates, is capable of providing sensitive and interpretable diagnostic information.
 ...
PMID:Patterns of structural complexity in Alzheimer's disease and frontotemporal dementia. 1867 45

Accurate cortical thickness estimation in-vivo is important for the study of many neurodegenerative diseases. When using magnetic resonance images (MRI), accuracy may be hampered by artifacts such as partial volume (PV) as the cortex spans only a few voxels. In zones of opposed sulcal banks (tight sulci) the measurement can be even more difficult. The aim of this work is to propose a voxel-based cortical thickness estimation method from MR by integrating a mechanism for correcting sulci delineation after an improved partial volume classification. First, an efficient and accurate framework was developed to enhance partial volume classification with structural information. Then, the correction of sulci delineation is performed after a homotopic thinning of a cost function image. Integrated to our voxel-based cortical thickness estimation pipeline, the overall method showed a better estimate of thickness and a high reproducibility on real data (R2 > 0.9). A quantitative analysis on clinical data from an Alzheimer's disease study showed significant differences between normal controls and Alzheimer's disease patients.
 ...
PMID:Automatic delineation of sulci and improved partial volume classification for accurate 3D voxel-based cortical thickness estimation from MR. 1897 55

Cerebral volume loss has long been associated with normal aging, but whether this is due to aging itself or to age-related diseases, including incipient Alzheimer disease, is uncertain. To understand the changes that occur in the aging brain, we examined the cerebral cortex of 27 normal individuals ranging in age from 56 to 103 years. None fulfilled the criteria for the neuropathologic diagnosis of Alzheimer disease or other neurodegenerative disease. Seventeen of the elderly participants had cognitive testing an average of 6.7 months prior to death. We used quantitative approaches to analyze cortical thickness, neuronal number, and density. Frontal and temporal neocortical regions had clear evidence of cortical thinning with age, but total neuronal numbers in frontal and temporal neocortical regions remained relatively constant during a 50-year age range. These data suggest that loss of neuronal and dendritic architecture, rather than loss of neurons, underlies neocortical volume loss with increasing age in the absence of Alzheimer disease.
 ...
PMID:Preservation of neuronal number despite age-related cortical brain atrophy in elderly subjects without Alzheimer disease. 1901 41

The aim of this study was to investigate the effect of demographic factors (age of onset, sex and years of education) on the distribution of cortical thickness in a large sample of patients with Alzheimer's disease (AD). The study participants consisted of 193 AD patients and 142 controls with no cognitive impairment (NCI) that were measured with cortical thickness across the entire brain. The effects of demographic factors on cortical thickness were analyzed by applying linear regression after controlling confounding factors. Older individuals in NCI group showed more cortical thinning in frontal, temporal association cortices and insula than younger participants. Early onset AD was associated with cortical thinning in the parietal lobe, whereas late onset AD was associated with cortical thinning in the medial temporal region. The NCI group demonstrated sex-related differences in cortical thickness, although those differences were not present in the AD group. While the education effect was absent in NCI individuals, high levels of education in the AD group correlated with cortical thinning in the frontal and temporoparietal association cortices. Our results show that AD with earlier onset and higher education had suffered more pronounced cortical atrophy in specific parts of the brain than their counterparts, which may be related to cognitive reserve theory.
 ...
PMID:Effects of demographic factors on cortical thickness in Alzheimer's disease. 1932 Dec 33


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>