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See detailNeuroimaging of REM sleep and dreaming
Dang-Vu, Thien Thanh; Schabus, Manuel; Desseilles, Martin ULg et al

in Stickgold, Robert; Walkerld, Matthew (Eds.) The Neuroscience of Sleep (2009)

Detailed reference viewed: 10 (2 ULg)
See detailNeuroimaging of REM sleep and dreaming
Dang Vu, Thien Thanh ULg; Schabus, Manuel; Desseilles, Martin ULg et al

in McNamara, Patrick; Barrett, Deirdre (Eds.) The New Science of Dreaming (2007)

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See detailNeuroimaging of the interaction between circadian and homeostatic processes
Vandewalle, Gilles ULg; Schmidt, Christina ULg

in Neuroimaging of Sleep and Sleep Disorders (2013)

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See detailNeuroimaging techniques
Dang-Vu, Thien Thanh; Maquet, Pierre ULg; Desseilles, Martin ULg

in Thomas, R.; Chokroverty, S. (Eds.) Atlas of Sleep Medicine, Edition 2 (2013)

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See detailNeuroimaging the effects of light on non-visual brain functions
Vandewalle, Gilles ULg; Dijk, Derk-Jan

in Neuroimaging of Sleep and Sleep Disorders (2013)

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See detailNeuroimaging tools to rate regional atrophy, subcortical cerebrovascular disease, and regional cerebral blood flow and metabolism: consensus paper of the EADC
Frisoni, G. B.; Scheltens, P. H.; Galluzzi, S. et al

in Journal of Neurology, Neurosurgery & Psychiatry (2003), 74(10), 1371-1381

Neuroimaging is a mainstay in the differential diagnosis of patients with cognitive impairment. The often equivocal clinical pictures, the prognostic uncertainty of the earliest stages of mild cognitive ... [more ▼]

Neuroimaging is a mainstay in the differential diagnosis of patients with cognitive impairment. The often equivocal clinical pictures, the prognostic uncertainty of the earliest stages of mild cognitive impairment, and the subtle brain changes mean that neuroimaging techniques are of potentially great incremental diagnostic value. A number of methods, ranging from very simple subjective visual ratings to highly sophisticated computerised tools, have been developed, which allow rating of structural and functional brain changes. The choice of the method is not obvious, and current guidelines provide no indications on which tools should be preferred. In this paper, we give indications for tools with demonstrated accuracy for detecting regional atrophy, cerebrovascular disease, and regional brain function, and discuss these according to increasing technological complexity, ranging from those with high feasibility that can be used at the patient's bedside to highly technological ones that require trained personnel and specific hardware and software. [less ▲]

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See detailNeuroimaging, cognition, light and circadian rhythms
Gaggioni, Giulia ULg; Maquet, Pierre ULg; Schmidt, Christina ULg et al

in Frontiers in Systems Neuroscience [=FNSYS] (2014)

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See detailNeuroimmune connections in jejunal and ileal Peyer's patches at various bovine ages: potential sites for prion neuroinvasion
Defaweux, Valérie ULg; Dorban, Gauthier ULg; Antoine, Nadine ULg et al

in Cell & Tissue Research (2007), 329(1), 35-44

During preclinical stages of cattle orally infected with bovine spongiform encephalopathy (BSE), the responsible agent is confined to ileal Peyer's patches (IPP), namely in nerve fibers and in lymph ... [more ▼]

During preclinical stages of cattle orally infected with bovine spongiform encephalopathy (BSE), the responsible agent is confined to ileal Peyer's patches (IPP), namely in nerve fibers and in lymph follicles, before reaching the peripheral and central nervous systems. No infectivity has been reported in other bovine lymphoid organs, including jejunal Peyer's patches (JPP). To determine the potential sites for prion neuroinvasion in IPP, we analyzed the mucosal innervation and the interface between nerve fibers and follicular dendritic cells (FDC), two dramatic influences on neuroinvasion. Bovine IPP were studied at three ages, viz., newborn calves, calves less than 12 months old, and bovines older than 24 months, and the parameters obtained were compared with those of JPP. No differences in innervation patterns between IPP and JPP were found. The major difference observed was that, in calves of less than 12 months, IPP were the major mucosal-associated lymphoid organ that possessed a large number of follicles with extended FDC networks. Using a panel of antibodies, we showed that PP in 24-month-old bovines were highly innervated at various strategic sites assumed to be involved in the invasion and replication of the BSE pathogen: the suprafollicular dome, T cell area, and germinal centers. In PP in calves of less than 12 months old, no nerve fibers positive for the neurofilament markers NF-L (70 kDa) and NF-H (200 kDa) were observed in contact with FDC. Thus, in view of the proportion of these protein subunits present in neurofilaments, the innervation of the germinal centers can be said to be an age-dependent dynamic process. This variation in innervation might influence the path of neuroinvasion and, thus, the susceptibility of bovines to the BSE agent. [less ▲]

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See detailNeuroimmune connections in ovine pharyngeal tonsil: potential site for prion neuroinvasion
Toppets, Vinciane ULg; Piret, Joëlle ULg; Kirschvink, Nathalie et al

in Cell & Tissue Research (2012)

Recent studies have proved the possible implication of nasal associated lymphoid tissues, mainly the pharyngeal tonsil, in prion pathogenesis. However, the mechanisms of this neuroinvasion are still being ... [more ▼]

