A childhood case of spinal tuberculosis misdiagnosed as muscular dystrophy

Tuberculosis is primarily a pulmonary disease, but extra-pulmonary manifestations are not uncommon, especially in children and adolescents. Ten percent of extra pulmonary tuberculosis localizes to the bones and joints, and 56% of such cases affect the spine. We treated a childhood case of spinal tuberculosis misdiagnosed as muscular dystrophy in a patient without specific constitutional symptoms. We report this case because the patient had an unusual presentation of spinal tuberculosis

Sleep experiences during different lifetime periods and in vivo Alzheimer pathologies

Background Very little is known for the direction or causality of the relationship between lifetime sleep experiences and in vivo Alzheimers disease (AD) pathologies. This study aimed to examine the relationship between sleep experiences during the young adulthood, midlife, and late-life periods and in vivo cerebral beta-amyloid (Aβ) deposition and AD signature regional neurodegeneration in cognitively normal (CN) old adults. Methods This study included 202 CN old adults who participated in the Korean Brain Aging Study for the Early Diagnosis and Prediction of Alzheimers Disease (KBASE) study. All participants underwent a comprehensive clinical assessment, [11C] Pittsburgh Compound B positron emission tomography (PET), [18F] Fluorodeoxyglucose-PET, and magnetic resonance imaging. The quality and duration of sleep were assessed for the following age periods: 20–30s, 40–50s, and the most recent month. All analyses were adjusted for age, gender, education, apolipoprotein E ε4 status, vascular risk score, Hamilton Depression Rating Scale score, and use of sleep medication. Results Bad sleep quality and short sleep duration during midlife were significantly associated with increased Aβ deposition and AD signature regional hypometabolism, respectively. Although current bad sleep quality appeared to be associated with increased Aβ accumulation, this association disappeared after controlling for the effects of midlife sleep quality. Neither the quality nor duration of sleep during young adulthood was related to Aβ burden or neurodegeneration. Conclusions Bad sleep quality during midlife increases pathological Aβ deposition in the brain, while short sleep duration during the same period accelerates regional hypometabolism.This study was supported by a grant from the Ministry of Science, ICT, and Future Planning, Republic of Korea (Grant No: NRF-2014M3C7A1046042) and a grant of the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health & Welfare, Republic of Korea (Grant No: HI18C0630). The funding source had no role in the design of the study; collection, analysis, and interpretation of the data; and writing of the manuscript

Synergistic interaction between APOE and family history of Alzheimers disease on cerebral amyloid deposition and glucose metabolism

Background Recently, the field of gene-gene or gene-environment interaction research appears to have gained growing interest, although it is seldom investigated in Alzheimers disease (AD). Hence, the current study aims to investigate interaction effects of the key genetic and environmental risks—the apolipoprotein ε4 allele (APOE4) and family history of late-onset AD (FH)—on AD-related brain changes in cognitively normal (CN) middle-aged and older adults. Methods [11C] Pittsburg compound-B (PiB) positron emission tomography (PET) imaging as well as [18F] fluoro-2-deoxyglucose (FDG) PET that were simultaneously taken with T1-weighted magnetic resonance imaging (MRI) were obtained from 268 CNs from the Korean Brain Aging Study for Early Diagnosis and Prediction of AD (KBASE). Composite standardized uptake value ratios were obtained from PiB-PET and FDG-PET images in the AD signature regions of interests (ROIs) and analyzed. Voxel-wise analyses were also performed to examine detailed regional changes not captured by the ROI analyses. Results A significant synergistic interaction effect was found between the APOE4 and FH on amyloid-beta (Aβ) deposition in the AD signature ROIs as well as other regions. Synergistic interaction effects on cerebral glucose metabolism were observed in the regions not captured by the AD signature ROIs, particularly in the medial temporal regions. Conclusions Strong synergistic effects of APOE4 and FH on Aβ deposition and cerebral glucose metabolism in CN adults indicate possible gene-to-gene or gene-to-environment interactions that are crucial for pathogenesis of AD involving Aβ. Other unspecified risk factors—genes and/or environmental—that are captured by the positive FH status might either coexpress or interact with APOE4 to alter AD-related brain changes in CN. Healthy people with both FH and APOE4 need more attention for AD prevention.This study was supported by a grant from the Ministry of Science and ICT, Republic of Korea (grant no. NRF-2014M3C7A1046042). The funding source had no role in the study design, data collection, data analysis, data interpretation, writing of the manuscript, or decision to submit it for publication

Association of carotid and intracranial stenosis with Alzheimers disease biomarkers

