Prevalence of Substance use Among Depressed Female Patients

2021 ◽  
Vol 15 (12) ◽  
pp. 3562-3564
Author(s):  
Muhammad Iqbal Afridi ◽  
Chooni Lal ◽  
Rozeena Ameen Dharwarwala ◽  
Jawed Akbar Dars ◽  
Fariha Iqbal ◽  
...  

Depressive disorder is a common mental disorder and one of the leading causes of disability around the globe. It is characterized by depressed mood, lack of enjoyment, decreased activity, negative thoughts and reduced concentration for at least two weeks. Globally 350 million people are suffering from depression and 18.34 million people from Southeast Asia alone. Major depressive disorder is growing in overall disease burden around the world. It is predicted to be the leading cause of disease burden by 2030, and it is already the leading cause in women worldwide. Depression affects the prefrontal cortex, cingulate gyrus, amygdala, hippocampus, thalamus and hypothalamus. These brain regions are involved in the regulation of motivation, eating, sleeping, energy level, circadian rhythm, and responses to rewarding and aversive stimuli, which are all abnormal in depressed people.

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Jiao Li ◽  
Jakob Seidlitz ◽  
John Suckling ◽  
Feiyang Fan ◽  
Gong-Jun Ji ◽  
...  

AbstractMajor depressive disorder (MDD) has been shown to be associated with structural abnormalities in a variety of spatially diverse brain regions. However, the correlation between brain structural changes in MDD and gene expression is unclear. Here, we examine the link between brain-wide gene expression and morphometric changes in individuals with MDD, using neuroimaging data from two independent cohorts and a publicly available transcriptomic dataset. Morphometric similarity network (MSN) analysis shows replicable cortical structural differences in individuals with MDD compared to control subjects. Using human brain gene expression data, we observe that the expression of MDD-associated genes spatially correlates with MSN differences. Analysis of cell type-specific signature genes suggests that microglia and neuronal specific transcriptional changes account for most of the observed correlation with MDD-specific MSN differences. Collectively, our findings link molecular and structural changes relevant for MDD.


2021 ◽  
Author(s):  
Shasha Li ◽  
Ya Chen ◽  
Gaoxiong Duan ◽  
Yong Pang ◽  
Huimei Liu ◽  
...  

Abstract Background: Although the acupuncture treatment of major depressive disorder(MDD) has been recognized by the latest clinical practice guidelines of the American Academy of Internal Medicine, complex therapeutic mechanisms need further to clarify. The aim of the study is investigate whether the aberrant resting state brain network in MDD patients could be regulated by acupuncture at GV20 using functional magnetic resonance imaging(fMRI) combined with degree centrality(DC) method. Results: Compared to healthy subjects, MDD patients exhibited significantly aberrant DC in widely brain regions, including cortical(PFC, precuneus, temporal, insula) and sub-cortical (thalamus, putamen and caudate) structures. Furthermore, results showed that acupuncture at GV20 induced down-regulation the DC of abnormal brain regions in MDD patients. Conclusions: Our findings provide imaging evidence to support that GV20-related acupuncture stimulation may modulate the abnormal brain function state in MDD patients by using fMRI technique combined with DC analysis. This study may partly interpret the neural mechanisms of acupuncture at GV20 which is used to treat patients with MDD in clinical. Trial registration: ChiCTR, ChiCTR-IOR-15006357. Registered 05 May 2015, http://www.chictr.org.cn/showproj.aspx?proj=10922.


2019 ◽  
Vol 3 ◽  
pp. 247054701987788
Author(s):  
Megan M. Hoch ◽  
Gaelle E. Doucet ◽  
Dominik A. Moser ◽  
Won Hee Lee ◽  
Katherine A. Collins ◽  
...  

Background Digital therapeutics such as cognitive–emotional training have begun to show promise for the treatment of major depressive disorder. Available clinical trial data suggest that monotherapy with cognitive–emotional training using the Emotional Faces Memory Task is beneficial in reducing depressive symptoms in patients with major depressive disorder. The aim of this study was to investigate whether Emotional Faces Memory Task training for major depressive disorder is associated with changes in brain connectivity and whether changes in connectivity parameters are related to symptomatic improvement. Methods Fourteen major depressive disorder patients received Emotional Faces Memory Task training as monotherapy over a six-week period. Patients were scanned at baseline and posttreatment to identify changes in resting-state functional connectivity and effective connectivity during emotional working memory processing. Results Compared to baseline, patients showed posttreatment reduced connectivity within resting-state networks involved in self-referential and salience processing and greater integration across the functional connectome at rest. Moreover, we observed a posttreatment increase in the Emotional Faces Memory Task-induced modulation of connectivity between cortical control and limbic brain regions, which was associated with clinical improvement. Discussion These findings provide initial evidence that cognitive–emotional training may be associated with changes in short-term plasticity of brain networks implicated in major depressive disorder. Conclusion Our findings pave the way for the principled design of large clinical and neuroimaging studies.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Haixia Zheng ◽  
Bart N. Ford ◽  
Rayus Kuplicki ◽  
Kaiping Burrows ◽  
Peter W. Hunt ◽  
...  

