Changes In Cortical Thickness Research Articles

Analysis of changes in bone mineral density and cortical bone thickness after reconstruction of the mandible with fibula, is condyle preservation a critical influence factor?

This study aimed to investigate the features of bone mineral density (BMD) and cortical bone thickness in grafted fibula. Eighty-six patients who underwent mandibular reconstruction using vascularized fibula flaps were enrolled, all of whom were followed up at 3, 6, and 12 months after surgery. The patients were grouped according to whether the condyle was preserved. BMD and cortical bone thickness were also measured. Condyle-preserved group consisted of 65 patients and condyle-unpreserved group consisted of 21 patients. There was a significant correlation between thickness and BMD, which was significantly correlated with follow-up time. One year after surgery, the BMD of the condyle-preserved group decreased from 1029.61 ± 156.01mg/cm3 to 978.6 ± 141.90mg/cm3, and thickness decreased from 3.29 ± 0.65mm to 2.72 ± 0.72mm. BMD of the condyle-unpreserved group decreased from 1062.21 ± 126.01mg/cm3 to 851.26 ± 144.38mg/cm3, and thickness decreased from 3.46 ± 0.89mm to 2.56 ± 0.73mm. In the condyle-preserved and unpreserved groups, the absorption rates of BMD were 3.29 ± 11.97% and 17.09 ± 12.42% at 12 months, respectively, and the rate of thickness was 20.7 ± 11.45% and 26.39 ± 12.23% at 12 months, respectively. BMD and thickness showed a decreasing trend over time. Preserving the condyle can slow bone resorption of the fibula. Regarding implant restoration, we recommend doctors to perform the treatment within 6-12 months after surgery in order to effectively manage bone resorption. Our study found that condylar preservation can decrease the absorption rate of BMD and cortical bone thickness, helping doctors make better clinical decisions. ChiCTR2300069661 (March 22, 2023).

Early childhood family threat and longitudinal amygdala-mPFC circuit development: Examining cortical thickness and gray matter-white matter contrast

Early threat-associated cortical thinning may be interpreted as accelerated cortical development. However, non-adaptive processes may show similar macrostructural changes. Examining cortical thickness (CT) together with grey/white-matter contrast (GWC), a proxy for intracortical myelination, may enhance the interpretation of CT findings. In this prospective study, we examined associations between early life family-related threat (harsh parenting, family conflict, and neighborhood safety) and CT and GWC development from late childhood to middle adolescence. MRI was acquired from 4200 children (2069 boys) from the Generation R study at ages 8, 10 and 14 years (in total 6114 scans), of whom 1697 children had >1 scans. Linear mixed effect models were used to examine family factor-by-age interactions on amygdala volume, caudal and rostral anterior cingulate (ACC) and medial orbitofrontal cortex (mOFC) CT and GWC. A neighborhood safety-by-age-interaction was found for rostral ACC GWC, suggesting less developmental change in children from unsafe neighborhoods. Moreover, after more stringent correction for motion, family conflict was associated with greater developmental change in CT but less developmental change in GWC. Results suggest that early threat may blunt ACC GWC development. Our results, therefore, do not provide evidence for accelerated threat-associated structural development of the amygdala-mPFC circuit between ages 8–14 years.

