Eye-tracking evidence of a relationship between attentional bias for emotional faces and depression severity in patients with treatment-resistant depression.

In a retrospective study, 54 patients with treatment-resistant major depressive disorder (TRD) completed a free-viewing task in which they had to freely explore pairs of faces (an emotional face (happy or sad) opposite to a neutral face). Attentional bias to emotional faces was calculated for early and sustained attention. We observed a significant negative correlation between depression severity as measured by the 10-item Montgomery-Åsberg Depression Rating Scale (MADRS) and sustained attention to happy faces. In addition, we observed a positive correlation between depression severity and sustained attention to sad faces. No significant correlation between depression severity and early attention was found for either happy or sad faces. Although conclusions from the current study are limited by the lack of comparison with a control group, the eye-tracking free-viewing task appears to be a relevant, accessible and easy-to-use tool for measuring depression severity through emotional attentional biases in TRD.

Caregivers in anorexia nervosa: is grief underlying parental burden?

ABSTARCT: PURPOSE: Anorexia Nervosa (AN) is a severe chronic disorder and parents' experience of caregiving is usually marked by emotional distress and burden. Severe chronic psychiatric disorders are known to be linked with the concept of grief. Grief has not been investigated in AN. The aim of this study was to explore parents' and adolescents' characteristics that may be related to parental burden and grief in AN, and the link between these two dimensions. METHODS: Eighty mothers, 55 fathers and their adolescents (N = 84) hospitalized for AN participated in this study. Evaluations of clinical characteristics of the adolescent's illness were completed, as well as self-evaluations of adolescent and parental emotional distress (anxiety, depression, alexithymia). Levels of parental burden were evaluated with the Experience of Caregiving Inventory and levels of parental grief with the Mental Illness Version of the Texas Revised Inventory of Grief. RESULTS: Main findings indicated that the burden was higher in parents of adolescents with a more severe AN; fathers' burden was also significantly and positively related to their own level of anxiety. Parental grief was higher when adolescents' clinical state was more severe. Paternal grief was related to higher anxiety and depression, while maternal grief was correlated to higher alexithymia and depression. Paternal burden was explained by the father's anxiety and grief, maternal burden by the mother's grief and her child's clinical state. CONCLUSION: Parents of adolescents suffering from AN showed high levels of burden, emotional distress and grief. These inter-related experiences should be specific targets for intervention aimed at supporting parents. Our results support the extensive literature on the need to assist fathers and mothers in their caregiving role. This in turn may improve both their mental health and their abilities as caregivers of their suffering child. LEVEL OF EVIDENCE: Level III: Evidence obtained from cohort or case-control analytic studies.

Correction to: ACE2 activation protects against cognitive decline and reduces amyloid pathology in the Tg2576 mouse model of Alzheimer's disease.

Unfortunately, the acknowledgement section was not included in the original publication.

ACE2 activation protects against cognitive decline and reduces amyloid pathology in the Tg2576 mouse model of Alzheimer's disease.

Mid-life hypertension and cerebrovascular dysfunction are associated with increased risk of later life dementia, including Alzheimer's disease (AD). The classical renin-angiotensin system (cRAS), a physiological regulator of blood pressure, functions independently within the brain and is overactive in AD. cRAS-targeting anti-hypertensive drugs are associated with reduced incidence of AD, delayed onset of cognitive decline, and reduced levels of Aß and tau in both animal models and human pathological studies. cRAS activity is moderated by a downstream regulatory RAS pathway (rRAS), which is underactive in AD and is strongly associated with pathological hallmarks in human AD, and cognitive decline in animal models of CNS disease. We now show that enhancement of brain ACE2 activity, a major effector of rRAS, by intraperitoneal administration of diminazene aceturate (DIZE), an established activator of ACE2, lowered hippocampal Aß and restored cognition in mid-aged (13-14-month-old) symptomatic Tg2576 mice. We confirmed that the protective effects of DIZE were directly mediated through ACE2 and were associated with reduced hippocampal soluble Aß42 and IL1-ß levels. DIZE restored hippocampal MasR levels in conjunction with increased NMDA NR2B and downstream ERK signalling expression in hippocampal synaptosomes from Tg2576 mice. Chronic (10 weeks) administration of DIZE to pre-symptomatic 9-10-month-old Tg2576 mice, and acute (10 days) treatment in cognitively impaired 12-13-month-old mice, prevented the development of cognitive impairment. Together these data demonstrate that ACE2 enhancement protects against and reverses amyloid-related hippocampal pathology and cognitive impairment in a preclinical model of AD.