PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 15338563

Gender differences in cortical complexity.

Eileen Luders·Katherine L Narr·Paul M Thompson·David E Rex·Lutz Jancke·Helmuth Steinmetz·Arthur W Toga
View original source ↗Export metadata ↓

Abstract

Cortical complexity, a measure that quantifies the spatial frequency of gyrification and fissuration of the brain surface, has not been thoroughly characterized with respect to gender differences in the human brain. Using a new three-dimensional (3D) analytic technique with magnetic resonance imaging, we found greater gyrification in women than men in frontal and parietal regions. Increased complexity implies more cortical surface area, which may offset gender differences in brain volume and account for behavioral gender differences.

Explore related subjects

Cerebral CortexFemaleHumansImaging, Three-DimensionalMaleSex CharacteristicsSex FactorsComparative StudyJournal ArticleResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, P.H.S.

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Eileen Luders, Katherine L Narr, Paul M Thompson, David E Rex, Lutz Jancke, Helmuth Steinmetz, Arthur W Toga. 2004. Gender differences in cortical complexity.. https://doi.org/10.1038/nn1277

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2026

Histone H3K9 methyltransferases regulate cortical growth by coordinating heterochromatin formation and neural progenitor dynamics.

DNA packaging into heterochromatin is a fundamental mechanism of transcriptional silencing, yet its role in regulating neural progenitor behavior during brain development remains poorly understood. Trimethylation of histone H3 lysine 9 (H3K9me3), catalyzed by the methyltransferases SETDB1, SUV39H1, and SUV39H2, is a defining feature of heterochromatin, but functional redundancy among these enzymes has obscured their developmental roles. Here, we generated a cortex-specific triple knockout mouse model lacking Setdb1, Suv39h1, and Suv39h2 to directly interrogate H3K9me3 function during corticogenesis. Combined loss of H3K9 methyltransferases caused genome-wide depletion of H3K9me3, disruption of neural progenitor cell-cycle progression, and impaired cortical neurogenesis, resulting in microcephaly. H3K9 methyltransferases preserve neural progenitor identity and function by silencing clustered protocadherins, meiosis-associated genes, and a cell-cycle restraint program through H3K9me3 deposition. Loss of H3K9me3 promoted local chromatin opening and increased transcription factor occupancy, enabling transposable elements to acquire cryptic enhancer activity and modulate proximal gene expression. Together, these findings establish H3K9me3 heterochromatin as an active regulator of neural progenitor dynamics and lineage fidelity, revealing a central epigenetic mechanism that restricts aberrant transcriptional programs to ensure cortical growth.

Cerebral Cortex↗
PubMed2005

Motor training as treatment in focal hand dystonia.

Focal hand dystonia may arise as a result of aberrant plasticity from excessive repetitive use. Improvement might be possible with appropriate motor training. Focusing on trying to decrease abnormal overflow of movement to fingers not involved in a task, we developed a motor training program for individualized finger movements. Ten patients with writer's cramp participated in the motor training program. Evaluation was done with the Fahn dystonia scale, kinematic analysis of handwriting, transcranial magnetic stimulation (TMS), and electroencephalography (EEG). Clinical improvement of dystonia was significant using the Fahn dystonia scale, and 6 patients reported an improvement in writing. The handwriting analysis showed a trend for improvement after training in simple exercises. There were no changes in cortical excitability measured by TMS and EEG. Whereas this method of motor training for 4 weeks led to mild subjective improvement and some improvement in handwriting, it is not sufficient to reverse motor cortex abnormalities measured by TMS and EEG.

Cerebral Cortex↗
PubMed2004

Differential localization of hamartin and tuberin and increased S6 phosphorylation in a tuber.

In a tuberous sclerosis patient with a mutation in the TSC1 tumor suppressor gene, no second-hit mutation was found in a resected cortical tuber. Tuber giant cells showed predominantly nuclear hamartin, cytosolic tuberin, and hyperphosphorylation of S6. Differential accumulation of hamartin and tuberin in separate cellular compartments of giant cells may prevent formation of the hamartin-tuberin complex, resulting in increased S6 phosphorylation. These data provide an alternative mechanism for tuberogenesis.

Cerebral Cortex↗