Patterns of Brain Maturation in Autism and Their Molecular Associations

In the neurotypical brain, regions develop in coordinated patterns, providing a fundamental scaffold for brain function and behavior. Whether altered patterns contribute to clinical profiles in neurodevelopmental conditions, including autism, remains unclear. To examine if, in autism, brain regions develop differently in relation to each other and how these differences are associated with molecular/genomic mechanisms and symptomatology. This study was an analysis of one the largest deep-phenotyped, case-control, longitudinal (2 assessments separated by approximately 12-24 months) structural magnetic resonance imaging and cognitive-behavioral autism datasets (EU-AIMS Longitudinal European Autism Project [LEAP]; study dates, February 2014-November 2017) and an out-of-sample validation in the Brain Development Imaging Study (BrainMapASD) independent cohort. Analyses were performed during the 2022 to 2023 period. This multicenter study included autistic and neurotypical children, adolescents, and adults. Autistic participants were included if they had an existing autism diagnosis (DSM-IV/International Statistical Classification of Diseases and Related Health Problems, Tenth Revision or DSM-5 criteria). Autistic participants with co-occurring psychiatric conditions (except psychosis/bipolar disorder) and those taking regular medications were included. Neuroanatomy of neurotypical and autistic participants. Intraindividual changes in surface area and cortical thickness over time, analyzed via surface-based morphometrics. A total of 386 individuals in the LEAP cohort (6-31 years at first visit; 214 autistic individuals, mean [SD] age, 17.3 [5.4] years; 154 male [72.0%] and 172 neurotypical individuals, mean [SD] age, 16.35 [5.7] years; 108 male [62.8%]) and 146 individuals in the BrainMapASD cohort (11-18 years at first visit; 49 autistic individuals, mean [SD] age, 14.31 [2.4] years; 42 male [85.7%] and 97 neurotypical individuals, mean [SD] age, 14.10 [2.5] years; 58 male [59.8%]). Maturational between-group differences in cortical thickness and surface area were established that were mostly driven by sensorimotor regions (eg, across features, absolute loadings for early visual cortex ranged from 0.07 to 0.11, whereas absolute loadings for dorsolateral prefrontal cortex ranged from 0.005 to 0.06). Neurodevelopmental differences were transcriptomically enriched for genes expressed in several cell types and during various neurodevelopmental stages, and autism candidate genes (eg, downregulated genes in autism, including those regulating synaptic transmission; enrichment odds ratio =3.7; P =2.6 × -10). A more neurotypical, less autismlike maturational profile was associated with fewer social difficulties and more typical sensory processing (false discovery rate P <.05; Pearson r ≥0.17). Results were replicated in the independently collected BrainMapASD cohort. Results of this case-control study suggest that the coordinated development of brain regions was altered in autism, involved a complex interplay of temporally sensitive molecular mechanisms, and may be associated with both lower-order (eg, sensory) and higher-order (eg, social) clinical features of autism. Thus, examining maturational patterns may provide an analytic framework to study the neurobiological origins of clinical profiles in neurodevelopmental/mental health conditions.

Speech motor impairment in ALS is associated with multiregional cortical thinning beyond primary motor cortex.

Cortical thinning is well-documented in individuals with amyotrophic lateral sclerosis (ALS), yet its association with speech deterioration remains understudied. This study characterizes anatomical changes in the brain within the context of speech impairment patterns in individuals with ALS, providing insight into the disease's multiregional spread and biology. To evaluate patterns of cortical thickness in speakers with ALS with and without functional speech changes compared to healthy controls (HCs) using whole-brain and region of interest (ROI) analyses. Forty individuals with ALS and 22 HCs underwent a T1-weighted 3-Tesla magnetic resonance imaging (MRI). Individuals with ALS were divided into two groups based on the preserved speech [ps-ALS] (n = 18) or deteriorated speech [ds-ALS] (n = 22) as measured by the ALSFRSF-R speech subscore (=4 or <4 points, respectively). Sixteen a priori-defined and automatically segmented cortical and subcortical brain ROIs were selected based on their previously documented roles in speech production. Two cortical thickness analyses were performed: (1) group-level whole-brain surface-based analyses and (2) group-level ROI analyses. A case study of 6 ALS individuals examined the cortical thickness, and their speech was characterized using quantitative and qualitative measures. Based on the group-level whole-brain surface-based analyses, the ds-ALS group demonstrated significant cortical thinning compared to HCs in the left primary motor and somatosensory cortices and the right inferior parietal lobe with its adjacent lateral occipital cortical regions. The ps-ALS group demonstrated no significant cortical thinning compared to HCs. Based on the group-level ROI analyses, the ds-ALS group demonstrated significant cortical thinning compared to HCs in bilateral middle motor cortices, right posterior dorsal premotor cortex, and left anterior cingulate cortex. The case study analysis revealed that ALS speakers with speech features characteristic of spastic dysarthria exhibited cortical thinning, while those with speech features characteristic of flaccid dysarthria did not. Individuals with ALS have anatomical changes involving multiregional neocortical areas beyond the primary motor cortex that may manifest as subjective (i.e., clinical judgment) and objective (i.e., speaking rate) changes in speech production. Further longitudinal work in ALS is needed to better understand the link between MRI cortical thickness changes and bulbar dysfunction.