Background To clarify whether atherosclerosis of the carotid and intracranial arteries is related to Alzheimers disease (AD) pathology in vivo, we investigated the associations of carotid and intracranial artery stenosis with cerebral beta-amyloid (Aβ) deposition and neurodegeneration in middle- and old-aged individuals. Given different variations of the pathologies between cognitive groups, we focused separately on cognitively normal (CN) and cognitively impaired (CI) groups. Methods A total of 281 CN and 199 CI (mild cognitive impairment and AD dementia) subjects underwent comprehensive clinical assessment, [11C] Pittsburgh compound B-positron emission tomography, and magnetic resonance (MR) imaging including MR angiography. We evaluated extracranial carotid and intracranial arteries for the overall presence, severity (i.e., number and degree of narrowing), and location of stenosis. Results We found no associations between carotid and intracranial artery stenosis and cerebral Aβ burden in either the CN or the CI group. In terms of neurodegeneration, exploratory univariable analyses showed associations between the presence and severity of stenosis and regional neurodegeneration biomarkers (i.e., reduced hippocampal volume [HV] and cortical thickness in the AD-signature regions) in both the CN and CI groups. In confirmatory multivariable analyses controlling for demographic covariates and diagnosis, the association between number of stenotic intracranial arteries ≥ 2 and reduced HV in the CI group remained significant. Conclusions Neither carotid nor intracranial artery stenosis appears to be associated with brain Aβ burden, while intracranial artery stenosis is related to amyloid-independent neurodegeneration, particularly hippocampal atrophy.This study was supported by a grant from the Ministry of Science and ICT, Republic of Korea (grant nos. NRF-2014M3C7A1046042, 2017R1A2B2008412, and 2018M3C7A1056888); by a grant of the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health & Welfare, Republic of Korea (grant nos. HI18C0630 and HI19C0149); by a grant no. 04-20190500 from the SNUH Research Fund; and by a grant no. 06-20191860 from the Scientific Research Fund of the Korean Society of Magnetic Resonance in Medicine (2019). The funder had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; preparation, review, or approval of the manuscript; and decision to submit the manuscript for publication

Corrigendum: Behavioral and Neuroimaging Evidence for Facial Emotion Recognition in Elderly Korean Adults with Mild Cognitive Impairment, Alzheimer's Disease, and Frontotemporal Dementia

Background: Facial emotion recognition (FER) is impaired in individuals with frontotemporal dementia (FTD) and Alzheimer’s disease (AD) when compared to healthy older adults. Since deficits in emotion recognition are closely related to caregiver burden or social interactions, researchers have fundamental interest in FER performance in patients with dementia.Purpose: The purpose of this study was to identify the performance profiles of six facial emotions (i.e., fear, anger, disgust, sadness, surprise, and happiness) and neutral faces measured among Korean healthy control (HCs), and those with mild cognitive impairment (MCI), AD, and FTD. Additionally, the neuroanatomical correlates of facial emotions were investigated.Methods: A total of 110 (33 HC, 32 MCI, 32 AD, 13 FTD) older adult participants were recruited from two different medical centers in metropolitan areas of South Korea. These individuals underwent an FER test that was used to assess the recognition of emotions or absence of emotion (neutral) in 35 facial stimuli. Repeated measures two-way analyses of variance were used to examine the distinct profiles of emotional recognition among the four groups. We also performed brain imaging and voxel-based morphometry (VBM) on the participants to examine the associations between FER scores and gray matter volume.Results: The mean score of negative emotion recognition (i.e., fear, anger, disgust, and sadness) clearly discriminated FTD participants from individuals with MCI and AD and HC [F(3,106) = 10.829, p 2 = 0.235], whereas the mean score of positive emotion recognition (i.e., surprise and happiness) did not. A VBM analysis showed negative emotions were correlated with gray matter volume of anterior temporal regions, whereas positive emotions were related to gray matter volume of fronto-parietal regions.Conclusion: Impairment of negative FER in patients with FTD is cross-cultural. The discrete neural correlates of FER indicate that emotional recognition processing is a multi-modal system in the brain. Focusing on the negative emotion recognition is a more effective way to discriminate healthy aging, MCI, and AD from FTD in older Korean adults.</p

Bone Mineral Density is an Independent Determinant of Left Ventricular Mass Index in the General Female Population

