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Background: Computerized cognitive training (CCT) has been proposed as a potential therapy for cognitive decline. One of the benefits of CCT is a transfer effect, but its mechanism on the memory domain is unclear. This study aimed to investigate the transfer effect of non-memory multidomain CCT on the memory domain and its neural basis in patients with mild cognitive impairment (MCI) through a randomized controlled trial., Methods: Patients with MCI recruited from memory clinics were randomly assigned to either the CCT or the control group. The CCT group received multidomain CCT training excluding memory training, while the control group read educational books with learning-based quizzes twice a week for 8 weeks. Participants underwent memory tests yielding a composite score, other cognitive domain tests, non-cognitive scales, and resting-state functional magnetic resonance imaging (rsfMRI), at baseline and after intervention. Within- and between-group comparisons, group × time interactions, and seed-to-voxel analyses in memory-involving brain networks were performed., Results: The CCT group showed improvement over the control group in memory domain (Group × time, F = 5.87, P = 0.03, η 2  = 0.31), which was related with the increased connectivity in the hippocampal-frontal and fusiform-occipital network. No other cognitive and non-cognitive symptoms differed between groups after adjusting for covariates., Conclusion: Eight weeks of multidomain CCT without memory training improved memory function and restored functional network in the hippocampal and medial temporal region in MCI patients. These results can provide evidence for the transferring ability of CCT on memory functioning with its neural basis., (© 2024 The Author(s). Psychogeriatrics published by John Wiley & Sons Australia, Ltd on behalf of Japanese Psychogeriatric Society.)

Background: Metamemory is the process of monitoring and controlling one's memory. Improving metamemory may reduce the memory problem in old age. We hypothesized that metamemory training (MMT) would improve cognition in older adults with subjective memory complaints and change the brain region related to metacognition., Method: We recruited and randomized older adults to the multi-strategic memory training of 10 weekly 90-min sessions, based on the metamemory concept or usual care. Cognitive tests including the Elderly Verbal Learning Test, Simple Rey Figure Test, Digit Span, Spatial Span, Categorical Fluency, and the Boston Naming Test were done in 201 participants, together with magnetic resonance imaging (MRI) in 49 participants before and after training., Results: A total of 112 in the training group and 89 in the control group participated. The training group had a significant increase in long-term delayed free recall, categorical fluency, and the Boston Naming test. In MRI, the mean diffusivity of the bundles of axon tracts passing from the frontal lobe to the posterior end of the lateral sulcus decreased in the training group., Conclusion: These results indicate that the MMT program has a positive impact on enhancing older people' cognitive performance. Improved white matter integrity in the anterior and posterior cerebrum and increased cortical thickness of prefrontal regions, which related to metacognition, possibly suggest that the effects of the MMT would be induced via the enhancement of cognitive control., (© 2019 The Authors. Brain and Behavior published by Wiley Periodicals, Inc.)

The hallmark of atherosclerosis in its early pathogenic process is the overexpression of class A scavenger receptors (SR-A) by activated macrophages. In this study, dextran sulfate-coated superparamagnetic iron oxide nanoparticles (DS-SPIONs), as a magnetic resonance (MR) imaging contrast agent of atherosclerosis, was prepared via the facile co-precipitation method using a versatile double-hydrophilic block copolymer comprising of a DS segment (ligand for SR-A) and a poly(glyclerol methacrylate) segment (SPIONs surface-anchoring unit). The physicochemical properties of the DS-SPIONs were investigated using various instruments. DS-SPIONs exhibited high aqueous stability compared to dextran-coated SPIONs (Dex-SPIONs), which were used as controls. The cellular uptake behaviors of DS-SPIONs and Dex-SPIONs were evaluated using Prussian blue assay. Interestingly, the DS-SPIONs were effectively taken up by activated macrophages compared to Dex-SPIONs. However, the cellular uptake of DS-SPIONs by activated macrophages was remarkably reduced in the presence of free DS. These results suggest that activated macrophages internalize DS-SPIONs via receptor (SR-A)-mediated endocytosis. T2-weighted MR imaging of the cells demonstrated that activated macrophages treated with DS-SPIONs showed a significantly lower signal intensity compared to those treated with Dex-SPIONs. Overall, these results suggest that DS-SPIONs may be utilized as a potential contrast agent for atherosclerosis MR imaging., (Copyright © 2013 Elsevier Ltd. All rights reserved.)