Regional patterns of human cortex development correlate with underlying neurobiology

Human brain morphology undergoes complex changes over the lifespan. Despite recent progress in tracking brain development via normative models, current knowledge of underlying biological mechanisms is highly limited. We demonstrate that human cortical thickness development and aging trajectories unfold along patterns of molecular and cellular brain organization, traceable from population-level to individual developmental trajectories. During childhood and adolescence, cortex-wide spatial distributions of dopaminergic receptors, inhibitory neurons, glial cell populations, and brain-metabolic features explain up to 50% of the variance associated with a lifespan model of regional cortical thickness trajectories. In contrast, modeled cortical thickness change patterns during adulthood are best explained by cholinergic and glutamatergic neurotransmitter receptor and transporter distributions. These relationships are supported by developmental gene expression trajectories and translate to individual longitudinal data from over 8000 adolescents, explaining up to 59% of developmental change at cohort- and 18% at single-subject level. Integrating neurobiological brain atlases with normative modeling and population neuroimaging provides a biologically meaningful path to understand brain development and aging in living humans.

Comparative analysis of cortical anatomy inmale participants with internet gaming disorder or tobacco use disorder: Insights fromnormative modeling.

Research on individual differences in brain structural features of internet gaming disorder (IGD) and established addictions such as tobacco use disorder (TUD) is currently limited. This study utilized normative modeling to analyze the cortical thickness (CT) development patterns of male patients with IGD and TUD, aiming to provide further insights into whether IGD qualifies as an addiction. Surface-based brain morphometry (SBM) was used to calculate CT from T1-weighted magnetic resonance imaging data of 804 male participants (665 healthy individuals, 68 IGD and 71 TUD). Gaussian process regression was employed to generate normative models of CT development. Deviation maps were produced to depict deviations of IGD and TUD participants from the typical developmental patterns. Both addiction groups exhibited widespread cortical thinning, particularly in regions such as the bilateral temporal pole and medial orbitofrontal cortex. The TUD group demonstrated a higher degree of individualization and limited spatial overlap compared to the IGD group. Opposite trends in CT changes were observed between the two groups in the bilateral pericalcarine cortex and pars triangularis. These findings regarding the similarities and differences between IGD and TUD provide support for the idea that IGD shares common features with substance-related addictions and contribute to a deeper understanding of the neural mechanisms underlyingIGD.

Impact of Social Connectedness on Neuroinflammation and Brain Architecture in Non-Human Primates

