Human Central Nervous System (human + central_nervous_system)

Distribution by Scientific Domains


Selected Abstracts


TROSPIUM CHLORIDE IS UNDETECTABLE IN THE OLDER HUMAN CENTRAL NERVOUS SYSTEM

JOURNAL OF AMERICAN GERIATRICS SOCIETY, Issue 8 2010
David Staskin MD
No abstract is available for this article. [source]


The Immunohistochemical Characterization of Human Fetal Olfactory Bulb and Olfactory Ensheathing Cells in Culture as a Source for Clinical CNS Restoration

THE ANATOMICAL RECORD : ADVANCES IN INTEGRATIVE ANATOMY AND EVOLUTIONARY BIOLOGY, Issue 3 2010
Kai Liu
Abstract Clinical studies have expanded the therapeutic olfactory ensheathing cells (OECs) transplantation to different human Central Nervous System (CNS) diseases. In fact, the OEC transplantation in clinic is a mixture of olfactory bulb cells; they even have not demonstrated that they have such a subpopulation yet. However, as a source of OECs transplantation, the development and identification of human fetal OECs are still need more understanding, because some surgery try to restoration CNS injury with a more purity of OEC cultures generated by a number of different procedures. In this article, twelve human fetal olfactory bulb (OB) samples were obtained from six fetuses in 20 weeks of gestation, it was studied by immunofluorescence on histological sections and cultured cells with multiple antibodies under confocal microscopy. The P75NTR positive OB-OECs (olfactory ensheathing cell from the olfactory bulb) were present in both outer olfactory nerve layers and glomerular layer. The percentage of OB cells in culture, about 22.31 was P75NTR positive, 45.77 was S100,, and 31.92 was GFAP. P75NTR and GFAP were coexpressed with S100,, respectively; however, P75NTR was not coexpressed with GFAP in human fetal OECs. It is suggested that the localization and development of human OECs in OB are different to those in rodent, and the P75NTR immunohistological staining is still necessary to identify and characterize human fetal OECs in culture before transplantation. Anat Rec, 2010. © 2009 Wiley-Liss, Inc. [source]


Neural precursor cells from a fatal human motoneuron disease differentiate despite aberrant gene expression

DEVELOPMENTAL NEUROBIOLOGY, Issue 3 2007
Niklas Pakkasjärvi
Abstract Precursor cells of the human central nervous system can be cultured in vitro to reveal pathogenesis of diseases or developmental disorders. Here, we have studied the biology of neural precursor cells (NPCs) from patients of lethal congenital contracture syndrome (LCCS), a severe motoneuron disease leading to prenatal death before the 32nd gestational week. LCCS fetuses are immobile because of a motoneuron defect, seen as degeneration of the anterior horn and descending tracts of the developing spinal cord. The genetic defect for the syndrome is unknown. We show that NPCs isolated postmortem from LCCS fetuses grow and are maintained in culture, but display increased cell cycle activity. Global transcript analysis of undifferentiated LCCS precursor cells present with changes in EGF-related signaling when compared with healthy age-matched human controls. Further, we show that LCCS-derived NPCs differentiate into cells of neuronal and glial lineage and that the initial differentiation is not accompanied by overt apoptosis. Cells expressing markers Islet-1 and Hb9 are also generated from the LCCS NPCs, suggesting that the pathogenic mechanism of LCCS does not directly affect the differentiation capacity or survival of the cells, but the absence of motoneurons in LCCS may be caused by a noncell autonomous mechanism. © 2007 Wiley Periodicals, Inc. Develop Neurobiol, 2007 [source]


Recent development and potential use of µ- and ,-opioid receptor ligands in positron emission tomography studies

DRUG DEVELOPMENT RESEARCH, Issue 12 2006
Gjermund Henriksen
Abstract Quantitative non-invasive imaging of target structures in the human central nervous system provided by positron emission tomography (PET) permits investigation of the relationship between molecular events and pharmacological effects in living humans. Due to their prominent role in opiate and stimulant drug misuse and dependence, as well as in nociceptive signaling, µ- and ,-opioid receptors are potential targets for advances in neuro(psycho)pharmacological treatment of these illnesses and syndromes. In this review, we describe recent developments in specific positron emitting radiopharmaceuticals for these opioid receptor subclasses. Implications for further advances and clinical applications of the labeled ligands are discussed. Drug Dev. Res. 67:890,904, 2006. © 2007 Wiley-Liss, Inc. [source]


Identification of soluble CD14 as an endogenous agonist for Toll-like receptor 2 on human astrocytes by genome-scale functional screening of glial cell derived proteins