Purpose: Ictal single-photon emission computerized tomography (SPECT) is often nonlocalized in patients with partial epilepsy. We repeated ictal SPECT in patients with partial epilepsy whose first ictal SPECT was nonlocalized. We also performed subtraction ictal SPECT coregistered to magnetic resonance imaging (MRI) (SISCOM) to test the localizability of ictal SPECT., Methods: We recruited 69 patients with partial epilepsy (33 male and 36 female, mean plus or minus standard deviation age 29.5 ± 12.2 years), who had a repeated ictal SPECT. Ictal-interictal SPECT subtractions were performed, and the subtracted SPECTs were coregistered with their brain MRI studies. SISCOM results were considered to be localizing when the results were concordant with the final location of the epileptic focus, as determined by the presurgical evaluation. We compared seizure duration, tracer injection time, interictal and ictal scalp electroencephalography (EEG) patterns, presence and time of secondary generalization, and epilepsy classification between the localized and nonlocalized SISCOM groups., Key Findings: The SISCOM results of the second ictal SPECT were localized in 43 (62.3%) patients and nonlocalized in 26 (37.7%) patients. In the second ictal SPECT, the radiotracer injection time was significantly shorter in the localized group (25.1 ± 8.9 s), as compared to the nonlocalized group (49.2 ± 55.8 s) (p = 0.008). Furthermore, the radiotracer injection time of the second ictal SPECT was significantly shorter than the first ictal SPECT, only in the localized group (36.8 ± 23.8 s in the first and 25.1 ± 8.9 s in the second ictal SPECT in the localized group, p = 0.004). The percent injection time ([(tracer injection time-seizure onset time)/total seizure duration] × 100%) in the second SPECT was significantly shorter in the localized group, as compared to the nonlocalized group (37.9 ± 23.0% in the localized group and 72.3 ± 46.2% in the nonlocalized group, p < 0.001). The localized ictal EEG patterns at the time of injection were more frequent in the localized SISCOM group. The secondary generalization of seizures at the time of injection was more frequent in nonlocalized groups., Significance: Repeated ictal SPECT with SISCOM analysis is helpful for localizing an epileptic focus in patients with partial epilepsy who have a nonlocalized first ictal SPECT. The most important factor for increasing the localizability of repeated ictal SPECT is early injection time and a localizing ictal EEG pattern at the time of radiotracer injection., (Wiley Periodicals, Inc. © 2011 International League Against Epilepsy.)

Study Objectives: To investigate differences in brain gray matter concentrations or volumes in patients with obstructive sleep apnea syndrome (OSA) and healthy volunteers., Designs: Optimized voxel-based morphometry, an automated processing technique for MRI, was used to characterize structural differences in gray matter in newly diagnosed male patients., Setting: University hospital., Patients and Participants: The study consisted of 36 male OSA and 31 non-apneic male healthy volunteers matched for age (mean age, 44.8 years)., Interventions: Using the t-test, gray matter differences were identified. The statistical significance level was set to a false discovery rate P < 0.05 with an extent threshold of k(E) > 200 voxels., Measurements and Results: The mean apnea-hypopnea index (AHI) of patients was 52.5/h. On visual inspection of MRI, no structural abnormalities were observed. Compared to healthy volunteers, the gray matter concentrations of OSA patients were significantly decreased in the left gyrus rectus, bilateral superior frontal gyri, left precentral gyrus, bilateral frontomarginal gyri, bilateral anterior cingulate gyri, right insular gyrus, bilateral caudate nuclei, bilateral thalami, bilateral amygdalo-hippocampi, bilateral inferior temporal gyri, and bilateral quadrangular and biventer lobules in the cerebellum (false discovery rate P < 0.05). Gray matter volume was not different between OSA patients and healthy volunteers., Conclusions: The brain gray matter deficits may suggest that memory impairment, affective and cardiovascular disturbances, executive dysfunctions, and dysregulation of autonomic and respiratory control frequently found in OSA patients might be related to morphological differences in the brain gray matter areas.

Objective: This study was conducted to explore differences in cortical thickness between subjects with bipolar disorder and healthy comparison subjects using cortical surface-based analysis., Methods: Brain magnetic resonance images were acquired from 25 subjects with bipolar disorder and 21 healthy comparison subjects. Cortical surface-based analysis was conducted using the Freesurfer application. Group differences in cortical thickness, defined by the distance from gray/white boundary to the pial surface, were assessed using statistical difference maps., Results: Subjects with bipolar disorder exhibited significantly decreased cortical thickness in left cingulate cortex, left middle frontal cortex, left middle occipital cortex, right medial frontal cortex, right angular cortex, right fusiform cortex and bilateral postcentral cortices, relative to healthy comparison subjects (all p < 0.001). Duration of illness in bipolar subjects was inversely correlated with the cortical thickness of the left middle frontal cortex., Conclusions: Cortical thinning was present in multiple prefrontal cortices in bipolar disorder. There was also cortical thinning in sensory and sensory association cortices, which has not been reported in previous studies using region-of-interest or voxel-based morphometry methods. Cortical thinning observed in the current study may be related to impairment of emotional, cognitive, and sensory processing in bipolar disorder but longitudinal studies will be necessary to test this hypothesis.

