Summarize data on metabolic syndrome (MS) in bipolar disorder (BD).A systematic review of the literature was conducted using the Medline, Embase and PsycInfo databases, using the keywords "metabolic syndrome", "insulin resistance" and "metabolic X syndrome" and cross-referencing them with "bipolar disorder" or "mania". The following types of publications were candidates for review: (i) clinical trials, (ii) studies involving patients diagnosed with bipolar disorder or (iii) data about metabolic syndrome. A 5-point quality scale was used to assess the methodological weight of the studies.Thirty-nine articles were selected. None of studies reached the maximum quality score of 5 points. The prevalence of MS was significantly higher in BD individuals when compared to a control group. The analysis of MS subcomponents showed that abdominal obesity was heterogeneous. Individuals with BD had significantly higher rates of hypertriglyceridemia than healthy controls. When compared to the general population, there were no significant differences in the prevalence of low HDL-c in individuals with BD. Data on hypertension were also inconclusive. Rates of hyperglycemia were significantly greater in patients with BD compared to the general population.The overall results point to the presence of an association between BD and MS, as well as between their subcomponents.

Invasion of the central nervous system (CNS) by microorganisms is a severe and frequently fatal event during the course of many infectious diseases. It may lead to deafness, blindness, cerebral palsy, hydrocephalus, cognitive impairment or permanent neurological dysfunction in survivors. Pathogens can cross the blood-brain barrier by transcellular migration, paracellular migration and in infected macrophages. Pathogens may breach the blood-brain barrier and be recognized by antigen-presenting cells through the binding of Toll-like receptors. This induces the activation of nuclear factor kappa B or mitogen-activated protein kinase pathways and subsequently induces leukocyte infiltration and proliferation and the expression of numerous proteins involved in inflammation and the immune response. Many brain cells can produce cytokines, chemokines and other pro-inflammatory molecules in response to bacteria stimuli; as a consequence, polymorphonuclear cells are attracted and activated, and release large amounts of superoxide anion and nitric oxide, leading to peroxynitrite formation and oxidative stress. This cascade leads to lipid peroxidation, mitochondrial damage and blood-brain barrier breakdown, contributing to cellular injury during neuronal infection. Current evidence suggests that bacterial CNS infections can play a role in the etiopathogenesis of behavioral disorders by increasing pro-inflammatory cytokines and bacterial virulence factors. The aim of this review is to summarize the current knowledge of the relevant pathophysiologic steps in CNS infections.

To overview the development of the Sydney-based Black Dog Institute.The strengths and limitations of the Institute's predecessor (the Mood Disorders Unit) gave way to a more ambitious Black Dog Institute, and this article gives an overview of the Institute's structural and functional components.It is argued that the Institute serves as a model for modern psychiatric service delivery.The Institute's model of linking clinical, research, education and community activities to advance the understanding, diagnosis and management of mood disorders is detailed for wider consideration.

The use of clinical staging models is emerging as a novel and useful paradigm for diagnosing severe mental disorders. The term "neuroprogression" has been used to define the pathological reorganization of the central nervous system along the course of severe mental disorders. In bipolar disorder (BD), neural substrate reactivity is changed by repeated mood episodes, promoting a brain rewiring that leads to an increased vulnerability to life stress.A search in the PubMed database was performed with the following terms: "staging", "neuroprogression", "serum", "plasma", "blood", "neuroimaging", "PET scan", "fMRI", "neurotrophins", "inflammatory markers" and "oxidative stress markers", which were individually crossed with "cognition", "functionality", "response to treatments" and "bipolar disorder". The inclusion criteria comprised original papers in the English language. Abstracts from scientific meetings were not included.We divided the results according to the available evidence of serum biomarkers as potential mediators of neuroprogression, with brain imaging, cognition, functioning and response to treatments considered as consequences.The challenge in BD treatment is translating the knowledge of neuronal plasticity and neurobiology into clinical practice. Neuroprogression and staging can have important clinical implications, given that early and late stages of the disorder appear to present different biological features and therefore may require different treatment strategies.

Bipolar disorder (BD) is a prevalent, chronic and progressive illness. There is a growing body of evidence indicating that brain-derived neurotrophic factor (BDNF) plays an important role in the pathophysiology of BD.The aim of this study was to evaluate BDNF plasma levels in BD patients with long term illness in comparison with controls.87 BD type I patients and 58 controls matched by age, gender and education level were enrolled in this study. All subjects were assessed by the Mini-International Neuropsychiatric Interview and the patients by the Young Mania Rating Scale and the Hamilton Depression Rating Scale. The plasma levels of BDNF were measured by ELISA.On average, patients had suffered from BD for 23.4 years. In comparison with controls, BD patients with mania presented a 1.90-fold increase in BDNF plasma levels (p = .001), while BD patients in remission presented a 1.64-fold increase in BDNF plasma levels (p = .03). BDNF plasma levels were not influenced by age, length of illness or current medications.The present study suggests that long-term BD patients exhibit increased circulating levels of BDNF.