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

In this study, we analyzed differences in cortical thickness (CTH) between healthy controls (HC), subjects with stable mild cognitive impairment (S-MCI), progressive MCI (P-MCI), and Alzheimer's disease (AD), and assessed correlations between CHT and clinical disease severity, education, and apolipoprotein E4 (APOE) genotype. Automated CTH analysis was applied to baseline high-resolution structural MR images of 145 subjects with a maximum followup time of 7.4 years pooled from population-based study databases held in the University of Kuopio. Statistical differences in CTH between study groups and significant correlations between CTH and clinical and demographic factors were assessed and displayed on a cortical surface model. Compared to HC group (n = 26), the AD (n = 21) group displayed significantly reduced CTH in several areas of frontal and temporal cortices of the right hemisphere. Higher education and lower MMSE scores were correlated with reduced CTH in the AD group, whereas no significant correlation was found between CDR-SB scores or APOE genotype and CTH. The P-MCI group demonstrated significantly reduced CTH compared to S-MCI in frontal, temporal and parietal cortices even after statistically adjusting for all confounding variables. Ultimately, analysis of CTH can be used to detect cortical thinning in subjects with progressive MCI several years before conversion and clinical diagnosis of AD dementia, irrespective of their cognitive performance, education level, or APOE genotype.
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PMID:Differences in cortical thickness in healthy controls, subjects with mild cognitive impairment, and Alzheimer's disease patients: a longitudinal study. 2150 34

Mild cognitive impairment (MCI) may affect multiple neuropsychological domains. While amnestic MCI is associated with Alzheimer's disease, patterns of brain pathology in non-amnestic subtypes have been less studied. Twenty-three patients with attention/executive MCI (a/e MCI), seen at a university-based memory clinic, and 23 normal controls, matched according to age, gender, and education, were included in this study. All subjects were assessed with a neuropsychological test battery, including tests of memory, attention and executive function, and underwent magnetic resonance imaging. Diffusion tensor imaging derived white matter (WM) tract radial and mean diffusivity (DR and MD) were assessed using Tract-Based Spatial Statistics, and cortical thickness (CTH) was assessed using FreeSurfer. This study investigated changes of WM DR/MD and CTH in subjects with a/e MCI, and associations between these changes and different a/e subfunctions. WM DR/MD underlying rostral middle frontal, medial orbitofrontal, caudal anterior cingulate, posterior cingulate, retrosplenial and entorhinal cortices was higher for the a/e MCI than the control group, but CTH was not different from controls in any of the regions. WM DR/MD underlying superior frontal, rostral middle frontal, lateral/medial orbitofrontal and retrosplenial cortices were significantly associated with inhibition/switching performance, while caudal middle frontal CTH was significantly associated with attention and divided attention in the patient group. We conclude that increased WM DR/MD in frontal and cingulate regions and cortical thinning in caudal middle frontal region are both associated with executive dysfunction in MCI.
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PMID:Executive dysfunction in mild cognitive impairment is associated with changes in frontal and cingulate white matter tracts. 2184 Dec 61

The amnestic form of mild cognitive impairment (aMCI) is likely a precursor of Alzheimer disease (AD). Both verbal and visual memory tests are used in the diagnosis of aMCI; however, it is unknown which type of test is superior at predicting the underlying pathologic changes associated with AD. In this study, we compared the topography of cortical thinning among 3 subtypes of patients with aMCI: 33 patients with predominant verbal memory impairment (verbal-aMCI), 35 with predominant visual memory impairment (visual-aMCI), and 56 with both verbal and visual memory-predominant impairment (both-aMCI), and 143 patients with normal cognition. As a result, patients with verbal-aMCI showed cortical thinning in the left anterior and medial temporal regions compared with individuals with normal cognition, while those with visual-aMCI did not show significant cortical thinning. The cortical thinning areas of both-aMCI group overlapped those of verbal-aMCI but were more widespread involving the bilateral temporal regions. These findings suggest that the verbal-aMCI and both-aMCI are more likely to be a precursor of AD than visual-aMCI, and that both-aMCI may be more advanced subtype than verbal-aMCI on the spectrum from MCI to AD.
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PMID:Cortical thinning in verbal, visual, and both memory-predominant mild cognitive impairment. 2186 81

Submicroscopic deletions involving chromosome 1q43-q44 result in cognitive impairment, microcephaly, growth restriction, dysmorphic features, and variable involvement of other organ systems. A consistently observed feature in patients with this deletion are the corpus callosal abnormalities (CCAs), ranging from thinning and hypoplasia to complete agenesis. Previous studies attempting to delineate the critical region for CCAs have yielded inconsistent results. We conducted a detailed clinical and molecular characterization of seven patients with deletions of chromosome 1q43-q44. Using array comparative genomic hybridization, we mapped the size, extent, and genomic content of these deletions. Four patients had CCAs, and shared the smallest region of overlap that contains only three protein coding genes, CEP170, SDCCAG8, and ZNF238. One patient with a small deletion involving SDCCAG8 and AKT3, and another patient with an intragenic deletion of AKT3 did not have any CCA, implying that the loss of these two genes is unlikely to be the cause of CCA. CEP170 is expressed extensively in the brain, and encodes for a protein that is a component of the centrosomal complex. ZNF238 is involved in control of neuronal progenitor cells and survival of cortical neurons. Our results rule out the involvement of AKT3, and implicate CEP170 and/or ZNF238 as novel genes causative for CCA in patients with a terminal 1q deletion.
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PMID:Delineation of a deletion region critical for corpus callosal abnormalities in chromosome 1q43-q44. 2193 13

