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Abstract The cortical thickness is a characteristic biomarker for a wide variety of neurological disorders. While the structural organization of the cerebral cortex is tightly regulated and evolutionarily preserved, its thickness varies widely between 1.5 and 4.5 mm across the healthy adult human brain. It remains unclear whether these thickness variations are a cause or consequence of cortical development. Recent studies suggest that cortical thickness variations are primarily a result of genetic effects. Previous studies showed that a simple homogeneous bilayered system with a growing layer on an elastic substrate undergoes a unique symmetry breaking into a spatially heterogeneous system with discrete gyri and sulci. Here, we expand on that work to explore the evolution of cortical thickness variations over time to support our finding that cortical pattern formation and thickness variations can be explained – at least in part – by the physical forces that emerge during cortical folding. Strikingly, as growth progresses, the developing gyri universally thicken and the sulci thin, even in the complete absence of regional information. Using magnetic resonance images, we demonstrate that these naturally emerging thickness variations agree with the cortical folding pattern in n = 9 healthy adult human brains, in n = 564 healthy human brains ages 7–64, and in n = 73 infant brains scanned at birth, and at ages one and two. Additionally, we show that cortical organoids develop similar patterns throughout their growth. Our results suggest that genetic, geometric, and physical events during brain development are closely interrelated. Understanding regional and temporal variations in cortical thickness can provide insight into the evolution and causative factors of neurological disorders, inform the diagnosis of neurological conditions, and assess the efficacy of treatment options. 

Alzheimer's disease (AD) is a neurodegenerative disorder with slow onset, which could result in the deterioration of the duration of persistent neurological dysfunction. How to identify the informative longitudinal phenotypic neuroimaging markers and predict cognitive measures are crucial to recognize AD at early stage. Many existing models related imaging measures to cognitive status using regression models, but they did not take full consideration of the interaction between cognitive scores. In this paper, we propose a robust low-rank structured sparse regression method (RLSR) to address this issue. The proposed model simultaneously selects effective features and learns the underlying structure between cognitive scores by utilizing novel mixed structured sparsity inducing norms and low-rank approximation. In addition, an efficient algorithm is derived to solve the proposed non-smooth objective function with proved convergence. Empirical studies on cognitive data of the ADNI cohort demonstrate the superior performance of the proposed method.

 

This study aimed to quantify the 3D asymmetry of the maxilla in patients with unilateral cleft lip and palate (UCP) and investigate the defect factors responsible for the variability of the maxilla on the cleft side using a deep‐learning‐based CBCT image segmentation protocol.

Cone beam computed tomography (CBCT) images of 60 patients with UCP were acquired. The samples in this study consisted of 39 males and 21 females, with a mean age of 11.52 years (SD = 3.27 years; range of 8‐18 years).

The deep‐learning‐based protocol was used to segment the maxilla and defect initially, followed by manual refinement. Pairedt‐tests were performed to characterize the maxillary asymmetry. A multiple linear regression was carried out to investigate the relationship between the defect parameters and those of the cleft side of the maxilla.

The cleft side of the maxilla demonstrated a significant decrease in maxillary volume and length as well as alveolar length, anterior width, posterior width, anterior height and posterior height. A significant increase in maxillary anterior width was demonstrated on the cleft side of the maxilla. There was a close relationship between the defect parameters and those of the cleft side of the maxilla.

Based on the 3D volumetric segmentations, significant hypoplasia of the maxilla on the cleft side existed in the pyriform aperture and alveolar crest area near the defect. The defect structures appeared to contribute to the variability of the maxilla on the cleft side.