Scores of the performance scale of the Wechsler Adult Intelligence Scale (WAIS) declined linearly with age from the 6th decade, whereas those of the verbal scale did not. This decrease in performance intelligence was thought to be related to an age-related frontal atrophy. The relationship between scores of the WAIS and changes in regional cortical gray matter density were examined in healthy elderly subjects using voxel-based morphometry. Thirty healthy non-demented individuals >50 years of age were tested with the WAIS and scanned with brain magnetic resonance imaging (MRI). The right neocerebellum was significantly associated with scores of the performance intelligence scale while frontal lobes were not. The current study suggests that the cerebellum may play an important role in changes of intellectual capacity in old age.

A cadaveric study was performed to investigate the relationship between disc degeneration and morphological changes in the intervertebral foramen of cervical spine, including the effect on the nerve root. Seven fresh frozen human cadavers were dissected from C1 to T1, preserving the ligaments, capsules, intervertebral disc and the neural structures. The specimens were scanned with MRI and then scanned through CT scan in the upright position. Direct mid-sagittal and 45 degree oblique images were obtained to measure the dimension of the intervertebral disc height, foraminal height, width, area and segmental angles. Disc degeneration was inversely correlated with disc height. There was a significant correlation between disc degeneration and foraminal width (p<0.005) and foraminal area (p< 0.05), but not with foraminal height. Disc height was correlated with foraminal width but not with height. The segmental angles were decreased more in advanced degenerated discs. There was a correlation between nerve root compression and decreased foraminal width and area (p<0.005). This information and critical dimensions of the intervertebral foramen for nerve root compression should help in the diagnosis of foraminal stenosis of the cervical spine in patients presenting with cervical spondylosis and radiculopathy.

ObjectiveTo assess the effect of subsyndromal symptoms of depression (SSD) on ratings of disability for individuals with mild cognitive impairment (MCI).MethodsData from 405 MCI participants from the Alzheimer's Disease Neuroimaging Initiative (ADNI) study were analyzed. Participants were evaluated at baseline and at 6-month intervals over 2 years. Severity of depressive symptoms was rated utilizing the Geriatric Depression Scale. Disability was assessed utilizing the Functional Assessment Questionnaire (FAQ). Other clinical variables included white matter lesion (WML) and intracranial brain (ICV) volumes derived from magnetic resonance imaging, ratings of overall cognitive function (Alzheimer's Disease Assessment Scale, ADAS), and apolipoprotein E (ApoE) status. Demographic variables included age, education, and gender.ResultsSSD individuals had a lower volume of WML and higher frequency of ApoE ε4 alleles than nondepressed participants but the two groups did not differ with respect to other clinical or demographic variables. At baseline, SSD individuals were 1.77 times more likely to have poorer FAQ scores than individuals with no symptoms of depression after controlling for the effect of cognitive functioning, ICV, WML, and ApoE status. The presence of SSD at baseline was not associated with a poorer course of disability outcomes, cognitive functioning, or conversion to dementia over 24 months.ConclusionsSSD demonstrated a significant impact on disability for MCI individuals, who are also at high risk for functional limitations related to neurodegenerative disease. Therefore, the treatment of SSD may represent a significant avenue to reduce the burden of disability in this vulnerable patient population.