AbstractHuman cytomegalovirus (HCMV) is a neurotropic herpes virus known to cause neuropathology in patients with impaired immunity. Previously, we reported a reduction in the gray matter volume (GMV) of several brain regions in two independent samples of participants who were seropositive for HCMV (HCMV+) compared to matched participants who were seronegative for HCMV (HCMV−). In addition to an independent replication of the GMV findings, this study aimed to examine whether HCMV+ was associated with differences in resting-state functional connectivity (rsfMRI-FC). After balancing on 11 clinical/demographic variables using inverse probability of treatment weighting (IPTW), GMV and rsfMRI-FC were obtained from 99 participants with major depressive disorder (MDD) who were classified into 42 HCMV+ and 57 HCMV− individuals. Relative to the HCMV− group, the HCMV+ group showed a significant reduction of GMV in nine cortical regions. Volume reduction in the right lateral orbitofrontal cortex (standardized beta coefficient (SBC) = −0.32, [95%CI, −0.62 to −0.02]) and the left pars orbitalis (SBC = −0.34, [95%CI, −0.63 to −0.05]) in the HCMV+ group was also observed in the previous study. Regardless of the parcellation method or analytical approach, relative to the HCMV− group, the HCMV+ group showed hypoconnectivity between the hubs of the sensorimotor network (bilateral postcentral gyrus) and the hubs of the salience network (bilateral insula) with effect sizes ranging from SBC = −0.57 to −0.99. These findings support the hypothesis that a positive HCMV serostatus is associated with altered connectivity of regions that are important for stress and affective processing and further supports a possible etiological role of HCMV in depression.


2011 ◽  
Vol 26 (S2) ◽  
pp. 2085-2085
Author(s):  
T. Frodl

IntroductionThe underlying neurobiology of major depressive disorder (MDD) is likely to represent an interaction between genetic susceptibility and environmental factors like stress. There is growing evidence that epigenetic processes might mediate the effects of the social environment during childhood on gene expression.ObjectivesWe investigated in multimodal high-resolution MRI-genetic studies whether microstructural and functional brain changes are the result of gene-environment interactions.MethodsPatients with major depressive disorder (MDD), high-risk subjects for developing MDD and healthy participants were investigated using high-resolution magnetic resonance imaging (MRI), high angular resolution diffusion imaging (HARDI) and functional MRI. Furthermore, we assessed early life adversity and measured the serotonin transporter polymorphisms (5-HTTLPR).ResultsWe demonstrated that patients with MDD have smaller hippocampal and frontal cortex volumes associated with gen-environment interactions. Healthy Subjects at risk for developing depression, who manage to stay healthy, show better activation of the frontal cognitive control system. Those who had stronger fibre connections between frontal and temporal brain regions also better managed incidences of adversity in early life.ConclusionsStress x gene interactions seem to account for at least some of the structural brain changes. Resilience against environmental stressors might be associated with stronger neural fibre connections and more effective cognitive control networks.


Author(s):  
Jill M. Goldstein ◽  
L. Holsen ◽  
S. Cherkerzian ◽  
M. Misra ◽  
R.J. Handra

Studies have demonstrated that major depressive disorder (MDD) is intimately tied to neuroendocrine dysregulation. This arises, in part, from the fact that brain regions that regulate mood also regulate primary neuroendocrine axes and metabolic functions. We and others demonstrated that the origin of MDD-neuroendocrine deficits begins in fetal development, is sex-dependent, emerges just post-puberty, and can be catalyzed by pregnancy (postpartum) and menopause. Here, we critically review clinical and preclinical studies to argue that higher MDD risk in women may arise, in part, from hormone-dependent pathogenic processes initiated during fetal development that drive sex-dependent developmental alterations of HPA circuitry emerging post-puberty with lifelong consequences.


Author(s):  
Revathy U. Chottekalapanda ◽  
Paul Greengard ◽  
Yotam Sagi

Major depressive disorder (MDD) affects more than 20 million people in the United States. Depression is comorbid with other psychiatric disorders and can increase risks of drug and alcohol abuse and suicide. Available antidepressants have limited efficacy and new therapeutic targets are needed. MDD and antidepressant responses are mediated via neurotransmitter signaling mechanisms and inflammatory responses involving an integrated network of limbic brain regions that include hippocampus, prefrontal cortex, and nucleus accumbens. Although this limbic circuit is broadly described, researchers do not understand how the properties of neurons within the circuit are altered in depression. The authors present the regulation of the p11 signaling module in this circuit, describe the diagnostic aspects of p11 function, and lay out a cellular and molecular framework for the understanding of MDD and the development of novel antidepressant therapies.


2015 ◽  
Vol 5 (9) ◽  
pp. e636-e636 ◽  
Author(s):  
F Mamdani ◽  
B Rollins ◽  
L Morgan ◽  
R M Myers ◽  
J D Barchas ◽  
...  

Abstract Stress can be a predisposing factor to psychiatric disorders and has been associated with decreased neurogenesis and reduced hippocampal volume especially in depression. Similarly, in white blood cells chronic psychological stress has been associated with telomere shortening and with mood disorders and schizophrenia (SZ). However, in previous post-mortem brain studies from occipital cortex and cerebellum, no difference in telomere length was observed in depression. We hypothesized that in psychiatric disorders, stress-driven accelerated cellular aging can be observed in brain regions particularly sensitive to stress. Telomere length was measured by quantitative-PCR in five brain regions (dorsolateral prefrontal cortex, hippocampus (HIPP), amygdala, nucleus accumbens and substantia nigra (SN)) in major depressive disorder (MDD), bipolar disorder, SZ and normal control subjects (N=40, 10 subjects per group). We observed significant differences in telomere length across brain regions suggesting variable levels of cell aging, with SN and HIPP having the longest telomeres and the dorsolateral prefrontal cortex the shortest. A significant decrease (P<0.02) in telomere length was observed specifically in the HIPP of MDD subjects even after controlling for age. In the HIPP of MDD subjects, several genes involved in neuroprotection and in stress response (FKBP5, CRH) showed altered levels of mRNA. Our results suggest the presence of hippocampal stress-mediated accelerated cellular aging in depression. Further studies are needed to investigate the cellular specificity of these findings.


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