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Background: Lower functioning and higher symptom severity are observed when panic disorder (PD) co-occurs with generalized anxiety disorder (PD + GAD). No research on cortical gyrification patterns in the PD + GAD group has been conducted to date, which could show the alterations in brain connectivity in the extended fear network (EFN). This study aimed to investigate the characteristics of cortical gyrification in the PD + GAD group, compared to that in the PD without comorbid GAD (PD-GAD) group.
Methods: This study included 90 patients with PD, with propensity score matching between the PD + GAD (n = 30) and PD-GAD groups (n = 60), and 65 healthy controls (HC). For clinical evaluation, we assessed the anxiety symptomatology, suicidality, and harm avoidance. The local gyrification index (LGI) was obtained from T1-weighted brain MRI data using FreeSurfer.
Results: In the PD group compared to the HC, the hypergyrification involved the EFN. In the PD + GAD group compared to the PD-GAD group, hypergyrification was shown in the pathological worry-related brain regions. Within the PD + GAD group, significant positive correlations were observed between the superior frontal gyrus LGI values and suicidality scores, as well as between the superior parietal gyrus LGI values and harm avoidance levels.
Limitations: Given the variability in cortical gyrification patterns, longitudinal studies are needed to assess the occurrence of hypergyrification in specific brain regions.
Conclusions: This study is the first to demonstrate cortical gyrification patterns in the PD + GAD group compared to those in the PD-GAD group. Notably, the EFN and pathological worry-related brain regions have been implicated in the pathology of PD + GAD.
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http://dx.doi.org/10.1016/j.jad.2024.12.001 | DOI Listing |
Neurol Ther
September 2025
Department of Neurology, The First Affiliated Hospital with Nanjing Medical University, No. 300 Guangzhou Road, Nanjing, 210029, China.
Introduction: The pathogenesis of levodopa-induced dyskinesia (LID) in Parkinson's disease (PD) remains uncertain. Our work sought to examine the cortical gyrification pattern and its corresponding functional connectivity alterations, along with the underlying neurotransmitter information, in LID of PD.
Methods: We included 30 PD patients with LID (PD-LID group), 30 without LID (PD-NLID group), and 30 age- and gender-matched healthy controls (HC group).
Sci Adv
September 2025
Department of Physiology, Anatomy and Genetics, University of Oxford, Oxford OX1 3QX, UK.
Apical-basal polarity (ABP) establishment and maintenance is necessary for proper brain development, yet how it is controlled is unclear. Galectin-3 (Gal-3) has been previously implicated in ABP of epithelial cells, and, here, we find that it is apically expressed in human embryonic stem cells (hESCs) during neural induction. Gal-3 blockade disrupts ABP and alters the distribution of junctional proteins in hESC-derived neural rosettes and is rescued by addition of recombinant Gal-3.
View Article and Find Full Text PDFQuant Imaging Med Surg
September 2025
Department of Radiology, Affiliated Hospital of Zunyi Medical University, Medical Imaging Center of Guizhou Province, Engineering Research Center of Intelligent Medical Imaging in Guizhou Higher Education Institutions, Zunyi, China.
Background: Spastic cerebral palsy (SCP) is associated with extensive alterations in regional cortical morphology. However, the specific effects of SCP on the topological organization of morphological brain networks remain largely unknown. This study aimed to investigate these effects and explore their potential correlations with clinical manifestations in SCP children.
View Article and Find Full Text PDFNat Commun
August 2025
Department of Molecules - Signaling - Development, Max Planck Institute for Biological Intelligence, Martinsried, Germany.
Folding of the mammalian cerebral cortex into sulcal fissures and gyral peaks is the result of complex processes that are incompletely understood. Previously we showed that genetic deletion of Flrt1/3 adhesion molecules causes folding of the smooth mouse cortex into sulci resulting from increased lateral dispersion and faster neuron migration, without progenitor expansion. Here, we show in mice that combining the Flrt1/3 double knockout with an additional genetic deletion that causes progenitor expansion, greatly enhances cortex folding.
View Article and Find Full Text PDFFront Aging Neurosci
August 2025
Department of Radiology and Center for Imaging Science, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul, Republic of Korea.
Purpose: To investigate the correlation between cortical thickness (CT), sulcal depth (SD), local gyrification index (LGI), and cognitive scores in patients with Alzheimer's disease (AD).
Methods: A total of 200 patients with AD from 2014 to 2021 were included, confirmed by 18F-florbetaben-positron emission tomography, and having a Clinical Dementia Rating score of 0.5 or 1.