Aim: The neurobiological substrates underlying the relationship of circadian rest‐activity rhythm (RAR) alteration with accelerated late‐life cognitive decline are not clearly understood. In the present study, the longitudinal relationship of objectively measured circadian RAR with in vivo Alzheimer disease (AD) pathologies and cerebrovascular injury was investigated in older adults without dementia. Methods: The present study included 129 participants without dementia who participated in the KBASE (Korean Brain Aging Study for Early Diagnosis and Prediction of Alzheimer's Disease) cohort. All participants underwent actigraphy at baseline and two consecutive [11C] Pittsburgh compound‐B positron emission tomography (PET), [18F] fluorodeoxyglucose‐PET, magnetic resonance imaging, and Mini‐Mental State Examination (MMSE) at baseline and at a 2‐year follow‐up assessment. The associations of circadian RAR with annualized change in neuroimaging measures including global amyloid‐beta retention, AD‐signature region cerebral glucose metabolism (AD‐CM), and white matter hyperintensity volume were examined. Results: Delayed acrophase at baseline was significantly associated with greater annualized decline of AD‐CM over a 2‐year period, but not with that of other neuroimaging measures. In contrast, other circadian RAR parameters at baseline had no association with annualized change of any neuroimaging measures. Annualized decline of AD‐CM was also significantly positively associated with the annual change in MMSE scores. Furthermore, a mediation analysis showed that greater reduction in AD‐CM mediated the effect of delayed acrophase at baseline on faster decline of MMSE score. Conclusion: The findings indicate that delayed acrophase in late life may cause or predict hypometabolism at AD‐signature brain regions, which underlies cognitive decline in the near future. [ABSTRACT FROM AUTHOR]

Background: Physical activities (PA) have been suggested to reduce the risk of Alzheimer's disease (AD) dementia. However, information on the neuropathological links underlying the relationship is limited.Objective: We investigated the role of midlife and late-life PA with in vivo AD neuropathologies in old adults without dementia.Methods: This study included participants from the Korean Brain Aging Study for Early Diagnosis and Prediction of Alzheimer's disease (KBASE). The participants underwent comprehensive clinical and neuropsychological assessment, [11C] Pittsburgh Compound B positron emission tomography (PET), [18F] fluorodeoxyglucose PET, and magnetic resonance imaging. Using the multi-modal brain imaging data, in vivo AD pathologies including global amyloid deposition, AD-signature region cerebral glucose metabolism (AD-CM), and AD-signature region cortical thickness (AD-CT) were quantified. Both midlife and late-life PA of participants were measured using the Lifetime Total Physical Activity Questionnaire.Results: This study was performed on 260 participants without dementia (195 with normal cognitive function and 65 with mild cognitive impairment). PA of neither midlife nor late-life showed direct correspondence with any neuroimaging biomarker. However, late-life PA moderated the relationship of brain amyloid-β (Aβ) deposition with AD-CM and AD-CT. Aβ positivity had a significant negative effect on both AD-CM and AD-CT in individuals with lower late-life PA, but those with higher late-life PA did not show such results. Midlife PA did not have such a moderation effect.Conclusion: The findings suggest that physically active lifestyle in late-life, rather than that in midlife, may delay AD-associated cognitive decline by decreasing Aβ-induced neurodegenerative changes in old adults. [ABSTRACT FROM AUTHOR]

Background: Despite the known associations between zinc levels and Alzheimer's disease (AD) dementia and related cognitive impairment, the underlying neuropathological links remain poorly understood. We tested the hypothesis that serum zinc level is associated with cerebral beta-amyloid protein (Aβ) deposition. Additionally, we explored associations between serum zinc levels and other AD pathologies [i.e., tau deposition and AD-signature cerebral glucose metabolism (AD-CM)] and white matter hyperintensities (WMHs), which are measures of cerebrovascular injury. Methods: A total of 241 cognitively normal older adults between 55 and 90 years of age were enrolled. All the participants underwent comprehensive clinical assessments, serum zinc level measurement, and multimodal brain imaging, including Pittsburgh compound B-positron emission tomography (PET), AV-1451 PET, fluorodeoxyglucose (FDG)-PET, and magnetic resonance imaging. Zinc levels were stratified into three categories: < 80 μg/dL (low), 80 to 90 μg/dL (medium), and > 90 μg/dL (high). Results: A low serum zinc level was significantly associated with increased Aβ retention. In addition, apolipoprotein E ε4 allele (APOE4) status moderated the association: the relationship between low zinc level and Aβ retention was significant only in APOE4 carriers. Although a low zinc level appeared to reduce AD-CM, the relationship became insignificant on sensitivity analysis including only individuals with no nutritional deficiency. The serum zinc level was associated with neither tau deposition nor the WMH volume. Conclusions: Our findings suggest that decreased serum zinc levels are associated with elevation of brain amyloid deposition. In terms of AD prevention, more attention needs to be paid to the role of zinc. [ABSTRACT FROM AUTHOR]

