Stigmatization of schizophrenia is widespread and its genetic explanation may potentially increase the stigma. The present study investigated whether seeing schizophrenia as a genetic or environmental disorder might influence perceived beliefs towards people with schizophrenia and whether social stigmatizing attitudes were differently perceived the 202 subjects who were recruited. Perceived social stigmatizing attitudes were compared among participants who read two vignettes depicting a person with schizophrenia. Then, the Standardized Stigmatization Questionnaire (SSQ) was administered. A genetic explanation of schizophrenia was more frequently associated with stigmatizing attitudes. Also, there were higher levels of perceived stigmatization in medical students and medical doctors than in other groups based on their social experience or background. However, the sample size was small and this was a non-experimental design; also the SSQ would benefit from more cross-validation. About half of the participants perceived stigmatizing social attitudes. Finally, considering schizophrenia as a genetic disorder influenced participants perception of other people's beliefs about dangerousness and unpredictability and people's desire for social distance.

Agomelatine actually represents an intriguing option in the treatment of affective disorders.

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Major depression is one of the leading causes of disability and psychosocial impairment worldwide. Although many advances have been made in the neurobiology of this complex disorder, the pathophysiological mechanisms are still unclear. Among the proposed theories, impaired neuroplasticity and hippocampal neurogenesis have received considerable attention. The possible association between hippocampal neurogenesis, neurotrophic factors, major depression, and antidepressant responses was critically analyzed using a comprehensive search of articles/book chapters in English language between 1980 and 2014. One common emerging theme was that chronic stress and major depression are associated with structural brain changes such as a loss of dendritic spines and synapses, as well as reduced dendritic arborisation, together with diminished glial cells in the hippocampus. Both central monoamines and neurotrophic factors were associated with a modulation of hippocampal progenitor proliferation and cell survival. Accordingly, antidepressants are generally suggested to reverse stress-induced structural changes augmenting dendritic arborisation and synaptogenesis. Such antidepressant consequences are supposed to stem from their stimulatory effects on neurotrophic factors, and possibly modulation of glial cells. Of course, accumulating evidence also suggested that glutamatergic systems are implicated in not only basic neuroplastic processes, but also in the core features of depression. Hence, it is critical that antidepressant strategies focus on links between the various neurotransmitter systems, neurotrophic processes of hippocampal neurogenesis, and neurotrophic factors with regards to depressive symptomology. The identification of novel alternative antidepressant medications that target these systems is discussed in this review.

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