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Sökning: LAR1:ki > (2000-2004) > Övrigt vetenskapligt/konstnärligt

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  • Aaberg, E, et al. (författare)
  • The role of neurogenesis in alcoholism
  • 2003
  • Ingår i: NORDIC JOURNAL OF PSYCHIATRY. - 0803-9488. ; 57:2, s. 94-94
  • Konferensbidrag (övrigt vetenskapligt/konstnärligt)
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  • Aarsland, D, et al. (författare)
  • Depression in Parkinson's disease
  • 2002
  • Ingår i: Acta psychiatrica Scandinavica. - 0001-690X. ; 106:3, s. 161-162
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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  • Aarum, Johan (författare)
  • Interactions between mouse CNS cells : microglia and neural precursor cells
  • 2004
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • The mammalian central nervous system (CNS) contains a variety of cells, all specialized to perform different functions. Most numerous are the three types of glia cells, whose basic role is to support the signaling units of the CNS, the neurons. The perspective of this thesis is from the glia cells; particularly the microglia cells, a non-neural population of cells that are spread throughout the CNS. In the healthy CNS these cells are resting, but as a consequence of various CNS disturbances they rapidly become activated, frequently together with astrocytes, the second type of glia cells (oligodendrocytes being the third). This can happen slowly, as in neurodegenerative diseases, or quickly as in acute CNS lesions such as stroke. Both processes involve microglia cells, and sometimes macrophages from the circulation. These latter cells are difficult to distinguish from the microglia cells. In an effort to generate microglia specific markers we used phage display technology to select microglia specific peptides from a random peptide library displayed on the phage surface. Two sets of selection strategies were compared with regard to phage-clone enrichment. The first strategy was based on phage binding to monolayers of primary microglia fixed to a solid surface, while the second strategy was based on fluorescence activated cell sorting (FACS) of microglia cells with bound phages. The latter protocol was found to be superior. Five phage-clones that preferentially bound to microglia cells were isolated. One of the selected clones was shown to be microglia specific by free peptide inhibition and selective in binding to microglia cells, as compared to blood-derived monocytes. Much of our current knowledge in neurobiology derives from studies of cells in culture, a less complex substitute for in vivo studies. As a bridge between monolayer CNS cell cultures and in vivo animal models we set up a three-dimensional culture system, so called aggregate cultures from mouse CNS cells. These aggregates were characterized in detail regarding cellular composition and dynamics, as well as the expression of several neuropeptides and neurotransmitters. All the principle brain cells were present in the aggregates and their numbers changed over time, neurons being the most numerous. The cells appeared to mature as judged by their morphology and, in the case of neurons, the increased expression of synapse specific proteins. Among the investigated neuropeptides, enkephalin and dynorphin were the most abundant followed by galanin, approximating their expression in CNS development. We also found that neural precursor cells, capable of self-renewal and differentiation into neurons, astrocytes and oligodendrocytes, were maintained in the aggregates, even after more than two months of culturing. Treating the aggregates with EGF led to the formation of an outer layer of nestin-positive precursor cells. Using the aggregate culture in part, we found that factor(s) secreted from microglia cells attracts neural precursor cells in a chemotactic manner. This finding may explain the preferred migration of precursor cells to sites of CNS injury. Furthermore, microglia derived factors could affect the differentiation of neural precursor cells, such that more neurons were formed. Together these results suggest important functions of microglia cells in CNS development and pathology. It is reasonable to believe that the migration of neural precursor cells is directed both by attractant and repellant cues. Reactive astrocytes are well known to inhibit growing axons and recently also suggested to inhibit the migration of neural precursor cells. We show that astrocytes in culture repel neural precursor cells and that this effect is mediated by secreted Slit proteins. This conclusion is based on several observations; astrocytes produce Slit and the astrocyte-repellant effect was blocked by the ectodomain of the Slit receptor, and finally, recombinant Slit could substitute for astrocyte derived Slit. Knowledge about the interplay between attractive and repulsive cues may be important for the manipulation of neural precursor cells for medical purposes.
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9.
  • Aase, Karin (författare)
  • On vascular endothelial growth factor B and platelet-derived growth factor C : two members of the VEGF/PDGF family of growth factors
  • 2001
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • Vascular endothelial growth factors (VEGFs), platelet-derived growth factors (PDGFs) and their receptors are important for normal development. They have also been implicated in many pathological conditions. VEGFs have been shown to play an important role in the development of both blood and lymphatic vessels. PDGFs on the other hand, are important regulators of the connective tissue cells of both the vascular network and other organs systems. The focus of the work presented in this thesis has been to elucidate the role of two members of the VEGF/PDGF family of growth factors, namely VEGF-B and PDGF-C. Embryonic analysis at the mRNA and protein level showed that VEGF-B was expressed in several organs, with highest expression in the developing muscles. VEGF-B was not detected in endothelial cells, where its receptor VEGFR-1 is expressed, which suggested that VEGF-B acts in a paracrine way. The expression of the two isoforms, VEGF-B167 and VEGF-B186 were investigated using techniques that can distinguish the two isoforms. The results showed that the VEGF-B167 isoform is predominantly expressed in most tissues. The VEGF-B186 isoform is expressed at lower levels and only in a limited numbers of organs. Moreover, the VEGF-B186 isoform is upregulated in mouse and human tumour cell lines and primary tumours compared with their corresponding normal tissues. These data suggest a fine genetic control of the expression of the two isoforms of VEGF-B, implying tissue- and cell-specific roles for the two VEGF-B isoforms. To elucidate the function in vivo, a VEGF-B knockout mouse strain was generated. The results showed that VEGF-B is not required for normal development of the cardiovascular system or for angiogenesis in adults. However, adult VEGF-B deficient mice have an atrial conduction abnormality characterised by a prolonged PQ interval in the electrocardiogram; thus VEGF-B appears to be required for normal heart function in adult animals. The second growth factor, PDGF-C contains a domain structure not present in other members of the VEGF/PDGF family. Following the signal sequence, PDGF-C contains an N-terminal CUB-domain and, in the C-terminus, the VEGF/PDGF homology domain. PDGF-C is synthesised as an inactive precursor protein that has to be proteolytically processed in the N-terminus before it can bind and activate its receptor, PDGFR-a. Expression analysis during mouse development suggests that PDGF-C acts in both paracrine and autocrine ways.