Background: Both elevated blood homocysteine and diabetes mellitus (DM) are related to cognitive impairments or dementia. A previous study also demonstrated that the association between homocysteine and cognitive decline was much stronger in individuals with DM than in those without DM.Objective: This study aimed to examine the interactive effect of blood homocysteine and DM on brain pathological changes including brain atrophy, amyloid-β and tau deposition, and small vessel disease (SVD) related to cognitive impairments.Methods: A total of 430 non-demented older adults underwent comprehensive clinical assessment, measurement of serum homocysteine level, [11C] Pittsburgh Compound B (PiB) PET, [18F] AV-1451 PET, and brain MRI.Results: The interactive effect of homocysteine with the presence of DM on brain atrophy, especially in aging-related brain regions, was significant. Higher homocysteine concentration was associated with more prominent brain atrophy in individuals with DM, but not in those without DM. In contrast, interaction effect of homocysteine and DM was found neither on Alzheimer's disease (AD) pathologies, including amyloid-β and tau deposition, nor white matter hyperintensity volume as a measure of SVD.Conclusion: The present findings suggest that high blood homocysteine level and DM synergistically aggravate brain damage independently of AD and cerebrovascular disease. With regard to preventing dementia or cognitive decline in older adults, these results support the importance of strictly controlling blood glucose in individuals with hyperhomocysteinemia and lowering blood homocysteine level in those with DM. [ABSTRACT FROM AUTHOR]

Background: Despite known associations between low blood hemoglobin level and Alzheimer's disease (AD) or cognitive impairment, the underlying neuropathological links are poorly understood. We aimed to examine the relationships of blood hemoglobin levels with in vivo AD pathologies (i.e., cerebral beta-amyloid [Aβ] deposition, tau deposition, and AD-signature degeneration) and white matter hyperintensities (WMHs), which are a measure of cerebrovascular injury. We also investigated the association between hemoglobin level and cognitive performance, and then assessed whether such an association is mediated by brain pathologies. Methods: A total of 428 non-demented older adults underwent comprehensive clinical assessments, hemoglobin level measurement, and multimodal brain imaging, including Pittsburgh compound B-positron emission tomography (PET), AV-1451 PET, fluorodeoxyglucose (FDG)-PET, and magnetic resonance imaging. Episodic memory score and global cognition scores were also measured. Results: A lower hemoglobin level was significantly associated with reduced AD-signature cerebral glucose metabolism (AD-CM), but not Aβ deposition, tau deposition, or WMH volume. A lower hemoglobin level was also significantly associated with poorer episodic memory and global cognition scores, but such associations disappeared when AD-CM was controlled as a covariate, indicating that AD-CM has a moderating effect. Conclusion: The present findings suggest that low blood hemoglobin in older adults is associated with cognitive decline via reduced brain metabolism, which seems to be independent of those aspects of AD-specific protein pathologies and cerebrovascular injury that are reflected in PET and MRI measures. [ABSTRACT FROM AUTHOR]

Background: Previous studies indicated an association between Alzheimer's disease (AD) dementia and air particulate matter (PM) with aerodynamic diameter <10μm (PM10), as well as smaller PM. Limited information, however, is available for the neuropathological links underlying such association.Objective: This study aimed to investigate the relationship between long-term PM10 exposure and in vivo pathologies of AD using multimodal neuroimaging.Methods: The study population consisted of 309 older adults without dementia (191 cognitively normal and 118 mild cognitive impairment individuals), who lived in Republic of Korea. Participants underwent comprehensive clinical assessments, 11C-Pittsburg compound B (PiB) positron emission tomography (PET), and magnetic resonance imaging scans. A subset of 78 participants also underwent 18F-AV-1451 tau PET evaluation. The mean concentration of PM with aerodynamic diameter <10μm over the past 5 years (PM10mean) collected from air pollution surveillance stations were matched to each participant's residence.Results: In this non-demented study population, of which 62% were cognitively normal and 38% were in mild cognitive impairment state, exposure to the highest tertile of PM10mean was associated with increased risk of amyloid-β (Aβ) positivity (odds ratio 2.19, 95% confidence interval 1.13 to 4.26) even after controlling all potential confounders. In contrast, there was no significant associations between PM10mean exposure and tau accumulation. AD signature cortical thickness and white matter hyperintensity volume were also not associated with PM10mean exposure.Conclusion: The findings suggest that long-term exposure to PM10 may contribute to pathological Aβ deposition. [ABSTRACT FROM AUTHOR]

