Publications by authors named "Sublette M"

Background: Early life adversity is a risk factor for psychopathology and is associated with epigenetic alterations in the 5-HT receptor gene promoter. The 5-HT receptor mediates neurotrophic effects, which could affect brain structure and function. We examined relationships between self-reported early childhood abuse, 5-HT receptor promoter DNA methylation, and gray matter volume (GMV) in Major Depressive Disorder (MDD).

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Background: Pro-inflammatory cytokines such as interleukin (IL)-6 and tumor necrosis factor (TNF)-α are elevated in response to psychosocial stress; however, less is known about other inflammatory markers.

Methods: We explored response to the Trier Social Stress Test (TSST) of 16 cytokines and growth factors in patients with major depressive disorder (MDD, n = 12) vs. healthy volunteers (HV, n = 16).

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Background: Childhood and lifetime adversity may reduce brain serotonergic (5-HT) neurotransmission by epigenetic mechanisms.

Aims: We tested the relationships of childhood adversity and recent stress to serotonin 1A (5-HT) receptor genotype, DNA methylation of this gene in peripheral blood monocytes and 5-HT receptor binding potential (BP) determined by positron emission tomography (PET) in 13 brain regions, in participants with major depressive disorder (MDD) and healthy volunteers (controls).

Method: Medication-free participants with MDD ( = 192: 110 female, 81 male, 1 other) and controls ( = 88: 48 female, 40 male) were interviewed about childhood adversity and recent stressors and genotyped for rs6295.

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Serotonin transporter (5-HTT) binding deficits are reported in major depressive disorder (MDD). However, most studies have not considered serotonin system anatomy when parcellating brain regions of interest (ROIs). We now investigate 5-HTT binding in MDD in two novel ways: (1) use of a 5-HTT tract-based analysis examining binding along serotonergic axons; and (2) using the Copenhagen University Hospital Neurobiology Research Unit (NRU) 5-HT Atlas, based on brain-wide binding patterns of multiple serotonin receptor types.

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Using magnetic resonance diffusion tensor imaging data from 45 patients with major depressive disorder (MDD) and 41 healthy controls (HCs), network indices based on a 246-region Brainnetcome Atlas were investigated in the two groups, and in the MDD subgroups that were subgrouped based on their duration of the disease. Correlation between the network indices and the duration of illness was also examined. Differences were observed between the MDD subgroup (short disease duration) and the HC group, but not between the MDD and HC groups.

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Objectives: The microbiome is a rapidly advancing biomedical frontier with relevance for psychiatric illness. The gut microbiota interact with the central nervous system bidirectionally through the gut-brain axis and generate substances that may influence host metabolism, including short-chain fatty acids such as butyrate. Understanding gut microbiota in bipolar disorder (BD) may suggest new disease markers and treatment approaches.

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Background: It has been argued that unipolar major depressive disorder (MDD) and bipolar disorder (BD) exist on a continuous spectrum, given their overlapping symptomatology and genetic diatheses. The Bipolarity Index (BI) is a scale that considers bipolarity as a continuous construct and was developed to assess confidence in bipolar diagnosis. Here we investigated whether BI scores correlate with gray matter volume (GMV) in a sample of unmedicated unipolar and bipolar depressed individuals.

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We evaluated associations of smoking heaviness markers and the effects of smoking cessation on the intestinal microbiota and cardiovascular disease risk factors in current smokers undertaking a quit attempt. Participants were current smokers enrolled in a prospective randomized clinical trial of smoking cessation therapies with visits at baseline, 2, and 12 weeks. Genomic DNA was extracted from fecal samples followed by 16S rRNA gene sequencing and analysis using the QIIME2 software workflow.

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