Social connectedness plays a critical role in the mental and physical health of primates, including humans.1-3 Social isolation and loneliness have been linked to a variety of negative health outcomes, such as increased risk of neurological disorders like Alzheimer’s, anxiety, and depression.2 Despite extensive research on the effects of early isolation, there is limited understanding of the neurobiological consequences of social deprivation during adulthood. This project aims to fill this gap by exploring how changes in social connectedness influence neuroinflammation and brain architecture in non-human primates (NHPs). The study utilized a longitudinal design involving 19 adult cynomolgus macaques to examine the effects of social living conditions on neuroinflammation and brain structure. The NHPs were first housed in group living conditions, transitioned to single-living conditions, and finally returned to group living. Multimodal neuroimaging was conducted to evaluate changes in cortical thickness, myelination, and brain connectivity across these phases. Blood and cerebrospinal fluid samples were collected at multiple time points to assess levels of pro-inflammatory cytokines (TNF-a, IL-1β, IL-6) and a biomarker for neuroplasticity (BDNF).4-6 Advanced biomarker detection technology, such as SIMOA, ELISA, and Luminex, could be leveraged to achieve highly sensitive measurements of these markers.7,8 Preliminary findings indicate that social deprivation leads to decreases in cortical thickness and myelination in key brain regions associated with social cognition; however, these changes may be reversible upon reintroduction to group living.9-12 This study hypothesizes that the observed structural changes correlate with increases in neuroinflammatory markers. If confirmed, these results could highlight the critical role of social connectedness in maintaining brain health and suggest potential biomarkers for loneliness and related neuropsychiatric conditions. This research could inform interventions aimed at mitigating the negative health impacts of social isolation and improve welfare standards in NHP research, enhancing the translational relevance of such models to human health. References Holt-Lunstad J, Steptoe A. Social Isolation: An underappreciated determinant of physical health. Current Opinion in Psychology. 2022;43:232-237. doi:10.1016/j.copsyc.2021.07.012 Bzdok D, Dunbar RIM. The neurobiology of social distance. Trends in Cognitive Sciences. 2020;24(9):717-733. doi:10.1016/j.tics.2020.05.016 Cacioppo JT, Cacioppo S. The growing problem of loneliness. The Lancet. 2018;391(10119):426. doi:10.1016/s0140-6736(18)30142-9 Magalhães DM, Mampay M, Sebastião AM, Sheridan GK, Valente CA. Age-related impact of social isolation in mice: Young vs middle-aged. Neurochemistry International. 2024;174:105678. doi:10.1016/j.neuint.2024.105678 Van Bogart K, Engeland CG, Sliwinski MJ, et al. The association between loneliness and inflammation: Findings from an older adult sample. Frontiers in Behavioral Neuroscience. 2022;15. doi:10.3389/fnbeh.2021.801746 Bathina S, Das UN. Brain-derived neurotrophic factor and its clinical implications. Archives of Medical Science. 2015;6:1164-1178. doi:10.5114/aoms.2015.56342 Lasseter HC, Provost AC, Chaby LE, Daskalakis NP, Haas M, Jeromin A. Cross-platform comparison of highly sensitive immunoassay technologies for cytokine markers: Platform performance in post-traumatic stress disorder and parkinson’s disease. Cytokine: X. 2020;2(2):100027. doi:10.1016/j.cytox.2020.100027 Platchek M, Lu Q, Tran H, Xie W. Comparative analysis of multiple immunoassays for cytokine profiling in drug discovery. SLAS Discovery. 2020;25(10):1197-1213. doi:10.1177/2472555220954389 Miller JG, López V, Buthmann JL, Garcia JM, Gotlib IH. A social gradient of cortical thickness in adolescence: Relationships with neighborhood socioeconomic disadvantage, family socioeconomic status, and depressive symptoms. Biological Psychiatry Global Open Science. 2022;2(3):253-262. doi:10.1016/j.bpsgos.2022.03.005 Yang Y, Cheng Z, Tang H, et al. Neonatal maternal separation impairs prefrontal cortical myelination and cognitive functions in rats through activation of Wnt Cerebral Cortex. Published online May 13, 2016. doi:10.1093/cercor/bhw121 Sallet J, Mars RB, Noonan MP, et al. Social network size affects neural circuits in macaques. Science. 2011;334(6056):697-700. doi:10.1126/science.1210027 Makinodan M, Rosen KM, Ito S, Corfas A critical period for social experience–dependent oligodendrocyte maturation and myelination. Science. 2012;337(6100):1357-1360. doi:10.1126/science.1220845

COVID-19 lockdown effects on adolescent brain structure suggest accelerated maturation that is more pronounced in females than in males

Adolescence is a period of substantial social-emotional development, accompanied by dramatic changes to brain structure and function. Social isolation due to lockdowns that were imposed because of the COVID-19 pandemic had a detrimental impact on adolescent mental health, with the mental health of females more affected than males. We assessed the impact of the COVID-19 pandemic lockdowns on adolescent brain structure with a focus on sex differences. We collected MRI structural data longitudinally from adolescents prior to and after the pandemic lockdowns. The pre-COVID data were used to create a normative model of cortical thickness change with age during typical adolescent development. Cortical thickness values in the post-COVID data were compared to this normative model. The analysis revealed accelerated cortical thinning in the post-COVID brain, which was more widespread throughout the brain and greater in magnitude in females than in males. When measured in terms of equivalent years of development, the mean acceleration was found to be 4.2 y in females and 1.4 y in males. Accelerated brain maturation as a result of chronic stress or adversity during development has been well documented. These findings suggest that the lifestyle disruptions associated with the COVID-19 pandemic lockdowns caused changes in brain biology and had a more severe impact on the female than the male brain.