This study aimed to investigate whether the midlife cognitive activity and physical activity moderate the relationship between apolipoprotein Eε4 (APOE4) and in vivo Alzheimer's disease (AD) pathologies. In total, 287 non-demented older adults (mean age 72 years) from the Korean Brain Aging Study for the Early diagnosis and prediction of Alzheimer's disease cohort were included. Participants underwent a comprehensive clinical assessment including the evaluation for midlife CA and physical activity, [11C]-Pittsburgh-Compound-B-positron emission tomography (PET), [18F]-fluorodeoxyglucose PET, structural magnetic resonance imaging (MRI), and APOE genotyping. We used linear regression and regression-based mediated-moderation models for statistical analyses. Neither midlife cognitive activity nor physical activity moderated the effect of APOE4 on β-amyloid (Aβ) retention itself. Midlife cognitive activity significantly moderated the effect of APOE4 on hippocampal volume [ B (SE) = − 627.580 (252.327), t = −2.488, p = 0.014]: APOE4 carriers had smaller hippocampal volume than non-carriers at relatively high cognitive activity state (p = 0.004), but not at relatively low cognitive activity condition (p = 0.937). Midlife physical activity significantly moderated the effect of Aβ retention, which was closely related to APOE4, on AD-signature region cerebral glucose metabolism [AD-CM; B (SE) = 0.004 (0.002), t = 2.030, p = 0.043]: higher Aβ accumulation was associated with lower AD-CM in relatively low physical activity condition (p < 0.001), whereas no such association was observed in relatively high physical activity state (p = 0.791). The findings suggest that high midlife cognitive activity may accelerate hippocampal atrophy induced by APOE4, whereas high midlife physical activity may delay AD-related cerebral hypometabolism by weakening the influence of APOE4-associated Aβ retention. [ABSTRACT FROM AUTHOR]

The primary goals of the present study were to develop and validate the Rappel Indicé 24 (RI-24), a shorter version of the original Rappel Indicé, which includes 48 items (RI-48), and to identify the specific brain regions that were correlated with scores on the RI-24. Using these clinical scales, the present study evaluated 91 elderly Korean participants who were classified into 3 groups: normal control (NC; n = 34), patients with mild cognitive impairment (MCI; n = 29), and patients with Alzheimer disease (AD; n = 28). Of the 91 participants, 77 also underwent magnetic resonance imaging scans. The RI-24 delayed cued recall (DCR) scores significantly differed among the NC, MCI, and AD groups. A receiver-operating characteristic curve analysis revealed that the RI-24 was very sensitive (89%) and specific (91%) for the detection of AD. Furthermore, although the time needed to administer the RI-24 was half that needed for the RI-48, the 24-item version showed a high correlation (r= .85 for the DCR score) with the 48-item version. In terms of brain morphological characteristics, voxel-based morphometry analyses revealed a significant positive correlation between DCR score and gray matter volume in the parahippocampal gyrus (r= .468), which plays a role in cued recall. Taken together, the present findings indicate that the RI-24 is a sensitive and reliable test for the detection of memory impairments in patients with MCI and AD despite its brief administration time. [ABSTRACT FROM AUTHOR]

Background: A standardized tool for evaluating semantic knowledge of the Korean population is needed.Objective: The purpose of this study was to develop a neuropsychological test for the evaluation of semantic knowledge in the Korean elderly population.Methods: The Korean version of the Size/Weight Attribute Test (SWAT-K) was developed in reference to the original version. The diagnostic validity of SWAT-K was evaluated with 95 elderly outpatients [67 normal controls; 18 with Alzheimer's disease (AD); 10 with semantic-variant progressive aphasia (SV-PPA)]. Voxel-based morphometry (VBM) was employed to examine associations between SWAT-K scores and morphological changes of the brain.Results: SWAT-K could discriminate the three subject groups (normal >AD, p <  0.001; AD >SV-PPA, p = 0.040), whereas Boston Naming Test could not distinguish SV-PPA from AD. ROC curve analysis confirmed high levels of sensitivity (0.90) and specificity (0.93) for SWAT-K. The test's inter-rater reliability (ICC = 0.827) and test-retest reliability (ICC = 0.666) were assessed as well. VBM found a significant positive correlation (uncorrected p <  0.005, k >  100) between SWAT-K scores and gray matter volume in right inferior frontal cortex (T = 4.08, k = 191) and bilateral temporal cortices (left, T = 4.42, k = 135; right, T = 3.55, k = 253), the areas the most affected in SV-PPA.Conclusions: SWAT-K is a sensitive and reliable test for evaluating semantic knowledge in the Korean elderly population. Strong positive correlations between SWAT-K scores and the brain areas responsible for semantic processing further corroborate the validity of SWAT-K. [ABSTRACT FROM AUTHOR]