Cardiovascular risk factors are associated with cognitive impairments. However, the effects of cardiovascular risk factors on the topography of cortical thinning have not yet been studied in patients with mild cognitive impairment (MCI) or dementia. Thus, we aimed to evaluate the topography of cortical thinning related to cardiovascular risk factors and the relationships among cardiovascular risk factors, white matter hyperintensities (WMH), and cortical atrophy. Participants included 226 patients with Alzheimer disease or subcortical vascular dementia and 135 patients with amnestic MCI or subcortical vascular MCI. We automatically measured the volume of WMH and cortical thickness. Hypertension was associated with cortical thinning in the frontal and perisylvian regions, and cortical thinning related to diabetes mellitus (DM) occurred in the frontal region. In path analyses, hypertension accounted for 0.04 of the frontal thinning with the mediation of WMH and 0.16 without the mediation of WMH. In case of DM, it accounted for 0.02 of the frontal thinning with the mediation of WMH and 0.13 without the mediation of WMH. Hypertension and DM predominantly affected frontal thinning both with and without the mediation of WMH, where the effects without the mediation of WMH were greater than those with the mediation of WMH.
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PMID:Cardiovascular risk factors cause cortical thinning in cognitively impaired patients: relationships among cardiovascular risk factors, white matter hyperintensities, and cortical atrophy. 2194 11

Schizophrenia is a severe psychiatric illness with widespread impairments of cognitive functioning; however, a certain percentage of subjects are known to perform in the normal range on neuropsychological measures. While the cognitive profiles of these individuals have been examined, there has been relatively little attention to the neuroanatomical characteristics of this important subgroup. The aims of this study were to statistically identify schizophrenia subjects with relatively normal cognition, examine their neuroanatomical characteristics relative to their more impaired counterparts using cortical thickness mapping, and to investigate relationships between these characteristics and demographic variables to better understand the nature of cognitive heterogeneity in schizophrenia. Clinical, neuropsychological, and MRI data were collected from schizophrenia (n = 79) and healthy subjects (n = 65). A series of clustering algorithms on neuropsychological scores was examined, and a 2-cluster solution that separated subjects into neuropsychologically near-normal (NPNN) and neuropsychologically impaired (NPI) groups was determined most appropriate. Surface-based cortical thickness mapping was utilized to examine differences in thinning among schizophrenia subtypes compared with the healthy participants. A widespread cortical thinning pattern characteristic of schizophrenia emerged in the NPI group, while NPNN subjects demonstrated very limited thinning relative to healthy comparison subjects. Analysis of illness duration indicated minimal effects on subtype classification and cortical thickness results. Findings suggest a strong link between cognitive impairment and cortical thinning in schizophrenia, where subjects with near-normal cognitive abilities also demonstrate near-normal cortical thickness patterns. While generally supportive of distinct etiological processes for cognitive subtypes, results provide direction for further examination of additional neuroanatomical differences.
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PMID:Cortical thickness in neuropsychologically near-normal schizophrenia. 2198 33

We retrospectively examined the clinical features and the neuroradiological findings on autopsy of 2 cases of young-onset dementia. The patient in case 1 was a 43-year-old woman who was unable to determine the time on the clock and who made frivolous remarks. Neuropsychological test batteries demonstrated memory impairment and frontal lobe dysfunction. T2-weighted magnetic resonance imaging (MRI) of the head revealed abnormal high-intensity signals around the lateral ventricles and thinning of the corpus callosum. Single photon emission computed tomography (SPECT) revealed patchy reduction in the accumulation of tracers in both the frontal lobes. Her neurological condition gradually deteriorated, and she died 13 years after the onset of the disease. She was clinically diagnosed with atypical Alzheimer's disease on the basis of visual cognitive impairment and memory impairment observed in the initial phase. However, the neuropathological diagnosis was adult-onset leukodystrophy with axonal spheroids. The patient in case 2 was a 43-year-old man who had gradually started behaving selfishly and had become ill-tempered and apathetic. He was admitted to a hospital. He was anosognosic and showed frontal lobe dysfunction. T2-weighted MRI scan of the brain showed abnormal high-intensity signals around the lateral ventricles; atrophy of the frontal and temporal lobes, hippocampus, and brainstem; and thinning of the corpus callosum. SPECT revealed patchy reduction in the accumulation of tracers in both the frontal lobes and the cerebellum. His neurological condition gradually deteriorated, and he died after being clinically ill for 7 years. The patient was clinically diagnosed with frontotemporal dementia on the basis of the clinical features and MRI findings. However, the neuropathological diagnosis was chronic meningoencephalitis. The frequency of neurological metabolic and inflammatory diseases is significantly high although it is not as high as that of degenerative diseases in young-onset dementia. Since such diseases may respond to therapy, they should be considered in the differential diagnosis of young-onset dementia, especially in patients presenting with atypical clinical features. Neuroradiological examination may contribute to the differential diagnosis of atypical dementia at young age.
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PMID:[A clinicopathological study of young-onset dementia: report of 2 autopsied cases]. 2198 68

