Social Support and Religion: Mental Health Service Use and Treatment of Schizophrenia

The perceptions and religious beliefs held by family members, mental health and health care professionals, and the community may affect the treatment of individuals with schizophrenia. To better identify and understand the influence of families, professionals and community members on individual’s treatment for schizophrenia, this review paper examines: (1) the religious perceptions of families, professionals, and the public towards schizophrenia; (2) religious perceptions of the etiology of schizophrenia; (3) how others perceive religion as a coping mechanism; and (4) how religion influences treatment engagement and help-seeking behaviors. MEDLINE and PsycInfo databases were systematically searched from 1980 to 2010 using the terms schizophrenia, schizoaffective, schizophreniform, psychotic disorder not otherwise specified and religion, religiosity, spirituality, and faith. Forty-three (n = 43) original research studies met the inclusion criteria. This study found that religious beliefs influence the treatment of schizophrenia in the following ways: Religious themes were positively associated with coping, treatment engagement and help-seeking behavior. Evidence of religious underpinnings was found in perceptions of etiology. The findings also indicate that there is often both a preference among family members and caregivers to utilize religious-based professionals and caution toward mental health professionals. Researchers and professionals may find avenues for improving treatment through examining the interaction of religious and schizophrenia at the social support level

Child mental health in Jordanian orphanages: effect of placement change on behavior and caregiving

Background: To assess the mental health and behavioral problems of children in institutional placements in Jordan to inform understanding of current needs, and to explore the effects of placement change on functioning and staff perceptions of goodness-of-fit. Methods: An assessment was completed of 134 children between 1.5? 12 years-of-age residing in Jordanian orphanages. The Child Behavior Checklist was used to assess prevalence rates of problems across externalizing and internalizing behavior and DSM-IV oriented subscales. Also included was caregiver perceived goodness-of-fit with each child, caregiving behavior, and two placement change-clock variables; an adjustment clock measuring time since last move, and an anticipation clock measuring time to next move. Results: 28% were in the clinical range for the internalizing domain on the CBCL, and 22% for the externalizing domain. The children also exhibited high levels of clinical range social problems, affective disorder, pervasive developmental disorder, and conduct problems. Internalizing problems were found to decrease with time in placement as children adjust to a prior move, whereas externalizing problems increased as the time to their next age-triggered move drew closer, highlighting the anticipatory effects of change. Both behavioral problems and the change clocks were predictive of staff perceptions of goodness-of-fit with the children under their care. Conclusions: These findings add to the evidence demonstrating the negative effects of orphanage rearing, and highlight the importance of the association between behavioral problems and child-caregiver relationship pathways including the timing of placement disruptions and staff perceptions of goodness-of-fit

A coding polymorphism in matrix metalloproteinase 9 reduces risk of scarring sequelae of ocular Chlamydia trachomatis infection.

BACKGROUND: Trachoma, an infectious disease of the conjunctiva caused by Chlamydia trachomatis, is an important global cause of blindness. A dysregulated extracellular matrix (ECM) proteolysis during the processes of tissue repair following infection and inflammation are thought to play a key role in the development of fibrotic sequelae of infection, which ultimately leads to blindness. Expression and activity of matrix metalloproteinase 9 (MMP-9), a major effector of ECM turnover, is up-regulated in the inflamed conjunctiva of trachoma subjects. Genetic variation within the MMP9 gene affects in vitro MMP9 expression levels, enzymatic activity and susceptibility to various inflammatory and fibrotic conditions. METHODS: We genotyped 651 case-control pairs from trachoma endemic villages in The Gambia for coding single nucleotide polymorphisms (SNPs) in the MMP9 gene using the high-throughput Sequenom system. Single marker and haplotype conditional logistic regression (CLR) analysis for disease association was performed. RESULTS: The Q279R mutation located in exon 6 of MMP9 was found to be associated with lower risk for severe disease sequelae of ocular Chlamydia trachomatis infection. This mutation, which leads to a nonsynonymous amino-acid change within the active site of the enzyme may reduce MMP-9-induced degradation of the structural components of the ECM during inflammatory episodes in trachoma and its associated fibrosis. CONCLUSION: This work supports the hypothesis that MMP-9 has a role in the pathogenesis of blinding trachoma

TMEM106B is a genetic modifier of frontotemporal lobar degeneration with C9orf72 hexanucleotide repeat expansions

