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Continuum mechanics-based computational modeling provides insights into the interplay between cell proliferation in different zones of the developing human brain and the evolving cortical folding patterns.

Variation in type XI collagen alters estrogen-dependent signaling in the extracellular matrix and is identified as a genetic risk factor for adolescent idiopathic scoliosis, a common childhood deformity.

The RNA helicase DDX3X controls neural progenitor division, cell fate, and translation during embryonic brain development.

Brain ventricular astrogliosis and neuroinflammation precede scoliosis onset in the zebrafish rpgrip1l ciliary mutant and anti-inflammatory treatment drastically reduces scoliosis while correcting urotensin related peptide level is ineffective.

Loss of functional dystroglycan disrupts the formation and function of CCK⁺/CB₁R⁺ inhibitory synapses in hippocampal CA1, resulting in reduced seizure thresholds in mouse models of dystroglycanopathy.

The brain and olfactory epithelium play a key role in pattering chondrogenic areas in the developing face, which is partly based on the release of SHH from neurosensory structures into the facial mesenchyme.

Genetic finding of pathogenic CRMP1 variants in three unrelated individuals with neurodevelopmental disorder, supported by structural simulation, biochemical and proof-of-principle data highlights the key role of CRMP1 in the development and functioning of the nervous system in humans.

FGF signaling is crucial for gyrus formation, proliferation of outer radial glial cells and expansion of upper layers of the cerebral cortex in gyrencephalic mammals.

Ts65dn mice exhibit structural, functional, molecular, and genetic alterations that are modulated but unrecovered by prenatal chronic GTE-EGCG, highlighting the importance of holistic studies to understand complex disorders and treatments.