The etiology of depression is still elusive and a matter of debate; however, inflammation and autoimmune processes have been proposed as 1 pathophysiologic pathway. In this cohort study of 194 483 women, Roberts and colleagues examined the temporal association between systemic lupus erythematosus (SLE) and depression and found a 2-fold increase of SLE in those women who had a history of depression. Thus, depression may change inflammatory processes and set the stage for the subsequent emergence of autoimmune diseases.
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Patients with schizophrenia have an excess cardiovascular mortality, but to our knowledge, no studies have investigated whether taking recommended treatments reduces this mortality. In a nationwide cohort of 105 018 patients with myocardial infarction, Kugathasan and colleagues showed that patients diagnosed with schizophrenia who did not receive cardioprotective treatment had the highest mortality rate, followed by treated patients diagnosed with schizophrenia and then by the general population. Thus, administration of proper cardiovascular treatment can reduce some of the increased cardiac mortality among patients with schizophrenia. In an Editorial, Druss discusses implications for the field.
Cognitive deterioration after schizophrenia onset is poorly understood. Niendam and colleagues followed up 87 patients with recent-onset schizophrenia and 93 healthy participants over 24 months and showed that patients had significantly impaired performance in a cognitive control task as well as reduced activation in dorsolateral prefrontal and parietal cortex, but the trajectory of activation changes was similar between patients and control individuals; younger age at onset was not associated with reduced cognition or activation. Thus, young patients do not show deterioration or disruption of ongoing brain development in the period following illness onset.
The mechanism of variable patient responses to antipsychotic medications remains unknown. Wang and colleagues conducted a 6-week multicenter open-label randomized clinical trial with 3023 patients of Chinese Han descent with schizophrenia and found that rare damaging variants in an N-methyl-d-aspartate–mediated synaptic current gene set were significantly enriched in the nonresponder group in a discovery and a replication sample. Thus, genetic variation in N-methyl-d-aspartate neurotransmission may be implicated in antipsychotic medication efficacy. Van den Oord and colleagues discuss the findings in an Invited Commentary.
Negative symptoms are associated with a range of poor clinical outcomes, but their structure is not well understood in schizophrenia. Using data from 3 instruments in 860 outpatients with schizophrenia, Strauss and colleagues found that a 5-factor model provided the most parsimonious fit for the latent structure of negative symptoms. These findings suggest that the trend toward conceptualizing negative symptoms as having 2 distinct dimensions does not adequately capture the complexity of the construct.