A Escala Multidimensional de Suporte Social Percebido (MSPSS), originalmente desenvolvida por Zimet, Dahlem, Zimet, e Farley (1988), foi criada para avaliar subjectivamente o suporte social proveniente da família, dos amigos e de outros significativos. Neste trabalho apresentam-se as características psicométricas da versão portuguesa da MSPSS. A escala foi avaliada num grupo de estudantes (n = 454), num grupo da população geral (n = 261) e num grupo de doentes com depressão major (n = 100). A análise factorial demonstrou a existência de três factores (Família, Amigos e Outros Significativos). Igualmente apresentou uma boa consistência interna, entre .85 e .95, considerando os três factores, os três grupos e ambos os géneros; apresentou uma adequada validade de construto e a estabilidade teste-reteste no grupo de estudantes e população geral apresentou valores entre .40 e .91. Os alfas de Cronbach no reteste oscilaram entre .87 e .95. A presente versão da MSPSS mostrou ter qualidades psicométricas adequadas para ser utilizada em estudantes, em sujeitos da população geral bem como em populações com psicopatologia depressiva, sendo necessária agora a continuação da investigação em outras amostras e utilizando estudos de seguimento.

The social rank and arrested defenses model for mood disorders bridges between animal and human models of psychopathology. There is increasing evidence that depression is associated with subordinated and loss of social rank, feeling inferior, shame, submissive behavior, and feeling defeated. These stressful states activate threat coping responses of fight and flight. If these are aroused but blocked, feelings of entrapment emerge with a negative impact on mood. The current study builds on previous studies and explores the association between depressive symptoms, social rank variables (of social comparison and submissive behavior), entrapment, and defeat in a sample of patients (n = 106) with major depression and in a sample of healthy controls (n = 116). Results showed that social rank variables, entrapment, and defeat were strongly associated with depressive symptoms in both samples. Entrapment and defeat showed significant association with other social rank variables. Logistic regression analysis revealed that defeat and internal entrapment were significant predictors of the belonging to the clinical or control groups. The present study extends previous research and supports the importance of defeat and external entrapment in clinical depression.

The Portuguese version of ACE-III has very good reliability and high diagnostic capacity in the context of MCI and dementia. ACE-III also holds concurrent and divergent validity.

Major depressive disorder (MDD) is a highly prevalent disorder, which has been associated with an abnormal response of the hypothalamus-pituitary-adrenal (HPA) axis. Reports have argued that an abnormal HPA axis response can be due to an altered P-Glycoprotein (P-GP) function. This argument suggests that genetic polymorphisms in ABCB1 may have an effect on the HPA axis activity; however, it is still not clear if this influences the risk of MDD. Our study aims to evaluate the effect of ABCB1 C1236T, G2677TA and C3435T genetic polymorphisms on MDD risk in a subset of Portuguese patients. DNA samples from 80 MDD patients and 160 control subjects were genotyped using TaqMan SNP Genotyping assays. A significant protection for MDD males carrying the T allele was observed (C1236T: odds ratio (OR)=0.360, 95% confidence interval [CI]: [0.140-0.950], p=0.022; C3435T: OR=0.306, 95% CI: [0.096-0.980], p=0.042; and G2677TA: OR=0.300, 95% CI: [0.100-0.870], p=0.013). Male Portuguese individuals carrying the 1236T/2677T/3435T haplotype had nearly 70% less risk of developing MDD (OR=0.313, 95% CI: [0.118-0.832], p=0.016, FDR p=0.032). No significant differences were observed regarding the overall subjects. Our results suggest that genetic variability of the ABCB1 is associated with MDD development in male Portuguese patients. To the best of our knowledge, this is the first report in Caucasian samples to analyze the effect of these ABCB1 genetic polymorphisms on MDD risk.

a b s t r a c tBackground: Hippocampal neurogenesis has been suggested as a downstream event of antidepressants (AD) mechanism of action and might explain the lag time between AD administration and the ther-apeutic effect. Despite the widespread use of AD in the context of Major Depressive Disorder (MDD) there are no reliable biomarkers of treatment response phenotypes, and a significant proportion of patients display Treatment Resistant Depression (TRD). Fas/FasL system is one of the best-known death-receptor mediated cell signaling systems and is recognized to regulate cell proliferation and tumor cell growth. Recently this pathway has been described to be involved in neurogenesis and neuroplasticity. Methods: Since FAS -670A4G and FASL -844T4C functional polymorphisms never been evaluated in the context of depression and antidepressant therapy, we genotyped FAS -670A 4G and FASL -844T4C in a subset of 80 MDD patients to evaluate their role in antidepressant treatment response phenotypes. Results: We found that the presence of FAS -670G allele was associated with antidepressant bad prog-nosis (relapse or TRD: OR ¼6.200; 95% CI: [1. .499]; p¼0.001), and we observed that patients carrying this allele have a higher risk to develop TRD (OR ¼10.895; 95% CI: [1.362-87.135]; p¼0.008). Moreover, multivariate analysis adjusted to potentials confounders showed that patients carrying G allele have higher risk of early relapse (HR ¼3.827; 95% CI: [1.072-13.659]; p¼0.039). FAS mRNA levels were down-regulated among G carriers, whose genotypes were more common in TRD patients. No association was found between FASL-844T 4C genetic polymorphism and any treatment phenotypes. Limitations: Small sample size. Patients used antidepressants with different mechanisms of action. Conclusion: To the best of our knowledge this is the first study to evaluate the role of FAS functional polymorphism in the outcome of antidepressant therapy. This preliminary report associates FAS -670A4G genetic polymorphism with Treatment Resistant Depression and with time to relapse. The current results may possibly be given to the recent recognized role of Fas in neurogenesis and/or neu-roplasticity.