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10.
  • Abbas Ahmed M Gadeh EL Dum, Nagat (författare)
  • Immunomodulation of cytokine and chemokine production in animal models of neuroinflammatory and neurodegenerative disorders
  • 2003
  • Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
    • Experimental autoimmune neuritis (EAN) is a CD4+ T cell-mediated autoimmune disease of the peripheral nervous system (PNS) that can be actively induced in susceptible animal species and strains by active immunization with heterogeneous peripheral nerve myelin or its component P2 or PO proteins or their peptides emulsified in Freund's complete adjuvant. EAN represents an animal model for studying the immunopathogenesis and therapy of Guillain-Barré syndrome (GBS ) which is a major inflammatory demyelinating disease of the PNS in humans. The close clinical, histopathological, and electrophysiological similarities between EAN and GBS make EAN an especially suitable model, capable of offering insights into the pathophysiology of GBS. EAN is also considered to represent a general model for studying CD4+-mediated autoimmune diseases. Alzheimer's disease (AD) is a progressive neurodegenerative disorder and the most common cause of dementia in the Western world. It is characterised neuropathologically by the deposition of extracellular amyeloid plaques containing aggregates of the amyloid protein beta (A-beta) peptide, as well as by intracellular aggregation of neurofibrillary tangles and selective neuronal loss accompanied by cerebrovascular amyloidosis. The mechanism of AD has not been completely defined. The inflammatory cytokines have been implicated as mediators in response to brain injury in AD. A-beta precursor protein APP transgenic mice (Tg2576) are one of the most widely used animal model for A-beta plaques in cortical regions of the brain, which over-expresses human APP with the Swedish double mutation. Peak numbers of macrophage inflammatory protein (MIP)- 1 alpha-positive cells in the sciatic nerve were seen on day 14 post-immunization (p.i.), which coincided with the development of severe clinical signs. Administration of an anti-MIP-1 alpha antibody suppressed clinical signs of EAN and inhibited inflammation and demyelination in the sciatic nerve. Peak numbers of monocyte chemotactic protein (MCP)-1-positive cells in the sciatic nerve were detected on day 7 p.i. (i.e., tile onset of clinical EAN). Administration of an anti-MCP-1 antibody caused a delay of onset of EAR The numbers of MIP-2-positive cells reached a maximum on day 21 p.i. Anti-MIP-2 antibody failed to suppress clinical signs of EAN and inflammation and demyelination in the sciatic nerve. EAN was strongly suppressed by Rolipram administered twice daily intraperitoneally from day 9 p.i., after onset of clinical EAN, to day 18 p.i., over 10 days. This clinical effect was associated with dose-dependent downregulation of interferon (IFN)-gamma and the chemokines MIP-1alpha, MIP-2 and MCP-1 as well as up-regulated interleukin (IL)-4 production in sciatic nerve sections from Rolipram-treated EAN rats at the maximum of clinical EAN, i.e., on day 14 p.i. These findings suggest that Rolipram could be useful in certain T cell-dependent autoimmune diseases and inflammatory neuropathies. ABR-215062, which is a new synthetic immunomodulatory compound derived from Linomide, administered daily subcutaneously from the day of inoculation strongly suppressed EAN in a dose-dependent manner. ABR215062 reduced the incidence of EAN, ameliorated clinical signs, and inhibited PO peptide 180-199-specific T and B cell responses and also decreased inflammation and demyelination in the peripheral nerves. The suppression of clinical EAN is associated with inhibition of the inflammatory cytokines IFN-gamma and tumor necrosis factor-alpha as well as the enhancement of the anti-inflammatory cytokine IL-4 in peripheral nerve tissues. The suppressive effects of ABR-215062 on EAN are quite similar to those of Linomide on EAN. These findings suggest that ABR-215062 could be useful in certain T cell-mediated autoimmune diseases. To elucidate the mechanisms involved in A-beta-mediated inflammation, we used immunocytochemistry and in situ hybridization to study the potential role of the cytokines interferon-gamma (IFN-gamma), interleukin (IL)-12 and IL-4 in transgenic mice Tg2576. Cytokine and cytokine mRNA expression was detected in brain sections from cortical regions at various postnatal ages ranging from 3 to 19 months. High levels of IFN-gamma and IL-12 mRNA expression, as well as their protein production appeared early at 9 months and peaked at 17-19 months in Tg2576 mice. Significantly increased transcripts of IFN-gamma and IL-12 genes were found in the reactive microglia. and astrocytes surrounding AP deposits. Both findings indicate a role for the pro-inflammatory cytokines IFN-gamma and IL-12 in early disease development and are consistent with microglial activation related to AP formation. In contrast, transcription and production of IL-4 in brain sections was almost undetectable in transgenic mice up to post-natal ages of 17-19 months. These results suggest a major pro-inflammatory role for IL-12 and IFN- gamma in Tg2576 transgenic mice that may provide the association between AP plaque formation, microglial and astrocyte activation in these animals. These observations call for further studies on the potential role of anti-inflammatory therapeutic strategies for AD.
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