A randomized controlled trial of a homeâ based training programme to decrease depression in family caregivers of persons with dementia

AimsThe aim of this study was to explore distinct trajectories of caregiversâ depressive symptoms and the effects of a training programme on these trajectories over 18 months after the programme.BackgroundOverall effects of caregiverâ training programmes on family caregiversâ depressive symptoms have been reported, but few studies explored distinct courses of changes in caregiversâ depressive symptoms and followed up intervention effects on these distinct courses.DesignRandomized clinical trial.MethodsFamily caregivers (n = 116) were randomly assigned into experimental (n = 57) and control (n = 59) groups. The experimental group received the training programme with telephone consultation and the control group received written educational materials and social telephone followâ ups. Caregiversâ depressive symptoms were assessed from June 2009 â March 2012 by selfâ completed questionnaires before, at 2 weeks and 3, 6, 12 and 18 months after the intervention. Groups of individual trajectories were distinguished using groupâ based trajectory modelling.ResultsCaregiversâ depressive symptoms fell into three stable trajectories: nonâ depressed, mildly blue and depressed. After controlling for covariates, caregivers who received the caregiverâ training programme were less likely than those who did not experience persistent depressive symptoms (b = â 1·92, odds ratio = 0·15, P < 0·05).ConclusionDepressive symptoms of family caregivers of persons with dementia were relatively stable and followed three distinct courses: nonâ depressed, mildly blue and depressed. Therefore, caregiversâ depressive symptoms should be assessed as early as possible. Caregivers in the experimental group had a lower probability of persistent depressive symptoms than caregivers in the control group. Therefore, this training programme can be used by healthcare providers for persons with dementia and their caregivers. Trial registration number: NCT02667951.Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/136266/1/jan13157.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/136266/2/jan13157_am.pd

A Post-hoc Study of D-Amino Acid Oxidase in Blood as an Indicator of Post-stroke Dementia

Stroke is an important risk factor for dementia. Epidemiological studies have indicated a high incidence of dementia in stroke patients. There is currently no effective biomarker for the diagnosis of post-stroke dementia (PSD). D-amino acid oxidase (DAO) is a flavin-dependent enzyme widely distributed in the central nervous system. DAO oxidizes D-amino acids, a process which generates neurotoxic hydrogen peroxide and leads to neurodegeneration. This study aimed to examine post-stroke plasma DAO levels as a biomarker for PSD. In total, 53 patients with PSD, 20 post-stroke patients without dementia (PSNoD), and 71 age- and gender-matched normal controls were recruited. Cognitive function was evaluated at more than 30 days post-stroke. Plasma DAO was measured using the enzyme-linked immunosorbent assay. White matter hyperintensity (WMH), a neuroimaging biomarker of cerebral small vessel diseases, was determined by magnetic resonance imaging. We found that plasma DAO levels were independently higher in PSD subjects than in PSNoD subjects or the controls and were correlated with the WMH load in stroke patients. Using an area under the curve (AUC)/receiver operating characteristic analysis, plasma DAO levels were significantly reliable for the diagnosis of PSD. The sensitivity and specificity of the optimal cut-off value of 321 ng/ml of plasma DAO for the diagnosis of PSD were 75 and 88.7%, respectively. In conclusion, our data support that plasma DAO levels were increased in PSD patients and correlated with brain WMH, independent of age, gender, hypertension, and renal function. Plasma DAO levels may therefore aid in PSD diagnosis

Validation of a Chinese version of disease specific quality of life scale (HFS-36) for hemifacial spasm in Taiwan

<p>Abstract</p> <p>Background and object</p> <p>There was no Chinese questionnaire to evaluate the health-related quality of life (HRQoL) in patients with hemifacial spasm (HFS). In this study, we aimed to validate a new disease-specific HRQoL scale for HFS (HFS-36) in Chinese version, and compared it to SF-36, a generic HRQoL scale.</p> <p>Patients and Methods</p> <p>The HFS-36 Chinese version was modified from English version of HFS-30, including subscales of mobility, activities of daily living (ADL), emotional well-being, stigma, social support, cognition, bodily discomfort, and communication. All the items were scored on the 5-point scales, ranging from 0(never) to 4(always). Patients with HFS were asked to answer HFS-36 and SF-36 questionnaires on the same day before and 6-8 weeks after Botulinum toxin (BTX) injections, respectively. The reliability and validity of HFS-36 scale were evaluated statistically.</p> <p>Results</p> <p>Totally, 103 patients (68 females; 35 males) were recruited in this study, with a mean age of 57.6 ± 11.5 years and a mean duration of HFS for 7.6 ± 5.8 years. The intra-class correlation (ICC) and Cronbach's α were over 0.7 in the majority of items. HFS-36 showed a good correlation to HFS severity before BTX treatment and a significant improvement of subscale scoring after BTX treatment. HFS-36 also had a significant correlation to the mental health of SF-36.</p> <p>Conclusions</p> <p>The Chinese version of HFS-36 demonstrated a good reliability and validity in subscales of motility, ADL, emotion well-being, stigma and bodily discomfort. The HRQoL was significantly improved after BTX treatment assessed by HFS-36 or SF-36. Compared to SF-36, HFS-36 scale was more sensitive and specific to evaluate the HRQoL in HFS.</p

