Altered patterns of association between cortical thickness and subcortical volume in patients with first episode major depressive disorder: A structural MRI study

Zhao, Ke; Liu, Haiyan; Yan, Rui; Lu, Hua; Chen, Yu; Shi, Jiabo; Yao, Zhijian; Lü, Qing

doi:10.1016/j.pscychresns.2016.12.001

Cited by 32 publications

(35 citation statements)

References 67 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…is a feature of older brain age relative to chronological age, which is accompanied by greater cognitive impairment (30). A thinner cortex has also been observed in categorical mental disorders spanning the Internalizing, Externalizing, and Thought Disorder diagnostic families (e.g., (31)(32)(33)). Meanwhile, accelerated thinning has been associated with worsening daily functioning and other symptoms in Alzheimer's disease (34,35).…”

Section: Discussionmentioning

confidence: 99%

“…The cohort is primarily white (93%), matching South Island demographics (12). Assessments were carried out at birth and ages 3,5,7,9,11,13,15,18,21,26,32,38, and most recently (completed April 2019) 45 years. The relevant ethics committees approved each phase of the Study and informed consent was obtained from all participants.…”

Section: Study Design and Populationmentioning

confidence: 99%

See 1 more Smart Citation

Pervasively thinner neocortex as a transdiagnostic feature of general psychopathology

Romer

Elliott

Knodt

et al. 2019

Preprint

View full text Add to dashboard Cite

AbstractObjectiveNeuroimaging research has revealed that structural brain alterations are common across broad diagnostic families of disorders rather than specific to a single psychiatric disorder. Such overlap in the structural brain correlates of mental disorders mirrors already well-documented phenotypic comorbidity of psychiatric symptoms and diagnoses, which can be indexed by a general psychopathology or p factor. We hypothesized that if general psychopathology drives the convergence of structural alterations common across disorders then 1) there should be few associations unique to any one diagnostic family of disorders, and 2) associations with the p factor should overlap with those for the broader diagnostic families.MethodsAnalyses were conducted on structural MRI and psychopathology data collected from 861 members of the population representative Dunedin Study at age 45.ResultsStudy members with high scores across three broad diagnostic families of disorders (Externalizing, Internalizing, Thought Disorder) exhibited highly overlapping patterns of reduced global and widely distributed parcel-wise neocortical thickness. Study members with high p factor scores exhibited patterns of reduced global and parcel-wise neocortical thickness nearly identical to those associated with the three broad diagnostic families.ConclusionsA pattern of pervasively reduced neocortical thickness appears common across all forms of mental disorders and may represent a transdiagnostic feature of general psychopathology. As has been documented with regard to symptoms and diagnoses, the underlying brain structural correlates of mental disorders may not exhibit specificity, the continued pursuit of which may limit progress toward more effective strategies for etiological understanding, prevention, and intervention.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Study Design and Populationmentioning

confidence: 99%

Pervasively thinner neocortex as a transdiagnostic feature of general psychopathology

Romer

Elliott

Knodt

et al. 2019

Preprint

View full text Add to dashboard Cite

show abstract

“…The OFC is involved in inhibiting background‐independent, redundant, or uncomfortable neural activity, feelings, and behaviors and also plays a crucial role in emotional/motivational management and decision making . It has been reported that the thickness of the right medial orbital cortex in MDD patients is thinner than that in healthy controls, and during treatment, increased cortical thickness was found in the OFC in MDD patients. Functional MRI results found reduced brain activity in the bilateral OFC .…”

Section: Significant Structural Brain Alterations In Mddmentioning

confidence: 99%

“…Structural brain hubs were identified by diffusion tensor imaging, and the nodes normalized to an intramodular degree higher than 1 were defined as hubs. 14,21 ACG, anterior cingulate and paracingulate gyri; CAL, calcarine fissure and surrounding cortex; HIP, hippocampus; INS, insula; L, left; MOG, middle occipital gyrus; MTG, middle temporal gyrus; PCUN, precuneus; PUT, putamen; R, right; SOG, superior occipital gyrus; SPG, superior parietal gyrus; SFGdor, dorsolateral part of the superior frontal gyrus; SFGmed, medial part of the superior frontal gyrus; THA, thalamus cortex in MDD patients is thinner than that in healthy controls, 37 and during treatment, increased cortical thickness was found in the OFC in MDD patients. Functional MRI results found reduced brain activity in the bilateral OFC.…”

