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Feeling Inferior Fi Has Substantially More For A House
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McGregor Thomas 1, Jonathan Savits 1, 2, Zhang 3, Kaiping Burrows 1, Ryan Smith 1, Leandra Figueroa-Hall 1, Reyes Kuplicki 1, Sahib S. Halsa 1, Uyasuyuki Taki 3, 4, 5, Tracy Kent Teague 6, 7, 8, Michael R. Irwin 9, 10, 11, Fang-Cheng yesh 12, Martin P. Paulus 1, 2, Haisia Cheng 1, * and on behalf of Tulsa 1000 Investigators †
Institute of Development, Aging and Cancer, Department of Aging and Geriatric Medicine Research, Tohoku University, Sendai 980-8575, Japan
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Received: 25 November 2021 / Revised: 17 December 2021 / Accepted: 22 December 2021 / Published: 28 December 2021
(1) Background: Increasing evidence suggests that inflammation can cause neural circuit dysfunction and play an important role in the pathogenesis of major depressive disorder (MDD). However, whether inflammation affects the integrity of white matter tracts remains understudied. . MDD. . These bundles include the bilateral cortico-striatal tract, thalamic projections, inferior longitudinal fasciculus, corpus callosum (part of the forceps and tapetum), cingulum bundle, and superior longitudinal fasciculus III. Importantly, the alliances bounced back after twelve potential opponents. Bilateral intercourse and partial thalamic radiation showed positive associations with CRP levels, but these associations did not remain significant after adjustment for confounders. (4) Conclusion: Peripheral inflammation may contribute to the etiology of MDD by affecting the microstructural integrity of corticocortical white matter tracts.
A growing body of human and animal research suggests that systemic inflammation can cause corticolimbic circuit dysfunction and contribute to the onset and maintenance of major depressive disorder (MDD) [ 1 , 2 , 3 , 4 , 5 , 6 ]. Neuroimaging studies have identified cortical and sub-cortical brain regions highly sensitive to inflammation, including the amygdala, ventral striatum, insula, cingulate cortex, orbitofrontal cortex, and hippocampus [ 4 , 5 , 6 ]. Previous studies have suggested that structural and functional abnormalities in this region may underlie several features of the depressive phenotype, including anhedonia, emotional dysregulation, cognitive impairment, and anxiety [ 3 , 7 , 8 , 9 ]. Interestingly, recent analyzes have shown that decreased resting state activity within and between these corticolimbic regions is associated with increased inflammatory symptoms [4, 10, 11, 12]. Given that white matter tracts support the functioning and functional connectivity of these brain regions, systemic inflammation may alter the structural connections between these regions, leading to functional changes. However, the relationship between systemic inflammation and integrity of white matter pathways is only beginning to be explored. Understanding this relationship should aid in mechanistic understanding of the interactions between peripheral inflammation and structural and functional brain changes observed in MDD.
Peripheral blood C-reactive protein (CRP) is often used as a marker of systemic inflammation in clinical practice. CRP is synthesized by the liver and regulated as part of the acute phase innate immunity [15, 16]. CRP is induced by interleukin (IL)-6 and is moderately correlated with concentrations of IL-6 and other inflammatory cytokines such as interleukin 1 beta (IL-1β) and tumor necrosis factor (TNF) [ 17 , 18 ]. Importantly, previous studies have shown a strong correlation between plasma CRP and cerebrospinal fluid CRP (r = 0.855) [18]. In the context of MDD, CRP is one of the most frequently repeated inflammatory markers associated with MDD, as at least five meta-analyses have reported increased CRP in MDD patients [19, 20, 21, 22, 23]. Furthermore, prospective data from longitudinal studies suggest that higher CRP is associated with an increased risk of developing depressive symptoms [22, 24]. Thus, CRP is a well-established inflammatory marker to study the relationship between systemic inflammation and white matter microstructural integrity in the context of MDD.
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The neuroinflammation hypothesis of depression suggests that systemic inflammation may enhance structural integrity of the brain through immune-mediated neurotoxic effects [ 1 , 2 , 3 , 4 , 25 , 26 ]. To our knowledge, there are three studies that have directly examined the relationship between peripheral inflammatory markers and white matter integrity in MDD, as indexed by decreased fractional anisotropy (FA) values. One study compared 35 depressive episode and drug-naïve MDD patients with 35 age- and sex-matched healthy controls and found that IL-1β was inversely correlated with FA values in bilateral inferior fronto-occipital fascicles, caudal fasciculus and corpus callosum gene in the MDD group [27]. Another study compared 22 patients with MDD and 22 healthy subjects. They reported similar findings, showing that peripheral TNF concentrations were negatively correlated with FA in several white matter regions, including the corpus callosum and left anterior and superior corona radiata [28]. A study combining MDD and healthy control participants (n = 590) showed that methylation-based CRP activity was associated with decreased FA area, and the strongest association was found in the external capsule and anterior limb of the internal capsule. [29]. However, all three of these studies used a tract-based spatial statistics (TBSS) approach that extrapolates volumetric data to the white matter region to gain statistical power through downscaling [ 30 ]. Although TBSS is a popular approach for voxel-based diffusion sensor imaging data analysis, this approach has been shown to have shortcomings relative to fully automated analysis methods [ 31 , 32 , 33 , 34 ]. One of the main concerns with TBSS is that the skeleton projection step differs greatly in anatomical specificity and accuracy, as skeletonization reduces white matter tracts in a single voxel-thick slice [ 34 ]. Therefore, results obtained from TBSS can be difficult to interpret and may not necessarily indicate pathology. Thus, although previous studies have provided some evidence to support the hypothesis that CRP levels affect white matter integrity in MDD, the anatomical specificity of this effect remains unclear.
Here, we hypothesize that individuals with high CRP levels exhibit reduced white matter integrity, particularly among brain regions that are more sensitive to peripheral inflammatory processes, than those with low CRP levels, indicating an ongoing inflammatory process. . To test this hypothesis, we used a novel connectivity analysis that can identify differences with high spatial specificity and comprehensively map white matter pathways affected by systemic inflammation in MDD patients. In addition, we examined the relationship between specific white matter tracts and depressive symptoms.
Study approval was obtained from the Western Institutional Review Board (#20101611), and written informed consent was obtained from all participants. The present study included 176 patients aged 18–55 years with a diagnosis of MDD (with or without anxiety disorder). All participants were assessed with the Mini International Neuropsychiatric Inventory (MINI) [36] by a trained psychiatric clinical interviewer. Participants were drawn from the first half of the Tulsa 1000 (T1000) study (the current half samples are not currently available) [37]. Data was collected from January 2015 to February 2017. Participants were recruited from Laureate Psychiatric Clinic and Hospital, other local mental and behavioral health providers, and through newspaper advertisements, flyers, online, radio, and other media in the Tulsa area.
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