Short-Term Family-Based Intervention with Schizophrenia: A Clinical Outcome Study

The University Archives has determined that this item is of continuing value to OSU's history.Presenter: Kia J. Bentley, Ph.D., ACSW, School of Social Work, Louisiana State University - "Short-Term Family-Based Intervention with Schizophrenia: A Clinical Outcome Study".The Ohio State University College of Social Wor

Review of \u3cem\u3eOut of Bedlam: The Truth about Deinstitutionalization.\u3c/em\u3e Ann Braden Johnson. Reviewed by Kia J. Bentley, Virginia Commonwealth University

Book Review. Ann Braden Johnson. Out of Bedlam: The Truth about Deinstitutionalization. New York: Basic Books, 1990. $13.00 paperback

Review of \u3cem\u3eMental Disorders in the Social Environment.\u3c/em\u3e Stuart A. Kirk (Ed.). Reviewed by Kia J. Bentley.

Book review of Stuart A. Kirk (Ed.), Mental Disorders in the Social Environment: Critical Perspectives. New York: Columbia University Press, 2005, $69.50 hardcover,$34.50 papercover

Review of \u3cem\u3eRefusing Care: Forced Treatment and the Rights of the Mentally Ill.\u3c/em\u3e Elyn R. Saks. Reviewed by Kai J. Bentley.

Book review of Elyn R. Saks, Refusing Care: Forced Treatment and the Rights of the Mentally Ill. Chicago: University of Chicago Press, 2003. $35.00 hardcover,$24.50 papercover

Moving beyond neurons: the role of cell type-specific gene regulation in Parkinson's disease heritability

Parkinson’s disease (PD), with its characteristic loss of nigrostriatal dopaminergic neurons and deposition of α-synuclein in neurons, is often considered a neuronal disorder. However, in recent years substantial evidence has emerged to implicate glial cell types, such as astrocytes and microglia. In this study, we used stratified LD score regression and expression-weighted cell-type enrichment together with several brain-related and cell-type-specific genomic annotations to connect human genomic PD findings to specific brain cell types. We found that PD heritability attributable to common variation does not enrich in global and regional brain annotations or brain-related cell-type-specific annotations. Likewise, we found no enrichment of PD susceptibility genes in brain-related cell types. In contrast, we demonstrated a significant enrichment of PD heritability in a curated lysosomal gene set highly expressed in astrocytic, microglial, and oligodendrocyte subtypes, and in LoF-intolerant genes, which were found highly expressed in almost all tested cellular subtypes. Our results suggest that PD risk loci do not lie in specific cell types or individual brain regions, but rather in global cellular processes detectable across several cell types

Identification of novel risk loci, causal insights, and heritable risk for Parkinson's disease: a meta-analysis of genome-wide association studies

Background Genome-wide association studies (GWAS) in Parkinson's disease have increased the scope of biological knowledge about the disease over the past decade. We aimed to use the largest aggregate of GWAS data to identify novel risk loci and gain further insight into the causes of Parkinson's disease. Methods We did a meta-analysis of 17 datasets from Parkinson's disease GWAS available from European ancestry samples to nominate novel loci for disease risk. These datasets incorporated all available data. We then used these data to estimate heritable risk and develop predictive models of this heritability. We also used large gene expression and methylation resources to examine possible functional consequences as well as tissue, cell type, and biological pathway enrichments for the identified risk factors. Additionally, we examined shared genetic risk between Parkinson's disease and other phenotypes of interest via genetic correlations followed by Mendelian randomisation. Findings Between Oct 1, 2017, and Aug 9, 2018, we analysed 7·8 million single nucleotide polymorphisms in 37 688 cases, 18 618 UK Biobank proxy-cases (ie, individuals who do not have Parkinson's disease but have a first degree relative that does), and 1·4 million controls. We identified 90 independent genome-wide significant risk signals across 78 genomic regions, including 38 novel independent risk signals in 37 loci. These 90 variants explained 16–36% of the heritable risk of Parkinson's disease depending on prevalence. Integrating methylation and expression data within a Mendelian randomisation framework identified putatively associated genes at 70 risk signals underlying GWAS loci for follow-up functional studies. Tissue-specific expression enrichment analyses suggested Parkinson's disease loci were heavily brain-enriched, with specific neuronal cell types being implicated from single cell data. We found significant genetic correlations with brain volumes (false discovery rate-adjusted p=0·0035 for intracranial volume, p=0·024 for putamen volume), smoking status (p=0·024), and educational attainment (p=0·038). Mendelian randomisation between cognitive performance and Parkinson's disease risk showed a robust association (p=8·00 × 10−7). Interpretation These data provide the most comprehensive survey of genetic risk within Parkinson's disease to date, to the best of our knowledge, by revealing many additional Parkinson's disease risk loci, providing a biological context for these risk factors, and showing that a considerable genetic component of this disease remains unidentified. These associations derived from European ancestry datasets will need to be followed-up with more diverse data. Funding The National Institute on Aging at the National Institutes of Health (USA), The Michael J Fox Foundation, and The Parkinson's Foundation (see appendix for full list of funding sources)

From Every Direction: Guilt, Shame, and Blame Among Parents of Adolescents with Co-occurring Challenges

This article explores the results of a qualitative inquiry into guilt, blame, and shame as experienced by parents of children with co-occurring mental health and substance use challenges. These interviews represent both the lived experience of parents, as well as the perspective of clinicians who work with these families. The parent–clinician alliance is taken as a central context for considering how these experiences may affect the dynamics of the helping relationship. Analyses of these results suggest that guilt, blame, and shame are often experienced by parents and have important implications for engagement and therapeutic processes. Parents associate feelings of blame with interactions from a number of helping professionals and connect personal characteristics, parenting behaviors, and relationship issues with experiences of shame and guilt surrounding their children’s behavioral health challenges. Finally, the information that is shared across these interviews is used to guide the development of a number of practice guidelines for social workers who work with families of adolescents that experience co-occurring mental health and substance use issues

Approaching Parental Guilt, Shame, and Blame in a Helping Relationship: Multiple Methods for Teaching and Learning

Social workers often feel ill-prepared to effectively engage parents in conversations about guilt, shame, and blame related to their children’s mental health or substance use challenges. To address that problem, we suggest that specific content should be integrated into social work courses to teach students how to acknowledge and sensitively manage these issues in their practice with families across cultures and family forms. Content, activities, and assignments are offered, built around three learning strategies (enhanced lecture, case-based learning, and experiential learning) to help students build therapeutic relationships based on a deep appreciation of parents’ emotional experiences