Section: Frontal Lobementioning

confidence: 99%

Brain structure alterations in depression: Psychoradiological evidence

et al. 2018

View full text Add to dashboard Cite

Depression is the leading cause of disability around the world, but little is known about its pathology. Currently, the diagnosis of depression is made based on clinical manifestations, with little objective evidence. Magnetic resonance imaging (MRI) has been used to investigate the pathological changes in brain anatomy associated with this disorder. MRI can identify structural alterations in depressive patients in vivo, which could make considerable contributions to clinical diagnosis and treatment. Numerous studies that focused on gray and white matter have found significant brain region alterations in major depressive disorder patients, such as in the frontal lobe, hippocampus, temporal lobe, thalamus, striatum, and amygdala. The results are inconsistent and controversial because of the different demographic and clinical characteristics. However, some regions overlapped; thus, we think that there may be a "hub" in MDD and that an impairment in these regions contributes to disease severity. Brain connections contain both structural connections and functional connections, which reflect disease from a different view and support that MDD may be caused by the interaction of multiple brain regions. According to previous reports, significant circuits include the frontal-subcortical circuit, the suicide circuit, and the reward circuit. As has been recognized, the pathophysiology of major depressive disorder is complex and changeable. The current review focuses on the significant alterations in the gray and white matter of patients with the depressive disorder to generate a better understanding of the circuits. Moreover, identifying the nuances of depressive disorder and finding a biomarker will make a significant contribution to the guidance of clinical diagnosis and treatment.

show abstract

“…Furthermore, LLD patients with reduced psychotherapeutic intervention response also demonstrated reduced cortical thickness in a variety of these and adjacent regions. In addition, first episode younger MDD patients exhibit reduced cortical thickness in a subset of these regions compared to healthy controls . Another study found increased cortical thickness in left middle temporal to superior and inferior temporal cortices, as well as the postcentral gyrus and right insula to superior temporal regions was found in non‐smoking younger MDD patients compared to controls .…”

Section: Introductionmentioning

confidence: 96%

Cortical thickness increases with levomilnacipran treatment in a pilot randomised double‐blind placebo‐controlled trial in late‐life depression

et al. 2019

View full text Add to dashboard Cite

Background Late‐life depression (LLD) is associated with significant medical comorbidity, cognitive impairment, and suboptimal treatment response compared to depression experienced earlier in life. Levomilnacipran (LVM) is a novel antidepressant the effects of which on neuroplasticity have not yet been investigated. We investigated the effect of LVM on cortical thickness in a pilot randomised placebo‐controlled trial in LLD. Methods Twenty‐nine adults (≥ 60 years) with major depression (48.3% female; mean age = 71.5 ± 5.8 years; mean education = 16.0 ± 1.7 years) were randomised to either LVM or placebo for 12 weeks. T1‐weighted images were acquired at baseline and 12 weeks. Thirteen subjects (six LVM and seven placebo) completed the study. Group differences in cortical thickness change across the study period were evaluated, with age and total intracranial volume included as covariates. Results Dropout rates did not differ significantly between groups. The LVM group had significantly more side effects, but no serious adverse events were reported. Lower LVM dose (≤ 40 mg) was better tolerated than higher doses (80–120 mg). Additionally, the LVM group showed a larger increase in cortical thickness in the right postcentral gyrus (primary somatosensory), supramarginal gyrus (sensory association region), and lateral occipital cortex (visual cortex) compared to the placebo group and greater reductions in the left insula. Conclusions LVM may be less tolerable by older adults with depression and the effects on cortical thickness across sensory and sensory association regions may be related to the experience of side effects. Larger studies are necessary to evaluate treatment efficacy, tolerability, and neural effects of LVM in LLD.

show abstract

Altered patterns of association between cortical thickness and subcortical volume in patients with first episode major depressive disorder: A structural MRI study

Cited by 32 publications

References 67 publications

Pervasively thinner neocortex as a transdiagnostic feature of general psychopathology

Pervasively thinner neocortex as a transdiagnostic feature of general psychopathology

Brain structure alterations in depression: Psychoradiological evidence

Cortical thickness increases with levomilnacipran treatment in a pilot randomised double‐blind placebo‐controlled trial in late‐life depression

Contact Info

Product

Resources

About