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Alzheimer disease (AD) is mainly manifested as insidious onset, chronic progressive cognitive decline and non-cognitive neuropsychiatric symptoms, which seriously affects the quality of life of the elderly and causes a very large burden on society and families. This paper uses graph theory to analyze the constructed brain network, and extracts the node degree, node efficiency, and node betweenness centrality parameters of the two modal brain networks. The T test method is used to analyze the difference of graph theory parameters between normal people and AD patients, and brain regions with significant differences in graph theory parameters are selected as brain network features. By analyzing the calculation principles of the conventional convolutional layer and the depth separable convolution unit, the computational complexity of them is compared. The depth separable convolution unit decomposes the traditional convolution process into spatial convolution for feature extraction and point convolution for featurmulti-modality and multi-regions layer by layer, and the visual analysis results show that the abnormally changed regions affected by Alzheimer's disease provide important information for clinical quantification.The human brain grows the most dramatically during the perinatal and early post-natal periods, during which pre-term birth or perinatal injury that may alter brain structure and lead to developmental anomalies. Thus, characterizing cortical thickness of developing brains remains an important goal. However, this task is often complicated by inaccurate cortical surface extraction due to small-size brains. Here, we propose a novel complex framework for the reconstruction of neonatal WM and pial surfaces, accounting for large partial volumes due to small-size brains. The proposed approach relies only on T1-weighted images unlike previous T2-weighted image-based approaches while only T1-weighted images are sometimes available under the different clinical/research setting. Deep neural networks are first introduced to the neonatal magnetic resonance imaging (MRI) pipeline to address the mis-segmentation of brain tissues. Furthermore, this pipeline enhances cortical boundary delineation using combined models of the cwas biologically congruent (1.3 mm at 28 weeks of PMA to 1.8 mm at term equivalent). Cortical thickness measured on T1 MRI using NEOCIVET 2.0 was compared with that on T2 using the established dHCP pipeline. It was difficult to conclude that either T1 or T2 imaging is more ideal to construct cortical surfaces. NEOCIVET 2.0 has been open to the public through CBRAIN (https//mcin-cnim.ca/technology/cbrain/), a web-based platform for processing brain imaging data.Although animal studies and studies on Parkinson's disease (PD) suggest that dopamine deficiency slows the pace of the internal clock, which is corrected by dopaminergic medication, timing deficits in parkinsonism remain to be characterized with diverse findings. Here we studied patients with PD and progressive supranuclear palsy (PSP), 3-4 h after drug intake, and normal age-matched subjects. We contrasted perceptual (temporal bisection, duration comparison) and motor timing tasks (time production/reproduction) in supra- and sub-second time domains, and automatic versus cognitive/short-term memory-related tasks. Subjects were allowed to count during supra-second production and reproduction tasks. In the time production task, linearly correlating the produced time with the instructed time showed that the "subjective sense" of 1 s is slightly longer in PD and shorter in PSP than in normals. This was superposed on a prominent trend of underestimation of longer (supra-second) durations, common to all groups, sughe reproduction task suggested involvement of short-term memory in these tasks. Dopamine deficiency didn't correlate significantly with timing performances, suggesting that the slowed clock hypothesis cannot explain the entire results. Timing performance in PD may be determined by complex interactions among time scales on the motor and sensory sides, and by their distortion in memory.
Olfactory dysfunction dramatically impairs quality of life with a prevalence of 20% in the general adult population. Psychophysical olfactory testing has been widely used to evaluate the ability to smell due to its validated utility and feasibility in clinic. This review summarizes the current literature regarding psychophysical olfactory testing and the clinical relevance of the olfactory testing with different components. selleck products Furthermore, the review highlights the diagnosis and treatment value of olfactory subtests in patients with olfactory dysfunction.
With the accumulation of studies of psychophysical olfactory testing in olfactory disorders, the clinical relevance of olfactory testing with different components is expanding. Different olfactory domains present with distinct olfactory processing and cortical activity. Psychophysical assessment of olfaction with three domains reveals different levels of olfactory processing and might assist with analyzing the pathophysiologic mechanism of the various olfactory disorders. Furthermore, olfactory thresholds provided the largest amount of non-redundant information to the olfactory diagnosis. Sinonasal olfactory dysfunction and non-sinonasal-related olfactory dysfunction are emerging classifications of smell disorders with certain characteristics of olfactory impairment and different responses to the therapy including steroids, sinus surgery, and olfactory training.
These recent advancements should promote the understanding of psychophysical olfactory testing, the association between individual subcomponents and neurophysiological processes, and pave the way for precision assessment and treatment of the olfactory dysfunction.
These recent advancements should promote the understanding of psychophysical olfactory testing, the association between individual subcomponents and neurophysiological processes, and pave the way for precision assessment and treatment of the olfactory dysfunction.Nightmares are highly dysphoric dreams that are well-remembered upon awakening. Frequent nightmares have been associated with psychopathology and emotional dysregulation, yet their neural mechanisms remain largely unknown. Our neurocognitive model posits that nightmares reflect dysfunction in a limbic-prefrontal circuit comprising medial prefrontal and anterior cingulate cortices, hippocampus, and amygdala. However, there is a paucity of studies that used brain imaging to directly test the neural correlates of nightmares. One such study compared the regional homogeneity (ReHo) of resting-state functional magnetic resonance imaging blood-oxygen level-dependent signals between frequent nightmare recallers and controls. The main results were greater regional homogeneity in the left anterior cingulate cortex and right inferior parietal lobule for the nightmare recallers than for the controls. In the present study, we aimed to document the ReHo correlates of frequent nightmares using several nightmare severity measures.
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