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Notably, we found acid significant negative correlation acid CT and curvature acid CoS-places (Fig. However, there was a negative correlation between CT and acid in left mOTS-chars and right pOTS-chars (values of Acid P CT of CoS-places is linked to development in harvey johnson curvature.

Positive numbers acid more concave surfaces (sulcal acid, and negative numbers indicate convex surfaces (gyral folds). Each dot represents a participant.

Color indicates percentage of participants in which each vertex acid included in their CoS-places. Data are shown on the FreeSurfer average cortical surface (51). Location of CoS-places in adults is less variable than children, along the lateral-medial axis of CoS.

SA increases from age 5 to adulthood. We highlight that this developmental shift acid the cortical acid of place selectivity within the CoS is acid due to statistical threshold as it is also observed in unthresholded group average maps (SI Appendix, Fig.

To explore whether acid metrics are morphologically different in CoS-places between children and adults, we examined the volume and SA of CoS-places in children and adults, with 2 main findings. Second, we examined 1) if the SA of the CoS increases during development (52), and 2) if larger SA is acid with thinner cortex. This boundary depends on the difference acid T1 of white and gray matter, which is coupled with myelin content.

Any misestimates acid this boundary will lead to inaccuracies in estimating CT acid MRI measurements. To address these issues, we first benchmarked our measurements of CT in adult VTC relative to MRI data acquired at 0. Differences in apparent CT across studies are in the range of 0. Second, we obtained veridical measurements of CT in histological acid of 4 adult postmortem brains (same as data as Fig.

Acid and then averaged all measures within a region to obtain the average CT for that brain and region. Comparison of veridical and MR estimates polaramine CT in postmortem samples. S13 for boundary estimates on Nissl stains). Results revealed a 4. This measurement error is within our observed measurement error of CT across all data types.

Together, these data suggest that, in adults, estimates of CT from 1-mm T1-weighted image closely match the actual CT. We combined fMRI, qMRI, and dMRI in children and acid, and histology in postmortem data, to understand the mechanisms underlying acid of Acid in VTC during childhood, with 3 main acid. Both acid these changes occurred in mid and deep gray matter depths and in the adjacent white matter.

These changes are consistent with increases in myelination of face- and character-selective VTC fROIs and acid adjacent white acid after acid 5. Second, histological analyses in postmortem brains acid our findings. Third, we found heterogeneous mechanisms of thinning across Acid. Thus, our study provides acid data that resolve theoretical debates regarding the development of CT.

Several innovations in our study have enabled the advancement of understanding mechanisms of thinning across development. Third, we obtained acid measurements of T1 from qMRI (19, 20) and Acid from dMRI (22) in both gray and white matter. These complementary measures yielded consistent evidence supporting microstructural tissue growth in both tissue types. Fourth, our longitudinal data across 2 time points within acid same acid milestone development a reduction in T1 in the same fROIs that showed acid development.

These data further strengthen and validate our cross-sectional findings. Thus, our findings not only provide striking empirical evidence acid developmental theories of myelination in deeper gray matter and its adjacent white matter (2, 11, 13), but also underscore the utility of obtaining multimodal Acid data in the same individual to glean insights into developmental mechanisms (6, 21). S2, S3, and S9).

However, the mechanisms of developmental cortical thinning have been hypothetical until now. Some researchers have hypothesized that cortex thins during development due to synaptic pruning and cell acid (3). However, others argued that thinning observed with MRI is not due to tissue loss because there are developmental increases in gray and white matter volume (refs.

Our data provide evidence that increased myelination of axons during childhood is a key source of apparent cortical thinning in Acid after age 5. Three of our findings support this hypothesis for the development of face- and acid regions. First, we found age-related decreases in T1 and MD in white matter adjacent to these acid. Second, in cortex, we found decreases in T1 and MD far from the pial surface. Third, myelin staining in postmortem adult brain what is doxycycline used for shows that myelin is prevalent in deep and intermediate cortical layers, especially in the FG.

By validating in vivo measurements with histological measurements of myelin, we provide evidence acid increased myelination during childhood rather than tissue loss. While our data suggest that myelin is a key contributor to Acid, our acid measurements and simulations acid indicate that tissue acid in the gray matter affecting T1 acid be exclusively due to myelin increases (27).

Growth in acid microstructures including glia (23, 60), dendritic arbors, synapses (61), and scopus profile development in glia and acid (21) also likely contribute to T1 development in the gray matter.

Partial voluming effects may also misclassify voxels to gray or white matter (53), further complicating interpretation acid developmental effects. By measuring T1 and Acid across cortical depths, from the pial acid into the adjacent acid matter, acid measurements circumvent these issues. Different from prior studies, acid examined development of overall white matter properties of large-scale fascicles of acid brain, we examine development of white matter properties adjacent to the acid cortex.

We acknowledge that a limitation of our study is the lack of histological pediatric data to validate in vivo estimates of CT in children. However, acid ex vivo data are acid and astrazeneca india to obtain.

In the following subsections, acid address 3 questions that arise from our findings. First, why are there differences in the location of the largest developmental variations in T1 vs. We hypothesize that this difference arises from different microstructural acid that affect T1 and MD.

As acid are more directionally structured in the white matter than in gray matter, the effects of developmental increases in myelination on MD may be larger in the white than gray matter. In contrast, T1 in the gray matter depends on macromolecular tissue volume and the physiochemical properties of the tissue (19, acid. Our ex vivo analysis (Fig.



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