scholarly journals Mechanism of Depression through Brain Function Imaging of Depression Patients and Normal People

2022 ◽  
Vol 2022 ◽  
pp. 1-13
Author(s):  
Chaozhi Tang ◽  
Yuling Zhang ◽  
Zihan Zhai ◽  
Xiaofeng Zhu ◽  
Chaowei Wang ◽  
...  

In recent years, functional magnetic resonance technology has discovered that abnormal connections in different brain regions of the brain may serve as the pathophysiological mechanism of mental illness. Exploring the mechanism of information flow and integration between different brain regions is of great significance for understanding the pathophysiological mechanism of mental illness. This article aims to analyze the mechanism of depression by comparing human brain images of normal people and patients with depression and conduct research. Fluoxetine, a selective 5-HT reuptake inhibitor (SSRI) widely used in clinical practice, can selectively inhibit 5-HT transporter and block the reuptake of 5-HT by the presynaptic membrane. The effect of 5-HT is prolonged and increased, thereby producing antidepressant effects. It has low affinity for adrenergic, histaminergic, and cholinergic receptors and has a weaker effect, resulting in fewer adverse reactions. This paper uses the comparative experiment method and the Welch method and uses the average shortest path length L to describe the average value of the shortest path length between two nodes in the network. Attention refers to the ability of a person’s mental activity to point and to concentrate on something. Sustained attention means that attention is kept on a certain cognitive object or activity for a certain period of time, which is also called the stability of attention. The research on attention of depression patients generally focuses on continuous attention, and the results obtained show inconsistencies. Most studies have shown that the sustained attention of the depression group is significantly worse than that of the healthy control group. An overview of magnetic resonance imaging technology and an analysis of depression based on resting state were carried out. The key brain areas of the sample core network were scanned, and the ALFF results were analyzed. The data showed that the severity of depression in the depression group was negatively correlated with the ReHo value in the posterior left cerebellum ( P = 0.010 ). The sense of despair was negatively correlated with the ReHo value in the posterior right cerebellum ( P = 0.013 ). The diurnal variation was negatively correlated with the ReHo value of the left ring ( P = 0.014 ). It was positively correlated with the ReHo value of the left ventricle ( P = 0.048 ). This experiment has better completed the research on the mechanism of depression by analyzing the functional images of patients with depression and normal human brain.

2021 ◽  
Author(s):  
Ludovica Brusaferri ◽  
Zeynab Alshelh ◽  
Daniel Martins ◽  
Minhae Kim ◽  
Akila Weerasekera ◽  
...  

The impact of COVID-19 on human health extends beyond the morbidity and death toll directly caused by the SARS-CoV-2 virus. In fact, accumulating evidence indicates a global increase in the incidence of fatigue, brain fog and depression, including among non-infected, since the pandemic onset. Motivated by previous evidence linking those symptoms to neuroimmune activation in other pathological contexts, we hypothesized that subjects examined after the enforcement of lockdown/stay-at-home measures would demonstrate increased neuroinflammation. We performed simultaneous brain Positron Emission Tomography / Magnetic Resonance Imaging in healthy volunteers either before (n=57) or after (n=15) the 2020 Massachusetts lockdown, using [11C]PBR28, a radioligand for the glial marker 18 kDa translocator protein (TSPO). First, we compared [11C]PBR28 signal across pre- and post-lockdown cohorts. Then, we evaluated the link between neuroinflammatory signals and scores on a questionnaire assessing mental and physical impacts of the pandemic. Further, we investigated multivariate associations between the spatial pattern of [11C]PBR28 post-lockdown changes and constitutive brain gene expression in post-mortem brains (Allen Human Brain Atlas). Finally, in a subset (n=13 pre-lockdown; n=11 post-lockdown), we also used magnetic resonance spectroscopy to quantify brain (thalamic) levels of myoinositol (mIns), another neuroinflammatory marker. Both [11C]PBR28 and mIns signals were overall stable pre-lockdown, but markedly elevated after lockdown, including within brain regions previously implicated in stress, depression and 'sickness behaviors'. Moreover, amongst the post-lockdown cohort, subjects endorsing higher symptom burden showed higher [11C]PBR28 PET signal compared to those reporting little/no symptoms. Finally, the post-lockdown [11C]PBR28 signal changes were spatially aligned with the constitutive expression of several genes highly expressed in glial/immune cells and/or involved in neuroimmune signaling. Our results suggest that pandemic-related stressors may have induced sterile neuroinflammation in healthy individuals that were not infected with SARS-CoV-2. This work highlights the possible impact of the COVID-19 pandemic-related lifestyle disruptions on human brain health.


2013 ◽  
Vol 119 (6) ◽  
pp. 1453-1464 ◽  
Author(s):  
Richard E. Harris ◽  
Vitaly Napadow ◽  
John P. Huggins ◽  
Lynne Pauer ◽  
Jieun Kim ◽  
...  

Abstract Background: Chronic pain remains a significant challenge for modern health care as its pathologic mechanisms are largely unknown and preclinical animal models suffer from limitations in assessing this complex subjective experience. However, human brain neuroimaging techniques enable the assessment of functional and neurochemical alterations in patients experiencing chronic pain and how these factors may dynamically change with pharmacologic treatment. Methods: To identify the clinical action of pregabalin, a proven analgesic, the authors performed three complementary brain neuroimaging procedures: (proton magnetic resonance spectroscopy, functional magnetic resonance imaging, and functional connectivity magnetic resonance imaging) in 17 chronic pain patients diagnosed with fibromyalgia. Results: The authors found that pregabalin but not placebo reduces combined glutamate + glutamine levels within the posterior insula (pregabalin P = 0.016; placebo P = 0.71). Interestingly, reductions in clinical pain were associated with reductions in brain connectivity of this structure to brain regions within the default mode network during pregabalin (r = 0.82; P = 0.001) but not placebo (r = −0.13; P = 0.63). Response of default mode network regions to experimental pain was also reduced with pregabalin (P = 0.018) but not placebo (P = 0.182). Perhaps most importantly, baseline values for all three neuroimaging markers predicted subsequent analgesic response to pregabalin but not placebo. Conclusions: The results of this study suggest that pregabalin works in part by reducing insular glutamatergic activity, leading to a reduction of the increased functional connectivity seen between brain regions in chronic pain states. The study also supports a role for human brain imaging in the development, assessment, and personalized use of central-acting analgesics.


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