From adolescence, women become more likely to experience fear dysregulation. Oral contraceptives (OCs) can modulate the brain regions involved in fear processes. OCs are generally used for years and often initiated during adolescence, a sensitive period where certain brain regions involved in the fear circuitry are still undergoing important reorganization. It remains unknown whether OC use during adolescence may induce long-lasting changes in the fear circuitry. This study aimed to examine whether age of onset moderated the relationship between duration of use and fear-related brain structures. We collected structural MRI data in 98 healthy adult women (61 current users, 37 past users) and extracted grey matter volumes (GMV) and cortical thickness (CT) of key regions of the fear circuitry. Non-linear multiple regressions revealed interaction effects between age of onset and quadratic duration of use on GMV of the right hippocampus and right ventromedial prefrontal cortex (vmPFC). Among women who initiated OCs earlier in adolescence, a short duration of use was associated with smaller hippocampal GMV and thicker vmPFC compared to a longer duration of use. For both GMV and CT of the right vmPFC, women with an early OC onset had more grey matter at a short duration of use than those with a later onset. Our results suggest that OC use earlier in adolescence may induce lasting effects on structural correlates of fear learning and its regulation. These findings support further investigation into the timing of OC use to better comprehend how OCs could disrupt normal brain development processes.

OBJECTIVE: Explore how anatomical measurements and field modeling can be leveraged to improve investigations of transcranial magnetic stimulation (TMS) effects on both motor and non-motor TMS targets.
METHODS: TMS motor effects (targeting the primary motor cortex [M1]) were evaluated using the resting motor threshold (rMT), while TMS non-motor effects (targeting the superior temporal gyrus [STG]) were assessed using a pain memory task. Anatomical measurements included scalp-cortex distance (SCD) and cortical thickness (CT), whereas field modeling encompassed the magnitude of the electric field (E) induced by TMS.
RESULTS: Anatomical measurements and field modeling values differed significantly between M1 and STG. For TMS motor effects, rMT was correlated with SCD, CT, and E values at M1 (p < 0.05). No correlations were found between these metrics for the STG and TMS non-motor effects (pain memory; all p-values > 0.05).
CONCLUSIONS: Although anatomical measurements and field modeling are closely related to TMS motor effects, their relationship to non-motor effects - such as pain memory - appear to be much more tenuous and complex, highlighting the need for further advancement in our use of TMS and virtual lesion paradigms.

Preterm-born (PTB) children are at an elevated risk for neurocognitive difficulties in general and language difficulties more specifically. Environmental factors such as socio-economic status (SES) play a key role for Term children\'s language development. SES has been shown to predict PTB children\'s behavioral developmental trajectories, sometimes surpassing its role for Term children. However, the role of SES in the neurocognitive basis of PTB children\'s language development remains uncharted. Here, we aimed to evaluate the role of SES in the neural basis of PTB children\'s language performance. Leveraging the Adolescent Brain Cognitive Development (ABCD) Study, the largest longitudinal study of adolescent brain development and behavior to date, we showed that prematurity status (PTB versus Term) and multiple aspects of SES additively predict variability in cortical thickness, which is in turn related to children\'s receptive vocabulary performance. We did not find evidence to support the differential role of environmental factors for PTB versus Term children, underscoring that environmental factors are significant contributors to development of both Term and PTB children. Taken together, our results suggest that the environmental factors influencing language development might exhibit similarities across the full spectrum of gestational age.

Development of attentional skills and inhibitory control rely on maturational changes in the brain across childhood and youth. However, both brain anatomy and different components of attention and inhibition show notable individual variation. Research on ADHD and inhibitory training and control have shown that variations in the thickness and surface area of particularly inferior cortical structures are associated with attentional control. However, the intricacies of how the development of inhibitory control is associated with the anatomical variations beyond the general age- and gender-dependent differences have not been resolved. Here, we sought to address these questions by quantifying the cortical thickness and surface area in frontal cortical regions and inhibitory control using the stop signal task performance in 6-14-year-old children. Our results showed that the thickness of the left medial orbitofrontal cortex and the surface area of the left caudal anterior cingulate were associated with the inhibitory performance, beyond the variance that could be explained by the subjects\' age and gender. The results highlight the importance of factoring in anatomical variations when following attentional development and the importance of evaluating multiple anatomical measures when aiming to link the properties of cortical structures with variations in cognitive performance.

