***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: IMPORTANCE The default mode network ( DMN ) is a collection of brain regions that reliably deactivate during goal -directed behaviors and is more active during a baseline , or so-called resting , condition . Coherence of neural activity , or functional connectivity , within the brain 's DMN is increased in major depressive disorder relative to healthy control ( HC ) subjects ; however , whether similar abnormalities are present in persons with dysthymic disorder ( DD ) is unknown . Moreover , the effect of antidepressant medications on DMN connectivity in patients with DD is also unknown . OBJECTIVE To use resting-state functional-connectivity magnetic resonance imaging ( MRI ) to study ( 1 ) the functional connectivity of the DMN in subjects with DD vs HC participants and ( 2 ) the effects of antidepressant therapy on DMN connectivity . DESIGN After collecting baseline MRI scans from subjects with DD and HC participants , we enrolled the participants with DD into a 10-week prospect i ve , double-blind , placebo-controlled trial of duloxetine and collected MRI scans again at the conclusion of the study . Enrollment occurred between 2007 and 2011 . SETTING University research institute . PARTICIPANTS Volunteer sample of 41 subjects with DD and 25 HC participants aged 18 to 53 years . Control subjects were group matched to patients with DD by age and sex . MAIN OUTCOME MEASURES We used resting-state functional-connectivity MRI to measure the functional connectivity of the brain 's DMN in persons with DD compared with HC subjects , and we examined the effects of treatment with duloxetine vs placebo on DMN connectivity . RESULTS Of the 41 subjects with DD , 32 completed the clinical trial and MRI scans , along with the 25 HC participants . At baseline , we found that the coherence of neural activity within the brain 's DMN was greater in persons with DD compared with HC subjects . Following a 10-week clinical trial , we found that treatment with duloxetine , but not placebo , normalized DMN connectivity . CONCLUSIONS AND RELEVANCE The baseline imaging findings are consistent with those found in patients with major depressive disorder and suggest that increased connectivity within the DMN may be important in the pathophysiology of both acute and chronic manifestations of depressive illness . The normalization of DMN connectivity following antidepressant treatment suggests an important causal pathway through which antidepressants may reduce depression The profile of cognitive dysfunction observed in patients with major depressive disorder ( MDD ) may be partially attributed to a deficit in the central executive component of working memory ( WM ) . This could be the consequence of a functional deficit in regions of cortex that are associated with WM function in healthy adults . In order to investigate this assertion , ten patients with a diagnosis of MDD and ten matched healthy controls undertook a parametric WM task ( i.e. the n-back task ) during the acquisition of blood oxygen level dependent echo planar magnetic resonance images ( BOLD EPI fMRI ) . There was no significant difference in the behavioral performance of depressed patients and controls . This was true for both accuracy and reaction time on the n-back task . R and om effects analysis of the functional imaging data ( using SPM99 ) revealed a significant difference in load-dependent activation in the medial orbitofrontal cortex/rostral anterior cingulate between patients and controls ( cluster size ( K(E))/volume = 128/1024 mm3 , P(corrected ) = 0.025 ) . While both participant groups exhibited a significant decrease in activation in this region with increased task difficulty , the magnitude of this decrease was smaller in patients with MDD than in controls . Therefore , this study implies that the performance of WM tasks is associated with a dysfunctional activation of the medial orbitofrontal and rostral anterior cingulate cortex in MDD . The study thus offers a rationale for explaining depressive cognitive impairment by the abnormal fronto-limbic activation found in clinical depression There is a need to identify clinical ly useful biomarkers in major depressive disorder ( MDD ) . In this context the functional connectivity of the orbitofrontal cortex ( OFC ) to other areas of the affect regulation circuit is of interest . The aim of this study was to identify neural changes during antidepressant treatment and correlates associated with the treatment outcome . In an exploratory analysis it was investigated whether functional connectivity measures moderated a response to mirtazapine and venlafaxine .  Twenty-three drug-free patients with MDD were recruited from the Department of Psychiatry and Psychotherapy of the Ludwig-Maximilians University in Munich . The patients were subjected to a 4-wk r and omized clinical trial with two common antidepressants , venlafaxine or mirtazapine .  Functional connectivity of the OFC , derived from functional magnetic resonance imaging with an emotional face-matching task , was measured before and after the trial . Higher OFC connectivity with the left motor areas and the OFC regions prior to the trial characterized responders ( p<0.05 , false discovery rate ) . The treatment non-responders were characterized by higher OFC-cerebellum connectivity . The strength of response was positively correlated with functional coupling between left OFC and the cau date nuclei and thalami . Differences in longitudinal changes were detected between venlafaxine and mirtazapine treatment in the motor areas , cerebellum , cingulate gyrus and angular gyrus . These results indicate that OFC functional connectivity might be useful as a marker for therapy response to mirtazapine and venlafaxine and to reconstruct the differences in their mechanism of action Abstract Objectives . Intensified repetitive transcranial magnetic stimulation ( rTMS ) applied to the left dorsolateral prefrontal cortex ( DLPFC ) may result in fast clinical responses in treatment resistant depression ( TRD ) . In these kinds of patients , subgenual anterior cingulate cortex ( sgACC ) functional connectivity ( FC ) seems to be consistently disturbed . So far , no de novo data on the relationship between sgACC FC changes and clinical efficacy of accelerated rTMS were available . Methods . Twenty unipolar TRD patients , all at least stage III treatment resistant , were recruited in a r and omized sham-controlled crossover high-frequency (HF)-rTMS treatment study . Resting-state ( rs )  functional MRI scans were collected at baseline and at the end of treatment . Results . HF-rTMS responders showed significantly stronger resting-state functional connectivity ( rsFC ) anti-correlation between the sgACC and parts of the left superior medial prefrontal cortex . After successful