Medial prefrontal neuroplasticity during extended-release naltrexone treatment of opioid use disorder – a longitudinal structural magnetic resonance imaging study

Opioid use disorder (OUD) has been linked to macroscopic structural alterations in the brain. The monthly injectable, extended-release formulation of μ-opioid antagonist naltrexone (XR-NTX) is highly effective in reducing opioid craving and preventing opioid relapse. Here, we investigated the neuroanatomical effects of XR-NTX by examining changes in cortical thickness during treatment for OUD. Forty-seven OUD patients underwent structural magnetic resonance imaging and subjectively rated their opioid craving ≤1 day before (pre-treatment) and 11 ± 3 days after (on-treatment) the first XR-NTX injection. A sample of fifty-six non-OUD individuals completed a single imaging session and served as the comparison group. A publicly available [¹¹C]carfentanil positron emission tomography dataset was used to assess the relationship between changes in cortical thickness and μ-opioid receptor (MOR) binding potential across brain regions. We found that the thickness of the medial prefrontal and anterior cingulate cortices (mPFC/aCC; regions with high MOR binding potential) was comparable between the non-OUD individuals and the OUD patients at pre-treatment. However, among the OUD patients, mPFC/aCC thickness significantly decreased from pre-treatment to on-treatment. A greater reduction in mPFC/aCC thickness was associated with a greater reduction in opioid craving. Taken together, our study suggests XR-NTX-induced cortical thickness reduction in the mPFC/aCC regions in OUD patients. The reduction in thickness does not appear to indicate a restoration to the non-OUD level but rather reflects XR-NTX’s distinct therapeutic impact on an MOR-rich brain structure. Our findings highlight the neuroplastic effects of XR-NTX that may inform the development of novel OUD interventions.

Patterns of cortical thickness alterations in degenerative cervical myelopathy: associations with dexterity and gait dysfunctions.

Degenerative cervical myelopathy (DCM) can lead to significant brain structural reorganization. The association between the cortical changes and specific motor symptoms in DCM has yet to be fully elucidated. We investigated the associations between cortical thickness changes with neurological symptoms, such as dexterity and gait abnormalities, in patients with DCM in a case-control study. A 3 Tesla MRI scanner was used to acquire high-resolution T1-weighted structural scans from 30 right-handed patients with DCM and 22 age-matched healthy controls. Pronounced cortical thinning was observed in DCM patients relative to healthy controls, particularly in the bilateral precentral and prefrontal gyri, left pars triangularis, left postcentral gyrus, right transverse temporal and visual cortices (P ≤ 0.04). Notably, cortical thickness in these regions showed strong correlations with objective motor deficits (P < 0.0001). Specifically, the prefrontal cortex, premotor area and supplementary motor area exhibited significant thickness reductions correlating with diminished dexterity (R2 = 0.33, P < 0.0007; R2 = 0.34, P = 0.005, respectively). Similarly, declines in gait function were associated with reduced cortical thickness in the visual motor and frontal eye field cortices (R2 = 0.39, P = 0.029, R2 = 0.33, P = 0.04, respectively). Interestingly, only the contralateral precuneus thickness was associated with the overall modified Japanese Orthopaedic Association (mJOA) scores (R2 = 0.29, P = 0.003). However, the upper extremity subscore of mJOA indicated an association with the visual cortex and the anterior prefrontal (R2 = 0.48, P = 0.002, R2 = 0.33, P = 0.0034, respectively). In conclusion, our findings reveal patterns of cortical changes correlating with motor deficits, highlighting the significance of combining objective clinical and brain imaging assessments for understanding motor network dysfunction in DCM.

Changes in cortical thickness: yet another indication of supraspinal adaptations in degenerative cervical myelopathy.

