No abstract

The present study is concerned with the stigma of mental illness. It examines the subjective element of the experience of stigma among a sample of in-patients with different mental disorders. The sample was taken from consecutive admissions of in-patients meeting International Classification of Diseases, 10th revision (ICD-10) criteria for mental disorders who had capacity to decide on participation in the study and were willing to respond to the structured interview. The study was undertaken in an Egyptian private psychiatric hospital. The structured clinical interview included aspects of the emotional, behavioral, and cognitive effects of having a psychiatric diagnosis on in-patients with various diagnostic labels in an Egyptian psychiatric hospital. It also studied whether this effect changes with specific disorders, total duration of illness, or sociodemographic variables as gender, age, or educational level. The study illustrated the core items of stigmatization attached to the diagnosis of mental illness ( 1 ), which more than half of the participants responded affirmatively. The study aimed to explore the most prevailing aspects of stigma or social disadvantage; hoping that this may offer a preliminary guide for clinicians to address these issues in their practice.

No abstract

Dementia is a global medical and societal challenge; it has devastating personal, social and economic costs, which will increase rapidly as the world’s population ages. Despite this, there are no disease-modifying treatments for dementia; current therapy modestly improves symptoms but does not change the outcome. Therefore, new treatments are urgently needed—particularly any that can slow down the disease’s progression. Many of the neurodegenerative diseases that lead to dementia are characterised by common pathological responses to abnormal protein production and misfolding in brain cells, raising the possibility of the broad application of therapeutics that target these common processes. The unfolded protein response (UPR) is one such mechanism. The UPR is a highly conserved cellular stress response to abnormal protein folding and is widely dysregulated in neurodegenerative diseases. In this review, we describe the basic machinery of the UPR, as well as the evidence for its overactivation and pathogenicity in dementia, and for the marked neuroprotective effects of its therapeutic manipulation in murine models of these disorders. We discuss drugs identified as potential UPR-modifying therapeutic agents—in particular the licensed antidepressant trazodone—and we review epidemiological and trial data from their use in human populations. Finally, we explore future directions for investigating the potential benefit of using trazodone or similar UPR-modulating compounds for disease modification in patients with dementia.