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Similarity in functional connectome architecture predicts teenage grit.

ABSTRACT: Grit is a personality trait that encapsulates the tendency to persevere and maintain consistent interest for long-term goals. While prior studies found that grit predicts positive behavioral outcomes, there is a paucity of work providing explanatory evidence from a neurodevelopmental perspective. Based on previous research suggesting the utility of the functional connectome (FC) as a developmental measure, we tested the idea that individual differences in grit might be, in part, rooted in brain development in adolescence and emerging adulthood (N = 64, 11-19 years of age). Our analysis showed that grit was associated with connectome stability across conditions and connectome similarity across individuals. Notably, inter-subject representational similarity analysis revealed that teenagers who were grittier shared similar FC architecture with each other, more so than those with lower grit. Our findings suggest that individuals with high levels of grit are more likely to exhibit a converging pattern of whole-brain functional connectivity, which may underpin subsequent beneficial behavioral outcomes.

SUBMITTER: Park S

PROVIDER: S-EPMC10549957 | biostudies-literature | 2023 Oct

REPOSITORIES: biostudies-literature

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Similarity in functional connectome architecture predicts teenage grit.

Park Sujin S Park Daeun D Kim M Justin MJ

Social cognitive and affective neuroscience 20231001 1

Grit is a personality trait that encapsulates the tendency to persevere and maintain consistent interest for long-term goals. While prior studies found that grit predicts positive behavioral outcomes, there is a paucity of work providing explanatory evidence from a neurodevelopmental perspective. Based on previous research suggesting the utility of the functional connectome (FC) as a developmental measure, we tested the idea that individual differences in grit might be, in part, rooted in brain ...[more]

PMID: 37700673

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Project description:Myelinated axons form long-range connections that enable rapid communication between distant brain regions, but how genetics governs the strength and organization of these connections remains unclear. We perform genome-wide association studies of 206 structural connectivity measures derived from diffusion magnetic resonance imaging tractography of 26,333 UK Biobank participants, each representing the density of myelinated connections within or between a pair of cortical networks, subcortical structures or cortical hemispheres. We identify 30 independent genome-wide significant variants after Bonferroni correction for the number of measures studied (126 variants at nominal genome-wide significance) implicating genes involved in myelination (SEMA3A), neurite elongation and guidance (NUAK1, STRN, DPYSL2, EPHA3, SEMA3A, HGF, SHTN1), neural cell proliferation and differentiation (GMNC, CELF4, HGF), neuronal migration (CCDC88C), cytoskeletal organization (CTTNBP2, MAPT, DAAM1, MYO16, PLEC), and brain metal transport (SLC39A8). These variants have four broad patterns of spatial association with structural connectivity: some have disproportionately strong associations with corticothalamic connectivity, interhemispheric connectivity, or both, while others are more spatially diffuse. Structural connectivity measures are highly polygenic, with a median of 9.1 percent of common variants estimated to have non-zero effects on each measure, and exhibited signatures of negative selection. Structural connectivity measures have significant genetic correlations with a variety of neuropsychiatric and cognitive traits, indicating that connectivity-altering variants tend to influence brain health and cognitive function. Heritability is enriched in regions with increased chromatin accessibility in adult oligodendrocytes (as well as microglia, inhibitory neurons and astrocytes) and multiple fetal cell types, suggesting that genetic control of structural connectivity is partially mediated by effects on myelination and early brain development. Our results indicate pervasive, pleiotropic, and spatially structured genetic control of white-matter structural connectivity via diverse neurodevelopmental pathways, and support the relevance of this genetic control to healthy brain function.

Project description:PurposePositron emission tomography (PET) with 18F-fluorodeoxyglucose (FDG) reveals altered cerebral metabolism in individuals with mild cognitive impairment (MCI) and Alzheimer's dementia (AD). Previous metabolic connectome analyses derive from groups of patients but do not support the prediction of an individual's risk of conversion from present MCI to AD. We now present an individual metabolic connectome method, namely the Kullback-Leibler Divergence Similarity Estimation (KLSE), to characterize brain-wide metabolic networks that predict an individual's risk of conversion from MCI to AD.MethodsFDG-PET data consisting of 50 healthy controls, 332 patients with stable MCI, 178 MCI patients progressing to AD, and 50 AD patients were recruited from ADNI database. Each individual's metabolic brain network was ascertained using the KLSE method. We compared intra- and intergroup similarity and difference between the KLSE matrix and group-level matrix, and then evaluated the network stability and inter-individual variation of KLSE. The multivariate Cox proportional hazards model and Harrell's concordance index (C-index) were employed to assess the prediction performance of KLSE and other clinical characteristics.ResultsThe KLSE method captures more pathological connectivity in the parietal and temporal lobes relative to the typical group-level method, and yields detailed individual information, while possessing greater stability of network organization (within-group similarity coefficient, 0.789 for sMCI and 0.731 for pMCI). Metabolic connectome expression was a superior predictor of conversion than were other clinical assessments (hazard ratio (HR) = 3.55; 95% CI, 2.77-4.55; P < 0.001). The predictive performance improved further upon combining clinical variables in the Cox model, i.e., C-indices 0.728 (clinical), 0.730 (group-level pattern model), 0.750 (imaging connectome), and 0.794 (the combined model).ConclusionThe KLSE indicator identifies abnormal brain networks predicting an individual's risk of conversion from MCI to AD, thus potentially constituting a clinically applicable imaging biomarker.

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Similarity in functional connectome architecture predicts teenage grit.

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Similarity in functional connectome architecture predicts teenage grit.

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