This scientific commentary refers to 'Patterns of cortical thickness alterations in degenerative cervical myelopathy: associations with dexterity and gait dysfunctions', by Muhammad et al. (https://doi.org/10.1093/braincomms/fcae279).

Association of Levels of CSF Osteopontin With Cortical Atrophy and Disability in Early Multiple Sclerosis.

To evaluate CSF inflammatory markers with accumulation of cortical damage as well as disease activity in patients with early relapsing-remitting MS (RRMS). CSF levels of osteopontin (OPN) and 66 inflammatory markers were assessed using an immune-assay multiplex technique in 107 patients with RRMS (82 F/25 M, mean age 35.7 ± 11.8 years). All patients underwent regular clinical assessment and yearly 3T MRI scans for 2 years while 39 patients had a 4-year follow-up. White matter lesion number and volume, cortical lesions (CLs) and volume, and global cortical thickness (CTh) were evaluated together with the 'no evidence of disease activity' (NEDA-3) status, defined by no relapses, no disability worsening, and no MRI activity, including CLs. The random forest algorithm selected OPN, CXCL13, TWEAK, TNF, IL19, sCD30, sTNFR1, IL35, IL16, and sCD163 as significantly associated with changes in global CTh. OPN and CXCL13 were most related to accumulation of atrophy after 2 and 4 years. In a multivariate linear regression model on CSF markers, OPN (p < 0.001), CXCL13 (p = 0.001), and sTNFR1 (p = 0.024) were increased in those patients with accumulating atrophy (adjusted R-squared 0.615). The 10 markers were added in a model that included all clinical, demographic, and MRI variables: OPN (p = 0.002) and IL19 (p = 0.022) levels were confirmed to be significantly increased in patients developing more CTh change over the follow-up (adjusted R-squared 0.619). CXCL13 and OPN also revealed the best association with NEDA-3 after 2 years, with OPN significantly linked to disability accumulation (OR 2.468 [1.46-5.034], p = 0.004) at the multivariate logistic regression model. These data confirm and expand our knowledge on the prognostic role of the CSF inflammatory profile in predicting changes in cortical pathology and disease activity in early MS. The data emphasize a crucial role of OPN.

Brain Charts for the Rhesus Macaque Lifespan.

Recent efforts to chart human brain growth across the lifespan using large-scale MRI data have provided reference standards for human brain development. However, similar models for nonhuman primate (NHP) growth are lacking. The rhesus macaque, a widely used NHP in translational neuroscience due to its similarities in brain anatomy, phylogenetics, cognitive, and social behaviors to humans, serves as an ideal NHP model. This study aimed to create normative growth charts for brain structure across the macaque lifespan, enhancing our understanding of neurodevelopment and aging, and facilitating cross-species translational research. Leveraging data from the PRIMatE Data Exchange (PRIME-DE) and other sources, we aggregated 1,522 MRI scans from 1,024 rhesus macaques. We mapped non-linear developmental trajectories for global and regional brain structural changes in volume, cortical thickness, and surface area over the lifespan. Our findings provided normative charts with centile scores for macaque brain structures and revealed key developmental milestones from prenatal stages to aging, highlighting both species-specific and comparable brain maturation patterns between macaques and humans. The charts offer a valuable resource for future NHP studies, particularly those with small sample sizes. Furthermore, the interactive open resource (https://interspeciesmap.childmind.org) supports cross-species comparisons to advance translational neuroscience research.

Genotype and environmental interactions determine the root digging time and essential oil production in vetiver (Chrysopogon zizanioides (L.) Roberty)

