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Altered peripheral immune/inflammatory system and brain volumetric changes have been implicated in the pathophysiology of bipolar disorder (BD). This study aimed to evaluate how peripheral levels of cytokines are related to volumetric brain changes in euthymic patients with BD.
Euthymic patients with BD (n = 21) and healthy controls (n = 22) were enrolled in this exploratory study. Blood samples were collected on the same day of clinical assessment and neuroimaging. Cytokines were measured through cytometric bead array method. Neuroimaging data were acquired using a sagittal three-dimensional magnetic resonance imaging T1-weighted fast field echo sequence and was processed using FreeSurfer.
Compared to controls, BD patients had significantly lower volumes in the cingulate, medial-orbitofrontal (MOF) and parahippocampal regions. We found a negative correlation between right MOF volume and interferon-gamma levels (β = −0.431, P = .049) and a positive correlation between interleukin-10 levels and left posterior cingulate volume (β = 0.457, P = .048).
Our results support the involvement of inflammatory pathways in structural brain changes in BD.
Mood disorders are the most common mental illnesses with a lifetime prevalence of up to 20% worldwide (1). Major depressive disorder (MDD) and bipolar disorder (BD) are significant health problems in the United States and worldwide (2). In the United States alone, the lifetime prevalence of MDD is up to 17%, and that of BD about 2.1% (2) that can go up to 4% of individuals with mood episodes not meeting episodic criteria included. Both are chronic illnesses characterized by recurrent episodes of depression and mania and depression in MDD and BD, respectively. Severe and disabling forms of BD and MDD are associated with increased risk of suicide, decline of physical health, and reduced productivity, and both conditions are associated with high rates of completed suicide of up to 8% (3).
To more effectively investigate, diagnose, and treat mood disorders, there is a need to move beyond standard clinical characterizations. While symptom-based nosology has provided a reliable and pragmatic framework for clinical practice, advances in neuroimaging research have permitted the possibility of identifying neurophysiologic biomarkers that index underlying pathophysiologic processes and provide an effective complement to clinical symptoms. Functional magnetic resonance imaging (fMRI) is one of the common state-of-the-art neuroimaging approaches for investigating brain disorders and has been very useful in providing a functional neuroanatomic account of neural disturbances in mood disorders.
Mood disorders such as depression and bipolar disorder are common mental illnesses, affecting millions of patients worldwide. The application of newly available brain imaging methods to the study of mood disorders holds substantial promise in uncovering the brain mechanisms affected in these illnesses. This comprehensive and authoritative text features contributions from leading international experts, providing easily accessible information on the study of the brain mechanisms involved in the causation of mood disorders and the available treatments. Topics covered include the potential of magnetoencephalography (MEG), neuroimaging brain inflammation in depression, electrophysiology studies in mood disorders, and the applications of machine learning, filling an important gap in available neuropsychiatric literature and highlighting new developments. An invaluable resource for practitioners in the fields of psychiatry, neurology, primary care medicine, and related mental health professions, as well as researchers, students, graduate and post-graduate trainees.
The history of pharmacological treatments for depression began in the 1950s, with the serendipitous discovery of the antidepressant potential of drugs like the tricyclic antidepressant, imipramine. Since then, many new, safer, and better tolerated, antidepressant drugs have appeared on the market (1), and now depression can be treated widely in primary care. However, finding a treatment effective for an individual patient is not a trivial task, with only around 30% of patients responding to their first antidepressant (AD) medication, most requiring multiple changes, and about one-third not responding at all (2).
Animal experimental studies have prompted concerns that widespread use of 3,4-methylenedioxymethamphetamine (MDMA; ‘ecstasy’) by young people may pose a major public health problem in terms of persistent serotonin neurotoxicity.
To determine the status of brain serotonin neurons in a group of abstinent MDMA users.
We assessed the integrity of brain serotonin neurons by measuring serotonin transporter (SERT) binding using positron emission tomography (PET) and [11C]DASB in 12 former MDMA users, 9 polydrug users who had never taken MDMA and 19 controls who reported no history of illicit drug use.
There was no significant difference in the binding potential of [11C]DASB between the groups in any of the brain regions examined.
To the extent that [11C]DASB binding provides an index of the integrity of serotonin neurons, our findings suggest that MDMA use may not result in long-term damage to serotonin neurons when used recreationally in humans.
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