structural covariance
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2022 ◽  
Vol 240 ◽  
pp. 1-21
Author(s):  
Konasale Prasad ◽  
Jonathan Rubin ◽  
Anirban Mitra ◽  
Madison Lewis ◽  
Nicholas Theis ◽  
...  

2022 ◽  
Author(s):  
Hyung Chan Kim ◽  
Dong Ah Lee ◽  
Ho-Joon Lee ◽  
Kyong Jin Shin ◽  
Kang Min Park

2022 ◽  
Vol 165 ◽  
pp. 108113
Author(s):  
Martin Göttlich ◽  
Macià Buades-Rotger ◽  
Juliana Wiechert ◽  
Frederike Beyer ◽  
Ulrike M. Krämer

2022 ◽  
Vol 239 ◽  
pp. 176-191
Author(s):  
Konasale Prasad ◽  
Jonathan Rubin ◽  
Anirban Mitra ◽  
Madison Lewis ◽  
Nicholas Theis ◽  
...  

2021 ◽  
Vol 13 ◽  
Author(s):  
Hsin-I Chang ◽  
Yu-Tzu Chang ◽  
Chi-Wei Huang ◽  
Kuo-Lun Huang ◽  
Jung-Lung Hsu ◽  
...  

The cognitive manifestations of Alzheimer’s disease (AD) are related to brain network degeneration, and genetic differences may mediate network degeneration. Several AD-susceptible loci have been reported to involve amyloid or tau cascades; however, their relationships with gray matter (GM) volume and cognitive outcomes have yet to be established. We hypothesized that single-nucleotide polymorphism genotype groups may interact with apolipoprotein E4 (ApoE4) status or independently exert an effect on cognitive outcomes. We also hypothesized that GM structural covariance networks (SCNs) may serve as an endophenotype of the genetic effect, which, in turn, may be related to neurobehavior test scores. Gray matter SCNs were constructed in 324 patients with AD using T1 magnetic resonance imaging with independent component analysis (ICA). We assessed the effects of 15 genetic loci (rs9349407, rs3865444, rs670139, rs744373, rs3851179, rs11136000, rs3764650, rs610932, rs6887649, rs7849530, rs4866650, rs3765728, rs34011, rs6656401, and rs597668) using additive, recessive, and dominant models on cognitive outcomes. Statistical analysis was performed to explore the independent role of each locus, interactions with ApoE4 status, and relationships to GM ICA network intensity score. For outcome measures, we used the Mini-Mental State Examination (MMSE), Cognitive Abilities Screening Instrument (CASI) total score, and short-term memory (STM) subscores, adjusted for the covariates of education, disease duration, and age. Clinically, the CD2AP G allele showed a protective role in MMSE, CASI total, and CASI-STM scores independently or via interactions with non-ApoE4 status, while the CR1 A genotype group was associated with lower STM subscores independent of ApoE4 status. Three loci showed synergic interactions with ApoE4: BIN 1, MS4A6A, and FTMT. Of the 15 meaningful ICA components, 5 SCNs (anterior and posterior hippocampus, right temporal, left thalamus, default mode network) showed relationships with general cognitive performance, in which only the ApoE4 and MS4A6A genotype groups were independently related to the hippocampus network. The genetic loci MS4A6A, BIN1, CLU, CR1, BIN1, PICALM, and FGF1 influenced the networks independently or in synergy. This study suggests that AD-susceptible loci may each exert clinical significance independently through interactions with ApoE4 status or through SCNs as an endophenotype and that this effect is associated with the cognitive outcomes.