The purpose of this preliminary study was to test the hypothesis that subsyndromal depression is associated with the volume of medial prefrontal regional gray matter and that of white matter lesions (WMLs) in the brains of cognitively normal older people. We also explored the relationships between subsyndromal depression and medial prefrontal regional gray matter volume, limbic regional gray matter volume, and lobar WMLs in the brains of patients with mild cognitive impairment (MCI) and Alzheimer's disease (AD). We performed a cross-sectional study comparing patients with subsyndromal depression and nondepressed controls with normal cognition (n = 59), MCI (n = 27), and AD (n = 27), adjusting for sex, age, years of education, and results of the Mini-Mental State Examination. Frontal WML volume was greater, and right medial orbitofrontal cortical volume was smaller in cognitively normal participants with subsyndromal depression than in those without subsyndromal depression. No volume differences were observed in medial prefrontal, limbic, or WML volumes according to the presence of subsyndromal depression in cognitively impaired patients. The absence of these changes in patients with MCI and AD suggests that brain changes associated with AD pathology may override the changes associated with subsyndromal depression. [ABSTRACT FROM AUTHOR]

The article reports a study which examined the effect of Brostrom-Gould repair on in vivo kinematics of the tibiotalar joint during quasistatic weightbearing loading. The results show that the modified Brostrom-Gould repair improved the abnormal joint motion observed in patients with lateral ankle instability, decreasing anterior translation and internal rotation of the talus. No significant differences in kinematics between repaired ankles and contralateral normal ankles were found.

Background: White matter hyperintensities (WMH) increase cognitive impairment in patients with dementia. Objective: We investigated the impact of WMH on the neuropsychological profiles in patients with mild to moderate dementia. Methods: We consecutively recruited newly diagnosed patients with mild to moderate dementia across South Korea for 1 year. The participants completed neuropsychological tests, magnetic resonance imaging, and structured neurological evaluations. The patients were divided into 3 categories, i.e. minimal, moderate, and severe WMH groups, according to the proportional degree of WMH. Results: 289 patients were recruited; 140 (48.3%) for the minimal WMH group, 99 (34.2%) for the moderate group, and 50 (17.5%) for the severe group. Both advanced age and low general cognitive level were significant contributors to WMH in patients with dementia. After adjusting for age, the neuropsychological correlates of the proportional impact of WMH were frontal executive, language, and attention profiles. However, the only significant neuropsychological correlate was the recognition memory profile after adjusting for both age and general cognitive level simultaneously. Conclusion: The results suggest that the most significant neuropsychological profile impacting the burden of WMH in patients with mild to moderate dementia was the recognition memory profile, regardless of age and general cognitive function. Copyright © 2011 S. Karger AG, Basel [ABSTRACT FROM AUTHOR]

The article presents a case study of a 27-year-old woman with epithelioid hemangioendotheliomas (EHE) who was taken to the hospital because of hyperkeratotic plaque on her left sole. Topics discussed include finding multiple nodules composed of epithelioid cells by histopathological evaluation, performing magnetic resonance imaging and diagnosing EHE.

Background: Late-life depression (LDD) results from multiple psychosocial and neurobiological changes occurring in later life. The current study investigated how patterns of clinical symptoms and brain structural features are classified into LDD subtypes.Method: Self-report scale of depression, behavioral rating of affective symptoms, and brain structural imaging of white matter change and cortical thickness were assessed in 541 older adults with no cognitive impairment or mild cognitive impairment. Latent profile analysis was used to identify distinct subtypes of depression.Results: The latent profile analysis identified four classes with mild to severe depressive symptoms and two classes with minimal symptoms. While the classes primarily differed in the overall severity, the combinatory patterns of clinical symptoms and neuropathological signature distinguished the classes with similar severity. The classes were distinguished in terms of whether or not neurodegenerative risk accompanied the corresponding depressive symptoms. The presence of the negative self-scheme and cortical thinning pattern notably characterized the subtypes of LDD.Limitations: The underlying etiologies of the biological subtypes are still speculative, and the current study lacks clinical history that differentiates late- and early-onset depression.Conclusions: Our finding provides insight in identifying heterogeneities of depressive disorder in later life and suggests that self-report and behavioral symptom profile in combination with white matter lesion and cortical thickness effectively characterizes distinct subtypes of LDD. [ABSTRACT FROM AUTHOR]