Thirty different vetiver genotypes were grown for evaluation in the experiments at CSIR- Central Institute for Medicinal and Aromatic Plants (CSIR-CIMAP), Lucknow, U.P. 226015, India, to assess the impact of genotype × environment interactions (GEI) on essential oil yield and chemical composition in vetiver lines grown in north India, as well as identifying appropriate genotypes and representative root digging times throughout the year for essential oil production. The interplay of genotype and environment is a significant constraint in crop development. The additive main effects and multiplicative interaction (AMMI) and the analysis of variance (ANOVA) revealed significant effects for genotype (G), environment (E), and genotype × environment (GE) (p < 0.01). The primary root transverse section confirmed the changes in cortical sclerenchyma thickness and variety observed in the dug-out roots from different vetiver genotypes after six and twelve months. The quantity and number of sclerenchyma rows in the peripheral cortical region vary throughout vetiver genotypes. Following root digging, one component (Khusol content) had 40 %, while Khusilal content had 20 % for genotype VTR-23. However, after twelve months, Khusol content had 19 %, whereas Khusilal content had 41 %. The shift in essential oil makeup was apparent. The level of essential oil did not alter considerably. Based on the GGE biplot analysis, VTR-1, 11, and 14 were identified as the most stable genotypes with high essential yields; therefore, it is recommended to use these genotypes in India's enormous agriculture.

Shared genetic architecture of cortical thickness alterations in major depressive disorder and schizophrenia

BackgroundMajor depressive disorder (MDD) and schizophrenia (SCZ) are heritable brain disorders characterized by alterations in cortical thickness. However, the shared genetic basis for cortical thickness changes in these disorders remains unclear. MethodsWe conducted a systematic literature search on cortical thickness in MDD and SCZ through PubMed and Web of Science. A coordinate-based meta-analysis was performed to identify cortical thickness changes. Additionally, utilizing summary statistics from the largest genome-wide association studies for depression (Ncase = 268,615, Ncontrol = 667,123) and SCZ (Ncase = 53,386, Ncontrol = 77,258), we explored shared genomic loci using conjunctional false discovery rate (conjFDR) analysis. Transcriptome-neuroimaging association analysis was then employed to identify shared genes associated with cortical thickness alterations, and enrichment analysis was finally carried out to elucidate the biological significance of these genes. ResultsOur search yielded 34 MDD (Ncase = 1621, Ncontrol = 1507) and 19 SCZ (Ncase = 1170, Ncontrol = 1043) neuroimaging studies for cortical thickness meta-analysis. Specific alterations in the left supplementary motor area were observed in MDD, while SCZ exhibited widespread reductions in various brain regions, particularly in the frontal and temporal areas. The conjFDR approach identified 357 genomic loci jointly associated with MDD and SCZ. Within these loci, 55 genes were found to be associated with cortical thickness alterations in both disorders. Enrichment analysis revealed their involvement in nervous system development, apoptosis, and cell communication. ConclusionThis study revealed the shared genetic architecture underlying cortical thickness alterations in MDD and SCZ, providing insights into common neurobiological pathways. The identified genes and pathways may serve as potential transdiagnostic markers, informing precision medicine approaches in psychiatric care.

More molar distal movement than pretreatment cone-beam computed tomography posterior space available at the root level in mandibular dentition distalization with microimplants.

To compare the mandibular posterior space available before treatment and the distance of molar distalization achieved after mandibular dentition distalization with microimplants. A total of 66 Class I or III adult patients (mean age = 24.46 ± 4.89 years) who underwent molar distalization using microimplants were retrospectively included. The posterior space available distal to the second molar before treatment and the distance of distalization achieved after treatment were measured using axial cone-beam computed tomography images (0, 2, 4, and 6 mm apical to the second molar root furcation). Changes in lingual cortical thickness and molar root length after treatment were examined. Paired t-test or Wilcoxon signed-rank test was performed to compare measurements before and after treatment. Spearman correlation analysis was performed to assess the relationship between thinning of the cortical plate and root resorption. Achieved distalization distance was significantly greater than pretreatment posterior space available by 0.8 mm at all root levels (P < .001). The difference was greater toward the root apex level and greater in the Class III group than the Class I group. Lingual cortical thickness was significantly decreased after treatment along with resorption of the second molar distal root (P < .001). In addition, a positive correlation was found between thinning of the cortical plate and distal root resorption of the molar (P < .001). Achieved distalization distance of the mandibular molar using microimplants was greater than the pretreatment posterior space available. Thinning of the lingual cortex and root resorption were observed after distalization.

Mapping brain morphology to cognitive deficits: a study on PD-CRS scores in Parkinson's disease with mild cognitive impairment.