Addiction ◽  
2021 ◽  
Author(s):  
Jonatan Ottino‐Gonzalez ◽  
Matthew D. Albaugh ◽  
Zhipeng Cao ◽  
Renata B. Cupertino ◽  
Nathan Schwab ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Dajung J. Kim ◽  
Manyoel Lim ◽  
June Sic Kim ◽  
Chun Kee Chung

AbstractDysfunctional thalamocortical interactions have been suggested as putative mechanisms of ineffective pain modulation and also suggested as possible pathophysiology of fibromyalgia (FM). However, it remains unclear which specific thalamocortical networks are altered and whether it is related to abnormal pain perception in people with FM. Here, we conducted combined vertex-wise subcortical shape, cortical thickness, structural covariance, and resting-state functional connectivity analyses to address these questions. FM group exhibited a regional shape deflation of the left posterior thalamus encompassing the ventral posterior lateral and pulvinar nuclei. The structural covariance analysis showed that the extent of regional deflation of the left posterior thalamus was negatively covaried with the left inferior parietal cortical thickness in the FM group, whereas those two regions were positively covaried in the healthy controls. In functional connectivity analysis with the left posterior thalamus as a seed, FM group had less connectivity with the periaqueductal gray compared with healthy controls, but enhanced connectivity between the posterior thalamus and bilateral inferior parietal regions, associated with a lower electrical pain threshold at the hand dorsum (pain-free point). Overall, our findings showed the structural thalamic alteration interacts with the cortical regions in a functionally maladaptive direction, leading the FM brain more responsive to external stimuli and potentially contributing to pain amplification.


2021 ◽  
Vol 11 (12) ◽  
pp. 1580
Author(s):  
Cecilia Grinsvall ◽  
Lukas Van Oudenhove ◽  
Patrick Dupont ◽  
Hyo Jin Ryu ◽  
Maria Ljungberg ◽  
...  

Somatization, defined as the presence of multiple somatic symptoms, frequently occurs in irritable bowel syndrome (IBS) and may constitute the clinical manifestation of a neurobiological sensitization process. Brain imaging data was acquired with T1 weighted 3 tesla MRI, and gray matter morphometry were analyzed using FreeSurfer. We investigated differences in networks of structural covariance, based on graph analysis, between regional gray matter volumes in IBS-related brain regions between IBS patients with high and low somatization levels, and compared them to healthy controls (HCs). When comparing IBS low somatization (N = 31), IBS high somatization (N = 35), and HCs (N = 31), we found: (1) higher centrality and neighbourhood connectivity of prefrontal cortex subregions in IBS high somatization compared to healthy controls; (2) higher centrality of left cerebellum in IBS low somatization compared to both IBS high somatization and healthy controls; (3) higher centrality of the anterior insula in healthy controls compared to both IBS groups, and in IBS low compared to IBS high somatization. The altered structural covariance of prefrontal cortex and anterior insula in IBS high somatization implicates that prefrontal processes may be more important than insular in the neurobiological sensitization process associated with IBS high somatization.


Author(s):  
Salvatore Nigro ◽  
Benedetta Tafuri ◽  
Daniele Urso ◽  
Roberto De Blasi ◽  
Alessia Cedola ◽  
...  

AbstractSemantic (svPPA) and nonfluent (nfvPPA) variants of primary progressive aphasia (PPA) have recently been associated with distinct patterns of white matter and functional network alterations in left frontoinsular and anterior temporal regions, respectively. Little information exists, however, about the topological characteristics of gray matter covariance networks in these two PPA variants. In the present study, we used a graph theory approach to describe the structural covariance network organization in 34 patients with svPPA, 34 patients with nfvPPA and 110 healthy controls. All participants underwent a 3 T structural MRI. Next, we used cortical thickness values and subcortical volumes to define subject-specific connectivity networks. Patients with svPPA and nfvPPA were characterized by higher values of normalized characteristic path length compared with controls. Moreover, svPPA patients had lower values of normalized clustering coefficient relative to healthy controls. At a regional level, patients with svPPA showed a reduced connectivity and impaired information processing in temporal and limbic brain areas relative to controls and nfvPPA patients. By contrast, local network changes in patients with nfvPPA were focused on frontal brain regions such as the pars opercularis and the middle frontal cortex. Of note, a predominance of local metric changes was observed in the left hemisphere in both nfvPPA and svPPA brain networks. Taken together, these findings provide new evidences of a suboptimal topological organization of the structural covariance networks in svPPA and nfvPPA patients. Moreover, we further confirm that distinct patterns of structural network alterations are related to neurodegenerative mechanisms underlying each PPA variant.


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