Abstract

The clinical and biological heterogeneity that pervades the field of neuropsychiatry has hindered progress in uncovering the pathophysiological mechanisms of psychiatric illnesses. Indeed, it is rare to come across well-replicated pathological findings within or across disorders, and when such findings do arise they merit our attention and focus. In this issue, Pantazopoulos et al. ( 1 Pantazopoulos H. Wiseman J.T. Markota M. Ehrenfeld L. Berretta S. Decreased numbers of somatostatin-expressing neurons in the amygdala of subjects with bipolar disorder or schizophrenia: Relationship to circadian rhythms. Biol Psychiatry. 2017; 81: 536-547 Abstract Full Text Full Text PDF PubMed Scopus (35) Google Scholar ) bring forward a pathological feature that is common to postmortem brains of patients with schizophrenia and bipolar disorder and that is shared by other psychiatric or neurodegenerative brain disorders ( 2 Lin L.C. Sibille E. Reduced brain somatostatin in mood disorders: A common pathophysiological substrate and drug target?. Front Pharmacol. 2013; 4: 110 Crossref PubMed Scopus (81) Google Scholar ). Decreased Numbers of Somatostatin-Expressing Neurons in the Amygdala of Subjects With Bipolar Disorder or Schizophrenia: Relationship to Circadian RhythmsBiological PsychiatryVol. 81Issue 6PreviewGrowing evidence points to a key role for somatostatin (SST) in schizophrenia (SZ) and bipolar disorder (BD). In the amygdala, neurons expressing SST play an important role in the regulation of anxiety, which is often comorbid in these disorders. We tested the hypothesis that SST-immunoreactive (IR) neurons are decreased in the amygdala of subjects with SZ and BD. Evidence for circadian SST expression in the amygdala and disrupted circadian rhythms and rhythmic peaks of anxiety in BD suggest a disruption of rhythmic expression of SST in this disorder. Full-Text PDF

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