treatment an inverted relative strength of the anti-correlations was observed in the perigenual prefrontal cortex ( pgPFC ) . No effects on sgACC rsFC were observed in non-responders . Conclusions . Strong rsFC anti-correlation between the sgACC and parts of the left prefrontal cortex could be indicative of a beneficial outcome . Accelerated HF-rTMS treatment design s have the potential to acutely adjust deregulated sgACC neuronal networks in TRD patients Sertraline , one of the oldest antidepressants , remains to be the most efficacious treatment for depression . However , major depression disorder ( MDD ) is characterized by altered emotion processing and deficits in cognitive control . In cognitive interference tasks , patients with MDD have shown excessive hypothalamus activity . The purpose of this study was to examine the effects of antidepressant treatment ( sertraline ) on hypothalamus-anchored resting brain circuitry . Functional magnetic resonance imaging was conducted on depressed patients ( n=12 ) both before and after antidepressant treatment .  After eight weeks of antidepressant treatment , patients with depression showed significantly increased connectivity between the hypothalamus and dorsolateral prefrontal cortex , orbitofrontal cortex , anterior cingulate cortex , insula , putamen , cau date , and claustrum . By contrast , decreased connectivity of the hypothalamus-related areas was primarily located in the inferior frontal gyrus , medial frontal gyrus , cingulated gyrus , precuneus , thalamus , and cerebellum . After eight weeks of antidepressant therapy , 8 out of the 12 depressed subjects achieved 70 % reduction or better in depressive symptoms , as measured on the Hamilton depression rating scale . Our findings may infer that antidepressant treatment can alter the functional connectivity of the hypothalamus resting brain to achieve its therapeutic effect Indices of functional connectivity in the default mode network ( DMN ) are promising neural markers of treatment response in late-life depression . We examined the differences in DMN functional connectivity between treatment-responsive and treatment-resistant depressed older adults . Forty-seven depressed older adults underwent MRI scanning pre- and post-pharmacotherapy . Forty-six never depressed older adults underwent MR scanning as comparison subjects . Treatment response was defined as achieving a Hamilton Depression Rating Scale of 10 or less post-treatment . We analyzed resting state functional connectivity using the posterior cingulate cortex as the seed region-of-interest . The result ing correlation maps were employed to investigate between-group differences . Additionally we examined the association between white matter hyperintensity burden and functional connectivity results . Comparison of pre- and post-treatment scans of depressed participants revealed greater post-treatment functional connectivity in the frontal pre central gyrus . Relative to treatment-responsive participants , treatment-resistant participants had increased functional connectivity in the left striatum . When adjusting for white matter hyperintensity burden , the observed differences lost significance for the PCC-prefrontal functional connectivity , but not for the PCC-striatum functional connectivity . The post-treatment " frontalization " of the DMN connectivity suggests a normalizing effect of antidepressant treatment . Moreover , our study confirms the central role of white matter lesions in disrupting brain functional connectivity It has been hypothesized that one of the effects of antidepressants is to increase functional connectivity between the cortical mood-regulating and the limbic mood-generating regions . One consequence of this antidepressant effect is thought to be decreased limbic activation in response to negative emotional stimuli . Twelve unmedicated unipolar depressed patients and 11 closely matched healthy comparison subjects completed two magnetic resonance imaging ( MRI ) scanning sessions at baseline and after 6 weeks . Depressed patients received treatment with sertraline between the two sessions . During each MRI session , subjects completed a resting state functional connectivity scan and a conventional block- design negative vs. neutral pictures regional brain activation scan . After 6 weeks of sertraline treatment resting state , functional connectivity between the ACC and limbic regions increased while limbic activation in response to negative versus neutral pictures decreased . The results of this study are consistent with the hypothesis that antidepressant treatment has reciprocal effects on corticolimbic functional connectivity and limbic activation in response to emotional stimuli The mechanisms by which antidepressant-induced neurochemical changes lead to physiological changes in brain circuitry and ultimately an antidepressant response remain unclear . This study investigated the effects of sertraline , a selective serotonin reuptake inhibitor antidepressant , on corticolimbic connectivity , using functional magnetic resonance imaging ( fMRI ) . In all , 12 unmedicated unipolar depressed patients and 11 closely matched healthy control subjects completed two fMRI scanning sessions at baseline and after 6 weeks . Depressed patients received treatment with sertraline between the two sessions . During each fMRI session , subjects first completed a conventional block- design experiment . Next , connectivity between cortical and limbic regions was measured using correlations of low-frequency blood oxygen level-dependent ( BOLD ) fluctuations ( LFBF ) during continuous exposure to neutral , positive , and negative pictures . At baseline , depressed patients had decreased corticolimbic LFBF correlations compared to healthy subjects during the resting state and on exposure to emotionally valenced pictures . At rest and on exposure to neutral and positive pictures , LFBF correlation between the anterior cingulate cortex and limbic regions was significantly increased in patients after treatment . However , on exposure to negative pictures , corticolimbic LFBF correlations remained decreased in depressed patients . The results of this study are consistent with the hypothesis that antidepressant treatment may increase corticolimbic connectivity , thereby possibly increasing the regulatory influence of cortical mood-regulating regions over limbic regions 
    Output:
    
It seems that both DMN and the connectivity between cortical and limbic structures consistently changes after antidepressant treatment .
However , the current evidence does not allow us to assure that the treatment of depression leads to changes in the CCN .
Finally , some papers suggest that changes in connectivity after antidepressant treatment might be partly related to the mechanisms of action of the treatment administered .