Background and Objectives: Left ventricular hypertrophy (LVH) is a well known cardiovascular prognostic predictor. Osteoporosis has been suggested to be associated with cardiovascular disease. According to studies of primary hyperparathyroidism, a pathophysiological association between calcium metabolism and LVH has been suggested but is not yet fully understood. This study was performed to investigate the association between bone mineral density (BMD) and left ventricular mass index (LVMI) in a general population. Subjects and Methods: Data from 460 subjects among 543 subjects sampled from a general population in a rural area in Korea were analyzed. BMD, echocardiography, brachial-ankle pulse wave velocity (baPWV), carotid intima-media thickness (IMT) measurement as well as the measurements of blood pressure, blood chemistry and metabolic parameters were analyzed. BMD was measured using the Sahara Clinical Bone Sonometer (Hologic Inc., Mass., USA). Results: Age of the subjects was 59.4??12.4 years. Males were 42.2% (n=194). In a simple correlation analysis on female subjects, age and waist circumference showed negative correlation, and body mass index (BMI) showed positive correlation with BMD. However, only age showed negative correlation with BMD in male subjects. After adjusting baPWV and carotid IMT, we found that BMD was an independent determinant of LVMI in female subjects (??=-13.703, p=0.016), but not in male subjects (??=-1.235, p=0.841). Conclusion: BMD is a consistent and independent determining factor of LVMI, BMI and carotid IMT in postmenopausal women. Copyright ?? 2010 The Korean Society of Cardiology

Prediction of Cerebral Amyloid With Common Information Obtained From Memory Clinic Practice

Background: Given the barriers prohibiting the broader utilization of amyloid imaging and high screening failure rate in clinical trials, an easily available and valid screening method for identifying cognitively impaired patients with cerebral amyloid deposition is needed. Therefore, we developed a prediction model for cerebral amyloid positivity in cognitively impaired patients using variables that are routinely obtained in memory clinics.Methods: Six hundred and fifty two cognitively impaired subjects from the Korean Brain Aging Study for the Early diagnosis and prediction of Alzheimer disease (KBASE) and the Alzheimer’s Disease Neuroimaging Initiative-2 (ADNI-2) cohorts were included in this study (107 amnestic mild cognitive impairment (MCI) and 69 Alzheimer’s disease (AD) dementia patients for KBASE cohort, and 332 MCI and 144 AD dementia patients for ADNI-2 cohort). Using the cross-sectional dataset from the KBASE cohort, a multivariate stepwise logistic regression analysis was conducted to develop a cerebral amyloid prediction model using variables commonly obtained in memory clinics. For each participant, the logit value derived from the final model was calculated, and the probability for being amyloid positive, which was calculated from the logit value, was named the amyloid prediction index. The final model was validated using an independent dataset from the ADNI-2 cohort.Results: The final model included age, sex, years of education, history of hypertension, apolipoprotein ε4 positivity, and score from a word list recall test. The model predicted that younger age, female sex, higher educational level, absence of hypertension history, presence of apolipoprotein ε4 allele, and lower score of word list recall test are associated with higher probability for being amyloid positive. The amyloid prediction index derived from the model was proven to be valid across the two cohorts. The area under the curve was 0.873 (95% confidence interval 0.815 to 0.918) for the KBASE cohort, and 0.808 (95% confidence interval = 0.769 to 0.842) for ADNI-2 cohort.Conclusion: The amyloid prediction index, which was based on commonly available clinical information, can be useful for screening cognitively impaired individuals with a high probability of amyloid deposition in therapeutic trials for early Alzheimer’s disease as well as in clinical practice

Intra-amniotic infection with genital mycoplasmas is characterized by an intense inflammatory response in the amniotic cavity and in the maternal compartment

OBJECTIVE: Genital mycoplasmas are the most frequent organisms responsible for intra-amniotic infection. Yet, they are considered to be less virulent than other bacteria. The purpose of this study was to compare the intensity of intra-amniotic and maternal inflammatory responses between cases of intra-amniotic infection (IAI) caused by genital mycoplasmas and IAI caused by other microorganisms. STUDY DESIGN: We studied the magnitude of the inflammatory response in 93 patients with preterm PROM and a positive amniotic fluid (AF) culture for microorganisms. Patients were divided into 2 groups: 1) those with genital mycoplasmas in the AF (ureaplasmas and/or Mycoplasma hominis, n 62); and 2) cases with other microorganisms (n 31). Patients with mixed infections (genital mycoplasmas and other microorganisms) were excluded. The intensity of intraamniotic inflammatory response was determined by the AF white blood cell (WBC) count, and that of the maternal inflammatory response was assessed by the concentration of C-reactive protein (CRP) and WBC count in maternal blood at the time of amniocentesis. RESULTS: 1) The median AF WBC count, maternal blood WBC count and plasma CRP concentration were significantly higher in cases with IAI caused by genital mycoplasmas than in those with IAI with other microorganisms (p 0.05 for each); and 2) there were no significant differences in maternal age, parity, gestational age at amniocentesis, rupture of membranes-to-amniocentesis interval, and use of corticosteroids and antibiotics before amniocentesis between the two groups. CONCLUSION: 1) Intra-amniotic infection caused by genital mycoplasmas results in a more intense inflammatory response in the amniotic cavity as well as in the maternal compartment than those caused by other microorganisms; 2) it is possible that chronicity can account for the more severe magnitude of intra-amniotic and maternal inflammatory response reported herein.