Identification of Gene Networks and Pathways Associated with Guillain-Barré Syndrome

BACKGROUND: The underlying change of gene network expression of Guillain-Barré syndrome (GBS) remains elusive. We sought to identify GBS-associated gene networks and signaling pathways by analyzing the transcriptional profile of leukocytes in the patients with GBS. METHODS AND FINDINGS: Quantitative global gene expression microarray analysis of peripheral blood leukocytes was performed on 7 patients with GBS and 7 healthy controls. Gene expression profiles were compared between patients and controls after standardization. The set of genes that significantly correlated with GBS was further analyzed by Ingenuity Pathways Analyses. 256 genes and 18 gene networks were significantly associated with GBS (fold change ≥2, P<0.05). FOS, PTGS2, HMGB2 and MMP9 are the top four of 246 significantly up-regulated genes. The most significant disease and altered biological function genes associated with GBS were those involved in inflammatory response, infectious disease, and respiratory disease. Cell death, cellular development and cellular movement were the top significant molecular and cellular functions involved in GBS. Hematological system development and function, immune cell trafficking and organismal survival were the most significant GBS-associated function in physiological development and system category. Several hub genes, such as MMP9, PTGS2 and CREB1 were identified in the associated gene networks. Canonical pathway analysis showed that GnRH, corticotrophin-releasing hormone and ERK/MAPK signaling were the most significant pathways in the up-regulated gene set in GBS. CONCLUSIONS: This study reveals the gene networks and canonical pathways associated with GBS. These data provide not only networks between the genes for understanding the pathogenic properties of GBS but also map significant pathways for the future development of novel therapeutic strategies

Exploring the aging process of cognitively healthy adults by analyzing cerebrospinal fluid metabolomics using liquid chromatography-tandem mass spectrometry

Abstract Background During biological aging, significant metabolic dysregulation in the central nervous system may lead to cognitive decline and neurodegeneration. However, the metabolomics of the aging process in cerebrospinal fluid (CSF) has not been thoroughly explored. Methods In this cohort study of CSF metabolomics using liquid chromatography-mass spectrometry (LC–MS), fasting CSF samples collected from 92 cognitively unimpaired adults aged 20–87 years without obesity or diabetes were analyzed. Results We identified 37 metabolites in these CSF samples with significant positive correlations with aging, including cysteine, pantothenic acid, 5-hydroxyindoleacetic acid (5-HIAA), aspartic acid, and glutamate; and two metabolites with negative correlations, asparagine and glycerophosphocholine. The combined alterations of asparagine, cysteine, glycerophosphocholine, pantothenic acid, sucrose, and 5-HIAA showed a superior correlation with aging (AUC = 0.982). These age-correlated changes in CSF metabolites might reflect blood–brain barrier breakdown, neuroinflammation, and mitochondrial dysfunction in the aging brain. We also found sex differences in CSF metabolites with higher levels of taurine and 5-HIAA in women using propensity-matched comparison. Conclusions Our LC–MS metabolomics of the aging process in a Taiwanese population revealed several significantly altered CSF metabolites during aging and between the sexes. These metabolic alterations in CSF might provide clues for healthy brain aging and deserve further exploration

Structural study of the microtubule-associated protein tau locus of Alzheimer's disease in Taiwan

Background: Haplotype structure of the microtubule-associated protein tau (MAPT) gene is associated with various tauopathies in the Caucasian population. With the knowledge that the association between MAPT structure and disease may be distinct in different ethnics, we intend to investigate the haplotype structure of MAPT in Taiwanese and test it for association with Alzheimer's disease (AD). Methods: One hundred and eight AD patients and 108 sex- and-age matched healthy controls were recruited from the dementia outpatient clinic of Chang Gung Medical center. We genotyped the del-In9 marker that defines the extended H1 and H2 clades. We selected 21 single-nucleotide polymorphisms (SNPs) in the extended MAPT region from Japanese SNPs database and dbSNP database. Using the software TagIt, we analyzed the linkage disequilibrium structure of MAPT and compared the allele and genotype distribution between patient group and control group. Results: All the Taiwanese participants were H1 haplotypes. Linkage disequilibrium analysis showed the haplotype blocks in Taiwanese population had a smaller size in comparison to that of the Caucasian population. Single locus association showed significant p value in one of the tagging variants (rs242557) in our Taiwanese AD case-control cohorts. Conclusion: MAPT gene has four haplotype blocks in the Taiwanese population, each of around 40 kbp. In both European study and our study, the SNP rs242557 showed association with AD. Given the position of this SNP, the most possible explanation is that genetic variability in tau expression contributes to the risk of developing AD