Increasing research has focused on the impact of air pollution on brain health. As the prevalence of air pollution is increasing alongside other environmental harms, the importance of studying the effects of these changes on human health has become more significant. Additionally, gaining insight into how air pollution exposure, measured at different points in the lifespan, can affect brain structure is critical, as this could be a precursor to cognitive decline later in life. The purpose of this review was to synthesize the literature on the association between air pollutant exposure and cortical thickness, a structural change with known associations with later cognition and neurodegenerative disease. After screening, twelve studies were included in this systematic review. Across a majority of studies, results suggest significant associations between increasing air pollution exposure and decreases in cortical thickness, primarily in areas such as prefrontal cortex, precuneus, and temporal regions of the brain. These results did differ somewhat between age groups and different air pollutants, with the most prominent results being found with exposure to PM2.5, the smallest particulate matter size included in the review. In the future, it is important to continue studying cortical thickness as it is essential to brain functioning and can be influential in disease progression. Furthermore, conducting more longitudinal studies in which air pollution is measured as a cumulation throughout the lifespan would help elucidate when exposure is most impactful and when brain structural changes become observable.

Significant evidence links obesity and schizophrenia (SZ), but the brain associations are still largely unclear. 48 people with SZ were divided into two subgroups: patients with lower waist circumference (SZ-LWC: n = 24) and patients with higher waist circumference (SZ-HWC: n = 24). Healthy controls (HC) were included for comparison (HC: n = 27). Using tract-based spatial statistics, we compared fractional anisotropy (FA) of the whole-brain white matter skeleton between these three groups (SZ-LWC, SZ-HWC, HC). Using Free Surfer, we compared whole-brain cortical thickness and the selected subcortical volumes between the three groups. FA of widespread white matter and the mean cortical thickness in the right temporal lobe and insular cortex were significantly lower in the SZ-HWC group than in the HC group. The FA of regional white matter was significantly lower in the SZ-LWC group than in the HC group. There were no significant differences in mean subcortical volumes between the groups. Additionally, the cognitive performances were worse in the SZ-HWC group, who had more severe triglycerides elevation. This study provides evidence for microstructural abnormalities of white matter, cortical thickness and neurocognitive deficits in SZ patients with excessive abdominal obesity.

BACKGROUND: Anhedonia is an enduring symptom of subthreshold depression (StD) and predict later onset of major depressive disorder (MDD). Brain structural covariance describes the inter-regional distribution of morphological changes compared to healthy controls (HC) and reflects brain maturation and disease progression. We investigated neural correlates of anhedonia from the structural covariance.
METHODS: T1-weighted brain magnetic resonance images were acquired from 79 young adults (26 StD, 30 MDD, and 23 HC). Intra-individual structural covariance networks of 68 cortical surface area (CSAs), 68 cortical thicknesses (CTs), and 14 subcortical volumes were constructed. Group-level hubs and principal edges were defined using the global and regional graph metrics, compared between groups, and examined for the association with anhedonia severity.
RESULTS: Global network metrics were comparable among the StD, MDD, and HC. StD exhibited lower centralities of left pallidal volume than HC. StD showed higher centralities than HC in the CSAs of right rostral anterior cingulate cortex (ACC) and pars triangularis, and in the CT of left pars orbitalis. Less anhedonia was associated with higher centralities of left pallidum and right amygdala, higher edge betweenness centralities in the structural covariance (EBSC) of left postcentral gyrus-parahippocampal gyrus and LIPL-right amygdala. More anhedonia was associated with higher centralities of left inferior parietal lobule (LIPL), left postcentral gyrus, left caudal ACC, and higher EBSC of LIPL-left postcentral gyrus, LIPL-right lateral occipital gyrus, and left caudal ACC-parahippocampal gyrus.
CONCLUSIONS: This study has a cross-sectional design.
CONCLUSIONS: Structural covariance of brain morphologies within the salience and limbic networks, and among the salience-limbic-default mode-somatomotor-visual networks, are possible neural correlates of anhedonia in depression.

BACKGROUND: Blood-derived microRNAs (miRNAs) are potential candidates for detecting and preventing subclinical cognitive dysfunction. However, replication of previous findings and identification of novel miRNAs associated with cognitive domains, including their relation to brain structure and the pathways they regulate, are still lacking.
METHODS: We examined blood-derived miRNAs and miRNA co-expression clusters in relation to cognitive domains, structural magnetic resonance imaging measures, target gene expression, and genetic variants in 2869 participants of a population-based cohort.
RESULTS: Five previously identified and 14 novel miRNAs were associated with cognitive domains. Eleven of these were also associated with cortical thickness and two with hippocampal volume. Multi-omics analysis showed that certain identified miRNAs were genetically influenced and regulated genes in pathways like neurogenesis and synapse assembly.
CONCLUSIONS: We identified miRNAs associated with cognitive domains, brain regions, and neuronal processes affected by aging and neurodegeneration, making them promising candidate blood-based biomarkers or therapeutic targets of subclinical cognitive dysfunction.
CONCLUSIONS: We investigated the association of blood-derived microRNAs with cognitive domains. Five previously identified and 14 novel microRNAs were associated with cognition. Eleven cognition-related microRNAs were also associated with cortical thickness. Identified microRNAs were linked to genes associated with neuronal functions. Results provide putative biomarkers or therapeutic targets of cognitive aging.