GLIA, Issue 5 2007
Malika Bsibsi
Abstract Human astrocytes express a limited repertoire of Toll-like receptor (TLR) family members including TLR1-4, which are expressed on the cell surface. Also, TLR3 but not TLR4 activation on astrocytes induces expression of several factors involved in neuroprotection and down-regulation of inflammation rather than in the onset of traditional pro-inflammatory reactions. The notion that astrocyte TLR may thus play a role not only in host defense but also in tissue repair responses prompted us to examine the possibility that endogenous TLR agonists could be expressed in the human central nervous system to regulate the apparently dual astrocyte functions during trauma or inflammation. As a potential source of endogenous agonists, a cDNA library derived from several human brain tumor cell lines was used. Gene pools of this library were transfected into COS-7 cells and the expression products were screened for their ability to induce TLR activation in human primary astrocytes. The screening resulted in the identification of soluble CD14. By using a panel of TLR-transfected HEK293 cells, we found that signaling by soluble CD14 was TLR2 dependent. Moreover, the CD14-triggered TLR2-mediated response in astrocytes lead to the production of CXCL8, IL-6, and IL12p40, whereas typical TLR-induced pro-inflammatory cytokines, like TNF-, and IL-1,, were not produced at detectable levels. In conclusion, our data indicate that apart from its well-known ability to act as a co-receptor for TLR-dependent signaling by peptidoglycans or LPS, soluble CD14 can also act as a direct agonist for TLR2. © 2007 Wiley-Liss, Inc. [source]


A Biochemical Comparison of Proteases from Pathogenic Naegleria fowleri and Non-Pathogenic Naegleria gruberi

THE JOURNAL OF EUKARYOTIC MICROBIOLOGY, Issue 5 2007
JESÚS SERRANO-LUNA
ABSTRACT. Naegleria fowleri is the etiologic agent of primary amoebic meningoencephalitis (PAM). Proteases have been suggested to be involved in tissue invasion and destruction during infection. We analyzed and compared the complete protease profiles of total crude extract and conditioned medium of both pathogenic N. fowleri and non-pathogenic Naegleria gruberi trophozoites. Using SDS-PAGE, we found differences in the number and molecular weight of proteolytic bands between the two strains. The proteases showed optimal activity at pH 7.0 and 35 °C for both strains. Inhibition assays showed that the main proteolytic activity in both strains is due to cysteine proteases although serine proteases were also detected. Both N. fowleri and N. gruberi have a variety of different protease activities at different pH levels and temperatures. These proteases may allow the amoebae to acquire nutrients from different sources, including those from the host. Although, the role of the amoebic proteases in the pathogenesis of PAM is not clearly defined, it seems that proteases and other molecules of the parasite as well as those from the host, could be participating in the damage to the human central nervous system. [source]


Viral vectors as tools to model and treat neurodegenerative disorders

THE JOURNAL OF GENE MEDICINE, Issue 5 2005
N. Déglon
Abstract The identification of disease-causing genes in familial forms of neurodegenerative disorders and the development of genetic models closely replicating human central nervous system (CNS) pathologies have drastically changed our understanding of the molecular events leading to neuronal cell death. If these achievements open new opportunities of therapeutic interventions, including gene-based therapies, the presence of the blood-brain barrier and the post-mitotic and poor regenerative nature of the target cells constitute important challenges. Efficient delivery systems taking into account the specificity of the CNS are required to administer potential therapeutic candidates. In addition, genetic models in large animals that replicate the late stages of the diseases are in most cases not available for pre-clinical studies. The present review summarizes the potential of viral vectors as tools to create new genetic models of CNS disorders in various species including primates and the recent progress toward viral gene therapy clinical trials for the administration of therapeutic candidates into the brain. Copyright © 2005 John Wiley & Sons, Ltd. [source]


Protective and detrimental immunity: lessons from stiff person syndrome and multiple sclerosis

ACTA NEUROLOGICA SCANDINAVICA, Issue 2009
T. Holmřy
Background,, The immune system may attack the brain and cause inflammatory disorders like multiple sclerosis (MS). On the other hand, the immune system may protect and support neurons. Methods, There are two obstacles to study this paradox in humans. First, the target antigens in many human central nervous system (CNS) disorders are unknown. Second, it is often difficult to separate pathogenic from protective events, as well as primary from secondary phenomena. Idiopathic stiff person syndrome (SPS) circumvents the first obstacle, because most patients secrete antibodies against glutamic acid decarboxylase (GAD) 65. The immune response against glatiramer acetate (GA) may circumvent the second obstacle. Migration of activated T helper cells to the intrathecal compartment could be a common denominator in GA treatment and SPS. Results, We here discuss recent results on T cells in MS and SPS, showing that GAD65-specific and GA-reactive lymphocytes in the cerebrospinal fluid are not a simple reflection of those in blood. Conclusion, The rules and mechanisms governing T cell selection and maintenance in the CNS may provide a key to the understanding of protective and detrimental aspects of CNS immunity. [source]