Hexanucleotide repeat expansions in chromosome 9 open reading frame 72 (C9orf72) have recently been linked to frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis, and may be the most common genetic cause of both neurodegenerative diseases. Genetic variants at TMEM106B influence risk for the most common neuropathological subtype of FTLD, characterized by inclusions of TAR DNA-binding protein of 43 kDa (FTLD-TDP). Previous reports have shown that TMEM106B is a genetic modifier of FTLD-TDP caused by progranulin (GRN) mutations, with the major (risk) allele of rs1990622 associating with earlier age at onset of disease. Here, we report that rs1990622 genotype affects age at death in a single-site discovery cohort of FTLD patients with C9orf72 expansions (n = 14), with the major allele correlated with later age at death (p = 0.024). We replicate this modifier effect in a 30-site international neuropathological cohort of FTLD-TDP patients with C9orf72 expansions (n = 75), again finding that the major allele associates with later age at death (p = 0.016), as well as later age at onset (p = 0.019). In contrast, TMEM106B genotype does not affect age at onset or death in 241 FTLD-TDP cases negative for GRN mutations or C9orf72 expansions. Thus, TMEM106B is a genetic modifier of FTLD with C9orf72 expansions. Intriguingly, the genotype that confers increased risk for developing FTLD-TDP (major, or T, allele of rs1990622) is associated with later age at onset and death in C9orf72 expansion carriers, providing an example of sign epistasis in human neurodegenerative disease

Genome-wide analyses as part of the international FTLD-TDP whole-genome sequencing consortium reveals novel disease risk factors and increases support for immune dysfunction in FTLD

Frontotemporal lobar degeneration with neuronal inclusions of the TAR DNA-binding protein 43 (FTLD-TDP) represents the most common pathological subtype of FTLD. We established the international FTLD-TDP whole genome sequencing consortium to thoroughly characterize the known genetic causes of FTLD-TDP and identify novel genetic risk factors. Through the study of 1,131 unrelated Caucasian patients, we estimated that C9orf72 repeat expansions and GRN loss-of-function mutations account for 25.5% and 13.9% of FTLD-TDP patients, respectively. Mutations in TBK1 (1.5%) and other known FTLD genes (1.4%) were rare, and the disease in 57.7% of FTLD-TDP patients was unexplained by the known FTLD genes. To unravel the contribution of common genetic factors to the FTLD-TDP etiology in these patients, we conducted a two-stage association study comprising the analysis of whole-genome sequencing data from 517 FTLD-TDP patients and 838 controls, followed by targeted genotyping of the most associated genomic loci in 119 additional FTLD-TDP patients and 1653 controls. We identified three genome-wide significant FTLD-TDP risk loci: one new locus at chromosome 7q36 within the DPP6 gene led by rs118113626 (pvalue=4.82e-08, OR=2.12), and two known loci: UNC13A, led by rs1297319 (pvalue=1.27e-08, OR=1.50) and HLA-DQA2 led by rs17219281 (pvalue=3.22e-08, OR=1.98). While HLA represents a locus previously implicated in clinical FTLD and related neurodegenerative disorders, the association signal in our study is independent from previously reported associations. Through inspection of our whole genome sequence data for genes with an excess of rare loss-of-function variants in FTLD-TDP patients (n≥3) as compared to controls (n=0), we further discovered a possible role for genes functioning within the TBK1-related immune pathway (e.g. DHX58, TRIM21, IRF7) in the genetic etiology of FTLD-TDP. Together, our study based on the largest cohort of unrelated FTLD-TDP patients assembled to date provides a comprehensive view of the genetic landscape of FTLD-TDP, nominates novel FTLD-TDP risk loci, and strongly implicates the immune pathway in FTLD-TDP pathogenesis

Conflicting Principles in Social Work Doctoral Programs: The Effects of Unspoken Power Dynamics

Doctoral students are guided by two distinct sets of principles - those of their profession and academe - that may conflict. The social work profession is built upon the collaborative principles of equity, diversity, social justice, anti-oppression, participation, respect for differences, and human dignity. In contrast, academe at the doctoral level promotes competition, productivity, research, publication, and the advancement of new knowledge and practice. When these frequently discordant tenets intersect in such areas as the supervisory relationship or the appointment of research and teaching assistants, the resulting unanticipated power dynamics can have a dramatic impact on students and faculty. Social work principles can be employed by faculty and students to identify and address these power dynamics, thus enriching the doctoral experience.Social Work, Graduate College o

Evidence-Based Family Psychoeducational Interventions for Children and Adolescents with Psychotic Disorders

Introduction: Family psychoeducational interventions have consistently been found to impact families positively and reduce relapse rates in individuals with psychotic disorders. Research finds that, for adults, family psychoeducational interventions are effective in preventing relapse and improving social and occupational functioning. Psychotic disorders are increasingly recognized as having early onset, yet limited psychoeducational evidence-based intervention services are available and no intervention has centered exclusively on youth with a psychotic disorders and their families. Method: This article reviews the evidence-based literature on family psychoeducational interventions for persons with a psychotic disorder, with a specific focus on the gaps, strengths, and limitations of family psychoeducational treatment for children and adolescents. This article incorporates current research in the proposed development of a family psychoeducational intervention exclusively for adolescents with a psychotic disorder and their parents. Results: A conceptual psychoeducational multiple family group intervention (PMFG) for adolescents with a psychotic disorder is presented. Conclusion: The impact of these disorders affects not only the diagnosed adolescents and their families, but places a significant burden on the health care system and society. This article adapts an evidence-based intervention to improve prognosis, social and peer functioning, and reduce relapse in children and adolescents throughout their life cycle