UNASSIGNED: The Parkinson\'s Disease-Cognitive Rating Scale (PD-CRS) is a widely used tool for detecting mild cognitive impairment (MCI) in Parkinson\'s Disease (PD) patients, however, the neuroanatomical underpinnings of this test\'s outcomes require clarification. This study aims to: (a) investigate cortical volume (CVol) and cortical thickness (CTh) disparities between PD patients exhibiting mild cognitive impairment (PD-MCI) and those with preserved cognitive abilities (PD-IC); and (b) identify the structural correlates in magnetic resonance imaging (MRI) of overall PD-CRS performance, including its subtest scores, within a non-demented PD cohort.
UNASSIGNED: This study involved 51 PD patients with Hoehn & Yahr stages I-II, categorized into two groups: PD-IC (n = 36) and PD-MCI (n = 15). Cognitive screening evaluations utilized the PD-CRS and the Montreal Cognitive Assessment (MoCA). PD-MCI classification adhered to the Movement Disorder Society Task Force criteria, incorporating extensive neuropsychological assessments. The interrelation between brain morphology and cognitive performance was determined using FreeSurfer.
UNASSIGNED: Vertex-wise analysis of the entire brain demonstrated a notable reduction in CVol within a 2,934 mm2 cluster, encompassing parietal and temporal regions, in the PD-MCI group relative to the PD-IC group. Lower PD-CRS total scores correlated with decreased CVol in the middle frontal, superior temporal, inferior parietal, and cingulate cortices. The PD-CRS subtests for Sustained Attention and Clock Drawing were associated with cortical thinning in distinct regions: the Clock Drawing subtest correlated with changes in the parietal lobe, insula, and superior temporal cortex morphology; while the PD-CRS frontal-subcortical scores presented positive correlations with CTh in the transverse temporal, medial orbitofrontal, superior temporal, precuneus, fusiform, and supramarginal regions. Additionally, PD-CRS subtests for Semantic and Alternating verbal fluency were linked to CTh changes in orbitofrontal, temporal, fusiform, insula, and precentral regions.
UNASSIGNED: PD-CRS performance mirrors neuroanatomical changes across extensive fronto-temporo-parietal areas, covering both lateral and medial cortical surfaces, in PD patients without dementia. The observed changes in CVol and CTh associated with this cognitive screening tool suggest their potential as surrogate markers for cognitive decline in PD. These findings warrant further exploration and validation in multicenter studies involving independent patient cohorts.

Apolipoprotein E (APOE) ε4, the strongest genetic risk for late-onset Alzheimer\'s disease (AD), confers greater risk in females than males. While APOE4-related modulation of structural brain integrity in AD is well documented, extant literature on sex-APOE interactions has focused on older adults. The understanding of the healthy brain as a part of the normal aging process and as distinct from explicit disease or pathology is essential before comparison can be made with pathological states. Hence, it is crucial to characterize and better understand these relationships in middle-age prior to the onset of overt clinical symptoms and advanced neurodegeneration. The present study examined the relationships between sex, APOE status, and cortical thickness in 128 healthy, cognitively unimpaired, middle-aged adults (ages 40-60, M(SD) = 49.97(6.04); 77 females). All participants underwent structural magnetic resonance imaging and were genotyped for APOE (APOE4 +  = 38; APOE4- = 90). Compared to males, females had thicker superior frontal cortices bilaterally, left middle temporal cortex, and left pars triangularis. APOE4 + had thinner left rostral middle frontal gyrus compared to APOE4-. Female compared to male APOE4- had thicker left banks of the superior temporal sulcus, left caudal anterior cingulate, left superior frontal, left superior parietal, and right precentral cortices. Female compared to male APOE4 + had thicker superior frontal cortices bilaterally. Female APOE4 + had thinner left rostral anterior cingulate cortex compared to female APOE4-. Overall, APOE-related differences in cortical thickness are more pronounced in females and detectable in middle age, well before the onset of overt clinical symptoms of AD.