High levels of human immunodeficiency virus (HIV) DNA in peripheral blood mononuclear cells (PBMCs), and specifically within CD14+ blood monocytes, have been found in HIV-infected individuals with neurocognitive impairment and dementia. The failure of highly active antiretroviral therapy (HAART) to eliminate cognitive dysfunction in HIV may be secondary to persistence of HIV-infected PBMCs which cross the blood-brain barrier, leading to perivascular inflammation and neuronal injury. This study assessed brain cortical thickness relative to HIV DNA levels and identified, we believe for the first time, a neuroimaging correlate of detectable PBMC HIV DNA in subjects with undetectable HIV RNA. Cortical thickness was compared between age- and education-matched groups of older (>40 years) HIV-seropositive subjects on HAART who had detectable (N = 9) and undetectable (N = 10) PBMC HIV DNA. Statistical testing revealed highly significant (P < 0.001) cortical thinning associated with detectable HIV DNA. The largest regions affected were in bilateral insula, orbitofrontal and temporal cortices, right superior frontal cortex, and right caudal anterior cingulate. Cortical thinning correlated significantly with a measure of psychomotor speed. The areas of reduced cortical thickness are key nodes in cognitive and emotional processing networks and may be etiologically important in HIV-related neurological deficits.
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PMID:Regional cortical thinning associated with detectable levels of HIV DNA. 2201 79

Patients with probable Alzheimer's disease (AD) and the amnesic form of mild cognitive impairment (aMCI) often demonstrate several types of neuropsychological deficits. These deficits are often related to cortical atrophy, induced by neuronal degradation. The purpose of this study is to investigate whether different anatomic patterns of cortical atrophy are associated with specific neuropsychological deficits. The participants were 170 patients with AD and 99 patients with aMCI. All participants underwent the Seoul Neuropsychological Screening Battery (SNSB), which includes tests that assess attention, language, visuospatial functions, verbal and visual memory, and frontal/executive functions. Cortical atrophy (thinning) was quantified by measuring the thickness of the cortical mantle across the entire brain using automated, three-dimensional magnetic resonance imaging. The relationship between cortical thickness and neuropsychological performance was analysed using stepwise multiple linear regression analyses. These analyses (corrected P<.001) showed that several specific brain regions with cortical thinning were associated with cognitive dysfunction including: digit span backward, verbal and picture recall, naming and fluency, drawing-copying, response inhibition and selective attention. Some of the other functions, however, were not associated with specific foci of cortical atrophy (digit span forward, the word reading portion of the Stroop test, word and picture recognition). Our study, involving a large sample of participants with aMCI and AD, provides support for the postulate that cortical thinning-atrophy in specific anatomic loci are pathological markers for specific forms of cognitive dysfunction.
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PMID:The cortical neuroanatomy of neuropsychological deficits in mild cognitive impairment and Alzheimer's disease: a surface-based morphometric analysis. 2201 76

Prior studies have shown that patients with AD have decreased functional or structural connectivity between the hippocampus and other brain areas. To the best of our knowledge, however, there have been no studies investigating the topography of cortical thinning areas and correlations with HA using surface based morphometry of three-dimensional (3D) T1-weighted magnetic resonance (MR) images. Cortical thickness was measured using SBM, and hippocampal volume was measured using an automated method, in 219 patients with AD and 54 subjects with no cognitive impairment (NCI). A partial correlation model was used in analysis of cortical thinning related to HA. Cortical thinning areas related to HA were found mostly within areas associated with polysynaptic or direct pathways of the hippocampus, a finding consistent with the disconnection hypothesis. Therefore, the cortical atrophy related to HA in patients with AD may represent disrupted cortical brain networks in connection with HA. However, since the topography of HA-related cortical thinning in groups with Clinical Dementia Ratings (CDR) of 0.5 and 1 corresponded to the stages I-II and III-IV of Braak and Braak staging, respectively, we could not exclude the possibility of the "concomitant hypothesis," i.e. that these areas are affected concomitantly with the hippocampus.
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PMID:Topography of cortical thinning areas associated with hippocampal atrophy (HA) in patients with Alzheimer's disease (AD). 2208 36


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