Cortical Thickness in Individuals at High Familial Risk of Mood Disorders as They Develop Major Depressive Disorder

Papmeyer, Martina; Giles, Stephen; Sussmann, Jessica E.; Kielty, Shauna; Stewart, Tiffany; Lawrie, Stephen M.; Whalley, Heather C.; McIntosh, Andrew M.

doi:10.1016/j.biopsych.2014.10.018

Cited by 100 publications

(80 citation statements)

References 63 publications

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“…Few imaging studies have applied this approach to depression. A study by Papmeyer et al followed early adult offspring (mean age, 21 yrs) at high- and low-familial risk for depression, but only across a two-year period (31). Offspring at high-risk for depression had thinner right temporal cortex, regardless of whether they developed the disorder themselves.…”

Section: Discussionmentioning

confidence: 99%

Stability of Cortical Thinning in Persons at Increased Familial Risk for Major Depressive Disorder Across 8 Years

Hao

Talati

Shankman

et al. 2017

Biological Psychiatry: Cognitive Neuroscience and Neuroimaging

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Background A biological marker of vulnerability should precede onset of illness and be independent of disease course. We previously reported that cortical thinning may serve as a potential biomarker for risk for familial depression. We now test stability of the cortical thinning across 8 years, and whether thinning mediates associations between familial risk and depressive traits. Method Participants were from a 3-generation family study of depression, where 2nd and 3rd generation offspring were characterized as being at high- or low-risk for depression based on the presence/absence of major depression in the 1st generation. The analysis includes 82 offspring with anatomical MRI scans across two assessment waves, 7.8 (S.D.1.3, range: 5.2-10.9) years apart. Results High-risk offspring had thinner bilateral superior and middle frontal gyri, and left inferior parietal lobule, at both time-points. High intra-subject correlation (0.60

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Section: Discussionmentioning

confidence: 99%

Stability of Cortical Thinning in Persons at Increased Familial Risk for Major Depressive Disorder Across 8 Years

Hao

Talati

Shankman

et al. 2017

Biological Psychiatry: Cognitive Neuroscience and Neuroimaging

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“…For example, the vertex-wise SBM approach been used to characterize patterns of GM changes in Alzheimer's disease (Blanc, et al, 2015), Parkinson's disease (Biundo, et al, 2015), and Depressive disorder (Qiu, et al, 2014), while the ROI-wise SBM approach has been used to depict brain morphometry involving socioeconomic status on children's brain structures (Jednoróg, et al, 2012), childhood maltreatment on brain structures (Kelly, et al, 2013), and brain structures of individuals with high familial risk of mood disorders (Papmeyer, et al, 2015). However, as far as we know, no studies have reported radiation-induced cortical thickness abnormalities in the normal-appearing GM for NPC patients with SBM approach.…”

Section: Introductionmentioning

confidence: 99%

Radiation-induced abnormal cortical thickness in patients with nasopharyngeal carcinoma after radiotherapy

Lin

Niu

et al. 2017

NeuroImage: Clinical

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Conventional MRI studies showed that radiation-induced brain necrosis in patients with nasopharyngeal carcinoma (NPC) in years after radiotherapy (RT) could involve brain gray matter (GM) and impair brain function. However, it is still unclear the radiation-induced brain morphological changes in NPC patients with normal-appearing GM in the early period after RT. In this study, we acquired high-resolution brain structural MRI data from three groups of patients, 22 before radiotherapy (pre-RT) NPC patients with newly diagnosed but not yet medically treated, 22 NPC patients in the early-delayed stage after radiotherapy (post-RT-ED), and 20 NPC patients in the late-delayed stage after radiotherapy (post-RT-LD), and then analyzed the radiation-induced cortical thickness alteration in NPC patients after RT. Using a vertex-wise surface-based morphometry (SBM) approach, we detected significantly decreased cortical thickness in the precentral gyrus (PreCG) in the post-RT-ED group compared to the pre-RT group. And the post-RT-LD group showed significantly increased cortical thickness in widespread brain regions, including the bilateral inferior parietal, left isthmus of the cingulate, left bank of the superior temporal sulcus and left lateral occipital regions, compared to the pre-RT group, and in the bilateral PreCG compared to the post-RT-ED group. Similar analysis with ROI-wise SBM method also found the consistent results. These results indicated that radiation-induced brain injury mainly occurred in the post-RT-LD group and the cortical thickness alterations after RT were dynamic in different periods. Our findings may reflect the pathogenesis of radiation-induced brain injury in NPC patients with normal-appearing GM and an early intervention is necessary for protecting GM during RT.

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“…49,[52][53][54][55][56][57][58] The specific involvement of the IFG adds to a converging body of evidence from structural and functional studies of BD. [59][60][61][62][63][64] Likewise, the involvement of the insula adds to a growing number of reports of structural and functional differences in HR cohorts. 23,[65][66][67] The involvement of a left-sided network is unique to the at-risk group (relative to CNs) and is not present in the bipolar group.…”

Section: Discussionmentioning

confidence: 99%

784. Structural Dysconnectivity of Key Cognitive and Emotional Hubs in Young People at High Genetic Risk for Bipolar Disorder

Mitchell

Breakspear

Roberts

et al. 2017

Biological Psychiatry

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Cortical Thickness in Individuals at High Familial Risk of Mood Disorders as They Develop Major Depressive Disorder

Cited by 100 publications

References 63 publications

Stability of Cortical Thinning in Persons at Increased Familial Risk for Major Depressive Disorder Across 8 Years

Stability of Cortical Thinning in Persons at Increased Familial Risk for Major Depressive Disorder Across 8 Years

Radiation-induced abnormal cortical thickness in patients with nasopharyngeal carcinoma after radiotherapy

784. Structural Dysconnectivity of Key Cognitive and Emotional Hubs in Young People at High Genetic Risk for Bipolar Disorder

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