Sleep studies often observe differences in slow wave activity (SWA) during non-rapid eye movement sleep between subjects. This study investigates to what extent these absolute differences in SWA can be explained with differences in grey matter volume, white matter volume or the thickness of skull and outer liquor rooms. To do this, we selected the 10-min interval showing maximal SWA of 20 young adult subjects and correlated these values lobe-wise with grey matter, skull and liquor thickness and globally with white matter as well as segments of the corpus callosum. Whereas grey matter, skull thickness and liquor did not correlate significantly with maximal slow wave activity, there were significant correlations with the anterior parts of the corpus callosum and with one other white matter region. In contrast, electroencephalogram power of higher frequencies correlates positively with grey matter volumes and cortical surface area. We discuss the possible role of white matter tracts on the synchronization of slow waves across the cortex.
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http://dx.doi.org/10.1111/j.1365-2869.2011.00916.x | DOI Listing |
Int J Mol Sci
December 2024
Neuroscience Research Institute, Gachon University, Incheon 21565, Republic of Korea.
To elucidate the potential roles of presynaptic and postsynaptic serotonergic activity in impulsivity traits, we investigated the relationship between self-reported impulsiveness and serotonin transporter (5-HTT) and 5-HT2A receptors in healthy individuals. In this study, 26 participants completed 3-Tesla magnetic resonance imaging and positron emission tomography with [C]DASB and [C]MDL100907. To quantify 5-HTT and 5-HT2A receptor availability, the binding potential (BP) of [C]DASB and [C]MDL100907 was derived using the simplified reference tissue model with cerebellar gray matter as the reference region.
View Article and Find Full Text PDFArch Public Health
January 2025
School of Physical Education, Liaoning Normal University, Dalian, 116029, China.
Background: 24-h movement behaviors have a close relationship with children and adolescents' cognition, gray matter volume, and academic performance. This systematic review aims to precisely explore the associations between meeting different combinations of guidelines and the aforementioned indicators, in order to better serve public health policy.
Methods: Computer retrieval was conducted on CNKI, Web of Science, PubMed, SPORT Discus and Cochrane library databases.
Neurobiol Dis
January 2025
Vulnerable Brain Lab, Department of Anatomy and Cell Biology, Schulich School of Medicine and Dentistry, Western University, London, Ontario N6A 5C1, Canada. Electronic address:
Alzheimer's disease (AD) is a progressive neurodegenerative disease that accounts for two-thirds of all dementia cases, and age is the strongest risk factor. In addition to the amyloid hypothesis, lipid dysregulation is now recognized as a core component of AD pathology. Gangliosides are a class of membrane lipids of the glycosphingolipid family and are enriched in the central nervous system (CNS).
View Article and Find Full Text PDFBiomed Phys Eng Express
January 2025
Shandong University of Traditional Chinese Medicine, Qingdao Academy of Chinese Medical Sciences, Jinan, Shandong, 250355, CHINA.
Mild cognitive impairment (MCI) is a significant predictor of the early progression of Alzheimer's disease, and it can be used as an important indicator of disease progression. However, many existing methods focus mainly on the image itself when processing brain imaging data, ignoring other non-imaging data (e.g.
View Article and Find Full Text PDFExp Physiol
January 2025
Department of Physiology, School of Medicine, University College Cork, Cork, Ireland.
Absence of the structural protein, dystrophin, results in the neuromuscular disorder Duchenne Muscular Dystrophy (DMD). In addition to progressive skeletal muscle dysfunction, this multisystemic disorder can also result in cognitive deficits and behavioural changes that are likely to be consequences of dystrophin loss from central neurons and astrocytes. Dystrophin-deficient mdx mice exhibit decreases in grey matter volume in the hippocampus, the brain region that encodes and consolidates memories, and this is exacerbated with ageing.
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