Abstract This study aimed to investigate the relationship of hypertension with beta-amyloid (Aβ) and neurodegeneration biomarkers of Alzheimer's disease (AD) and the modulating effect of apolipoprotein E-ε4 (APOE4). In total, 259 cognitively normal (CN) and 79 AD dementia older adults received clinical assessments including the evaluation for the presence of hypertension, [11C]-Pittsburgh-compound-B–positron emission tomography, magnetic resonance imaging, and APOE genotyping. We used a clinical stage-specific approach, separately focusing on CN and AD dementia stages. For the CN group, individuals with hypertension showed reduced AD signature cortical thickness compared with those without hypertension. Subsequent subgroup analyses showed that hypertension was associated with reduced AD signature cortical thickness only in APOE4 noncarriers, whereas hypertension was associated with elevated Aβ deposition in APOE4 carriers. Meanwhile, regardless of APOE4 status, AD dementia patients with hypertension had significantly lower Aβ deposition than those without hypertension. In conclusion, the findings suggest that hypertension contributes to AD primarily through the reduction of brain reserve. In case of APOE4 carriers, however, hypertension seems to additionally facilitate AD process through amyloid-dependent pathway. Highlights • Hypertension (HTN) is related to Alzheimer's disease (AD)-related neuronal injury. • HTN may contribute to AD mainly through the reduction of brain reserve. • HTN may additionally facilitate beta-amyloid deposition in APOE4 carrier. [ABSTRACT FROM AUTHOR]

Objectives: To investigate neural substrates of symptomatic rapid eye movement sleep behavior disorder (RBD) in Parkinson's disease (PD) by analyzing brain changes based on both hypothesis-free and hypothesis-driven neuroimaging analyses.Methods: A total of 63 subjects (14 PDRBD-, 24 PDRBD+, and 25 age-matched healthy controls = HC) were enrolled in this study. RBD was defined by RBD screening questionnaire with video-polysomnographic confirmation. All subjects underwent volumetric and diffusion tensor imaging. The whole brain gray- and white-matter changes were analyzed and the central ascending cholinergic pathway involving the pedunculopontine nucleus and thalamus was compared with a region-of-interest analysis and probabilistic tractography.Results: The PDRBD+ group showed decreased gray matter volume of the left posterior cingulate and hippocampus compared to the PDRBD- and additional gray matter decrease in the left precuneus, cuneus, medial frontal gyrus, postcentral gyrus and both inferior parietal lobule compared to the HC group (uncorrected p < 0.001, k = 50). There were no significant differences in white matter changes between the PDRBD- and PDRBD+ groups both by fractional anisotropy and mean diffusivities. However, both PD groups showed widespread changes by fractional anisotropy reductions and mean diffusivity increments compared to HC (p < 0.05 corrected). There were no significant differences in tract-based spatial statistics and the normalized tract volumes as well as the diffusion indices of both the thalamus and pedunculopontine nuclei among the study groups.Conclusions: The appearance of RBD in PD may be related to regional gray matter changes in the left posterior cingulate and hippocampus but not localized to the brainstem. [ABSTRACT FROM AUTHOR]

Irisin, an exercise-induced myokine, has been shown to have beneficial effects on cognitive and metabolic functions. However, previous studies assessing the levels of circulating irisin in patients with Alzheimer's disease (AD) or diabetes mellitus (DM) have provided inconsistent results. This suggests that the normal physiological action of irisin may be altered by disease-associated pathological conditions in target organs. To investigate the association of plasma levels of irisin with cognition and brain structures according to the presence or absence of AD and DM. Plasma levels of irisin, multi-domain cognition, and volumes of relevant brain regions were assessed using enzyme-linked immunoassay, neuropsychological test, and magnetic resonance imaging, respectively. We classified 107 participants by cognitive (cognitively normal [CN, n = 23], mild cognitive impairment [MCI, n = 49], and AD [n = 35]) and metabolic (non-DM [n = 75] and DM [n = 32]) states. Disease state-stratified multiple regression analyses showed that plasma levels of irisin were positively associated with cognition only in participants without AD (CN plus MCI). By contrast, in participants with AD, these associations lost significance, and furthermore, higher levels of irisin indicated smaller hippocampal, superior temporal, and inferior frontal volumes. The association between plasma irisin levels and cognition was not affected by the presence of DM. Consistently, moderation analysis revealed that the relationship between plasma irisin levels and cognition or brain structures was significantly modified by the presence of AD, not that of DM. Our findings suggest that the beneficial actions of circulating irisin on cognition may be attenuated by AD-induced pathological conditions in the brain. • Alzheimer's disease alters the relationship of irisin with cognition and brain volume. • Diminished beneficial effect of irisin in Alzheimer's disease supports "irisin resistance." • Relation of irisin to cognition and brain volume is unaffected by diabetes mellitus. [ABSTRACT FROM AUTHOR]