Matter Areas (matter + area)

Distribution by Scientific Domains

Kinds of Matter Areas

  • white matter area


  • Selected Abstracts


    Activation and deactivation of periventricular white matter phagocytes during postnatal mouse development

    GLIA, Issue 1 2010
    Mariya Hristova
    Abstract Brain microglia are related to peripheral macrophages but undergo a highly specific process of regional maturation and differentiation inside the brain. Here, we examined this deactivation and morphological differentiation in cerebral cortex and periventricular subcortical white matter, the main "fountain of microglia" site, during postnatal mouse development, 0,28 days after birth (P0,P28). Only macrophages in subcortical white matter but not cortical microglia exhibited strong expression of typical activation markers alpha5, alpha6, alphaM, alphaX, and beta2 integrin subunits and B7.2 at any postnatal time point studied. White matter phagocyte activation was maximal at P0, decreased linearly over P3 and P7 and disappeared at P10. P7 white matter phagocytes also expressed high levels of IGF1 and MCSF, but not TNFalpha mRNA; this expression disappeared at P14. This process of deactivation followed the presence of ingested phagocytic material but correlated only moderately with ramification, and not with the extent of TUNEL+ death in neighboring cells, their ingestion or microglial proliferation. Intravenous fluosphere labeling revealed postnatal recruitment and transformation of circulating leukocytes into meningeal and perivascular macrophages as well as into ramified cortical microglia, but bypassing the white matter areas. In conclusion, this study describes strong and selective activation of postnatally resident phagocytes in the P0,P7 subcortical white matter, roughly equivalent to mid 3rd trimester human fetal development. This presence of highly active and IGF1- and MCSF-expressing phagocytes in the neighborhood of vulnerable white matter could play an important role in the genesis of or protection against axonal damage in the fetus and premature neonate. © 2009 Wiley-Liss, Inc. [source]


    Heritability of regional and global brain structure at the onset of puberty: A magnetic resonance imaging study in 9-year-old twin pairs

    HUMAN BRAIN MAPPING, Issue 7 2009
    Jiska S. Peper
    Abstract Puberty represents the phase of sexual maturity, signaling the change from childhood into adulthood. During childhood and adolescence, prominent changes take place in the brain. Recently, variation in frontal, temporal, and parietal areas was found to be under varying genetic control between 5 and 19 years of age. However, at the onset of puberty, the extent to which variation in brain structures is influenced by genetic factors (heritability) is not known. Moreover, whether a direct link between human pubertal development and brain structure exists has not been studied. Here, we studied the heritability of brain structures at 9 years of age in 107 monozygotic and dizygotic twin pairs (N = 210 individuals) using volumetric MRI and voxel-based morphometry. Children showing the first signs of secondary sexual characteristics (N = 47 individuals) were compared with children without these signs, based on Tanner-stages. High heritabilities of intracranial, total brain, cerebellum, and gray and white matter volumes (up to 91%) were found. Regionally, the posterior fronto-occipital, corpus callosum, and superior longitudinal fascicles (up to 93%), and the amygdala, superior frontal and middle temporal cortices (up to 83%) were significantly heritable. The onset of secondary sexual characteristics of puberty was associated with decreased frontal and parietal gray matter densities. Thus, in 9-year-old children, global brain volumes, white matter density in fronto-occipital and superior longitudinal fascicles, and gray matter density of (pre-)frontal and temporal areas are highly heritable. Pubertal development may be directly involved in the decreases in gray matter areas that accompany the transition of our brains from childhood into adulthood. Hum Brain Mapp, 2009. © 2009 Wiley-Liss, Inc. [source]


    Water Apparent Diffusion Coefficient and T2 Changes in the Acute Stage of Maple Syrup Urine Disease: Evidence of Intramyelinic and Vasogenic-Interstitial Edema

    JOURNAL OF NEUROIMAGING, Issue 2 2003
    Andrea Righini MD
    ABSTRACT Background. The acute phase of the neonatal classical form of maple syrup urine disease (MSUD) is usually associated with generalized brain edema. Methods and Results. The authors present the case of a newborn infant in the acute stage of the classical form of MSUD in whom a remarkable decrease in the water apparent diffusion coefficient (ADC) in advanced myelinating white matter areas was associated with an increase in the T2 signal. This diffusion magnetic resonance imaging (MRI) pattern appears to be compatible with a rare kind of cytotoxic edema, the so-called intramyelinic edema. At the same time, an increase in the ADC was seen in unmyelinated areas together with an increase in the T2 signal, a sign of a coexistent vasogenic-interstitial edema. Conclusions. ADC measurements in MSUD provide more specific information than conventional MRI about the pathophysiology of white matter changes. [source]


    Altered White Matter Integrity in Adolescent Binge Drinkers

    ALCOHOLISM, Issue 7 2009
    Tim McQueeny
    Background:, White matter integrity has been found to be compromised in adult alcoholics, but it is unclear when in the course of alcohol exposure white matter abnormalities become apparent. This study assessed microstructural white matter integrity among adolescent binge drinkers with no history of an alcohol use disorder. Methods:, We used diffusion tensor imaging to examine fractional anisotropy (FA), a measure of directional coherence of white matter tracts, among teens with (n = 14) and without (n = 14) histories of binge drinking but no history of alcohol use disorder, matched on age, gender, and education. Results:, Binge drinkers had lower FA than controls in 18 white matter areas (clusters ,27 contiguous voxels, each with p < 0.01) throughout the brain, including the corpus callosum, superior longitudinal fasciculus, corona radiata, internal and external capsules, and commissural, limbic, brainstem, and cortical projection fibers, while exhibiting no areas of higher FA. Among binge drinkers, lower FA in 6 of these regions was linked to significantly greater lifetime hangover symptoms and/or higher estimated peak blood alcohol concentrations. Conclusions:, Binge drinking adolescents demonstrated widespread reductions of FA in major white matter pathways. Although preliminary, these results could indicate that infrequent exposure to large doses of alcohol during youth may compromise white matter fiber coherence. [source]


    Glial cytoplasmic inclusions and tissue injury in multiple system atrophy: A quantitative study in white matter (olivopontocerebellar system) and gray matter (nigrostriatal system)

    NEUROPATHOLOGY, Issue 3 2008
    Keisuke Ishizawa
    Glial cytoplasmic inclusions (GCIs) and microglia were quantified in 12 cases of multiple system atrophy (MSA) with special reference to their association with histologically defined lesion severity. The targets of the analysis were white matter (cerebellum, pontine base) and gray matter (putamen, substantia nigra). First, the lesion severity was defined: for white matter, the degree of demyelination and tissue rarefaction were semi-quantified on Klüver-Barrera (KB) sections as grade I (mildly injured), II (moderately injured), and III (severely injured); for gray matter, neurons and astrocytes were counted on KB and glial fibrillary acidic protein-immunostained sections, respectively. Next, the GCI burden was quantified on sections immunostained for ,-synuclein, phosphorylated ,-synuclein, and ubiquitin and the microglial burden was quantified on sections immunostained for HLA-DR. In white matter, the GCI and microglial burdens were the greatest when the tissue injury was mild and/or moderate (grade I and/or grade II), and they became less prominent when the tissue injury became more severe (grade III). In gray matter, in contrast, the GCI and microglial burdens failed to show significant correlations with the lesion severity. Our result suggests that the amount of GCIs as well as that of microglia is reduced when the tissue injury becomes severe in vulnerable white matter areas, but not in vulnerable gray matter areas, of MSA. It also suggests that there seems to be a difference between gray matter and white matter in the way GCIs and microglia participate in the degenerative process of MSA. [source]