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. 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. 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. 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.

Spatial and temporal patterns of cortical mean diffusivity in Alzheimer's disease and suspected non-Alzheimer's disease pathophysiology.

The spatial and temporal patterns of cortical mean diffusivity (cMD), as well as its association with Alzheimer's disease (AD) and suspected non-Alzheimer's pathophysiology (SNAP), are not yet fully understood. We compared baseline (n=617) and longitudinal changes (n=421) of cMD, cortical thickness, and gray matter volume and their relations to vascular risk factors, amyloid beta (Aβ), and tau positron emission tomography (PET), and longitudinal cognitive decline in Aβ PET negative and positive older adults. cMD increases were more sensitive to detecting brain structural alterations than cortical thinning and gray matter atrophy. Tau-related cMD increases partially mediated Aβ-related cognitive decline in AD, whereas vascular disease-related increased cMD levels substantially mediated age-related cognitive decline in SNAP. These findings revealed the dynamic changes of microstructural and macrostructural indicators and their associations with AD and SNAP, providing novel insights into understanding upstream and downstream events of cMD in neurodegenerative disease. Cortical mean diffusivity (cMD) was more sensitive to detecting structural changes than macrostructural factors. Tau-related cMD increases partially mediated amyloid beta-related cognitive decline in Alzheimer's disease (AD). White matter hyperintensity-related higher cMD mainly explained the age-related cognitive decline in suspected non-Alzheimer's pathophysiology (SNAP). cMD may assist in tracking earlier neurodegenerative signs in AD and SNAP.

Association of cortical morphology, white matter hyperintensity, and glymphatic function in frontotemporal dementia variants.

Frontotemporal dementia (FTD) can be phenotypically divided into behavioral variant FTD (bvFTD), nonfluent variant primary progressive aphasia (nfvPPA), and semantic variant PPA (svPPA). However, the neural underpinnings of this phenotypic heterogeneity remain elusive. Cortical morphology, white matter hyperintensities (WMH), diffusion tensor image analysis along the perivascular space (DTI-ALPS), and their interrelationships were assessed in subtypes of FTD. Neuroimaging-transcriptional analyses on the regional cortical morphological deviances among subtypes were also performed. Changes in cortical thickness, surface area, gyrification, WMH, and DTI-ALPS were subtype-specific in FTD. The three morphologic indices are related to whole-brain WMH volume and cognitive performance, while cortical thickness is related to DTI-ALPS. Neuroimaging-transcriptional analyses identified key biological pathways linked to the formation and/or spread of TDP-43/tau pathologies. We found subtype-specific changes in cortical morphology, WMH, and glymphatic function in FTD. Our findings have the potential to contribute to the development of personalized predictions and treatment strategies for this disorder. Cortical morphologic changes, white matter hyperintensities (WMH), and glymphatic dysfunction are subtype-specific. Cortical morphologic changes, WMH, and glymphatic dysfunction are inter-correlated. Cortical morphologic changes and WMH burden contribute to cognitive impairments.

Regional patterns of human cortex development correlate with underlying neurobiology.

Human brain morphology undergoes complex changes over the lifespan. Despite recent progress in tracking brain development via normative models, current knowledge of underlying biological mechanisms is highly limited. We demonstrate that human cortical thickness development and aging trajectories unfold along patterns of molecular and cellular brain organization, traceable from population-level to individual developmental trajectories. During childhood and adolescence, cortex-wide spatial distributions of dopaminergic receptors, inhibitory neurons, glial cell populations, and brain-metabolic features explain up to 50% of variance associated with a lifespan model of regional cortical thickness trajectories. In contrast, modeled cortical thickness change patterns during adulthood are best explained by cholinergic and glutamatergic neurotransmitter receptor and transporter distributions. These relationships are supported by developmental gene expression trajectories and translate to individual longitudinal data from over 8,000 adolescents, explaining up to 59% of developmental change at cohort- and 18% at single-subject level. Integrating neurobiological brain atlases with normative modeling and population neuroimaging provides a biologically meaningful path to understand brain development and aging in living humans.