Recent studies have proved the possible implication of nasal associated lymphoid tissues, mainly the pharyngeal tonsil, in prion pathogenesis. However, the mechanisms of this neuroinvasion are still being debated. To determine the potential sites for prion neuroinvasion inside the ovine pharyngeal tonsil, the topography of neurofilaments heavy (200 kDa) (NFH), neurofilaments light (70 kDa) (NFL) and glial fibrillar acidic protein (GFAP) was semi-quantitatively analysed inside the different compartments of the tonsil. The results showed that the most innervated areas were the interfollicular area and the connective tissue located beneath the respiratory epithelium. Even if the germinal centre of the lymphoid follicles was poorly innervated, the existence of rare follicular dendritic cell-nerve synapses inside the germinal centre indicates that this mechanism of neuroinvasion is possible but unlikely to be unique. The host PRNP genotype did not influence the pattern of innervation in these different tonsil compartments, unlike age: an increase of nerve endings in a zone of high trafficking cells beneath the respiratory epithelium occurred with ageing. A minimal age-related increase of innervation inside the lymphoid follicles was also observed. An increase in nerve fibre density around the lymphoid follicles, in an area rich in mobile cells able to transport PrPd, could ensure a more efficient infectivity, not in the early phase but in the advanced phase of lymphoinvasion after amplification of PrPd, or could act as direct site of entry during neuroinvasion. [less ▲]

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See detailNeuroimmunomodulation in Health and Disease
Geenen, Vincent ULg

Book published by Wiley Company (2015)

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See detailLa neuroinvasion dans les maladies à prions: étude de l'interface neuroimmune FDC - système nerveux sympathique
Demonceau, Caroline ULg

Doctoral thesis (2013)

Prion diseases are neurodegenerative diseases affecting the central nervous system (CNS) wherein the PrPd disease-associated prion infectious agent is an abnormal isoform of PrPc host-encoded cellular ... [more ▼]

Prion diseases are neurodegenerative diseases affecting the central nervous system (CNS) wherein the PrPd disease-associated prion infectious agent is an abnormal isoform of PrPc host-encoded cellular prion protein. The process through which the prion infectious agent is transferred to the CNS, the neuroinvasion, is still unknown, but secondary lymphoid organs seem to play an important role in prion amplification prior the invasion of the associated peripheral nervous system (PNS). In particular, modifications of follicular dendritic cells (FDC) and sympathetic nervous system (SNS) of lymphoid organs could influence the speed of neuroinvasion, and thus the length of the disease incubation period. It was shown that the lack of mature FDC prevents the replication of the infectious agent in secondary lymphoid organs. Likewise, sympathectomy delays the onset of the disease, and enhances sympathetic innervation reduces the incubation period. In mice, the relative positioning of FDC and sympathetic neural fibres plays a role in the incubation period following scrapie inoculation. This study thus focuses on the neuroimmune interface between FDC and sympathetic neural fibres. First, the number of close interactions between FDC and sympathetic neural fibres of five mouse strains with the same Prnpa genotype was estimated to check if it could explain the different incubation period observed after inoculation of primary bovine spongiform encephalopathy (BSE) infected-brain. Then we checked if scrapie infection, by oral or intraperitoneal route, could influence this neuroimmune interface between FDC and sympathetic neural fibres within Peyer’s patches (PP) and spleen of the C57BL/6 mouse strain. In the first part of this work, co-localizations between FDC and sympathetic neural fibres were observed in vivo within germinal centers (GC) of mouse spleen. Among the five mouse strains exhibiting the same Prnpa genotype, three strains (RIII-1, RIII-2 and 129/Ola) showed an incubation period about 100 days shorter than those of C57BL and C57BL/6 mouse strains when inoculated with primary BSE. Moreover, amplification by FDC seems an obligatory process before subsequent neuroinvasion as an intracerebral inoculation doesn’t reduce the incubation period observed with an intraperitoneal inoculation. A meticulous analysis revealed that the density of close interactions between FDC and sympathetic neural fibres is not higher for the three mouse strains with a shorter incubation period. However, these three mouse strains with a shorter incubation period after primary BSE inoculation have a higher proportion of FDC networks with close interactions than the mouse strains with a longer incubation period. These results suggest that it is not the quantity of sympathetic neural fibres close to FDC, but rather the percentage of FDC with close sympathetic neural endings that could influence the incubation period of prions diseases. In the second part of this work, it came out that prion infection did not result in neuronal loss within the PNS like observed in the CNS, and also did not modify the FDC-SNS neuroimmune interface of secondary lymphoid organs where PrPd deposits are observed within germinal centers. For a single mouse strain orally infected with scrapie, neither FDC networks hypertrophy nor sympathetic neural fibres closer than 10 μm from a FDC network were observed within GC of PP. Moreover, in our conditions, the prion strain did not seem to alter the neuroimmune interface between FDC and SNS in PP that could explain the different incubation periods observed with the 139A and ME7 scrapie strains. To check if prion infection does not modify the FDC-SNS neuroimmune interface, close interactions between FDC and sympathetic neural fibres already shown in the spleen were analyzed in the same mouse strain intraperitoneally infected with the 139A scrapie strain. In that case as well, no differences were observed in FDC network hypertrophy, in the in vivo density of sympathetic neural fibres closer than 10 μm from a FDC network, or in the proportion of well innervated FDC networks, compared to control mice. An in vitro model of coculture of splenic FDC from the same C57BL/6 mouse strain with nerve cells from dorsal root ganglia (DRG) also yielded similar results. FDC isolated from scrapie 139A infected mice exhibited the same neuritogenic or neurotrophic effects than FDC isolated from control mice. During these experiments, it was also noted that young-adult or middle-age mice showed both the same mean density of close interactions between FDC and SNS. However, with age, even if the splenic volume occupied by FDC networks halved, the proportion of FDC networks with close interactions almost doubled. It would be very interesting to check this last parameter in old mice that show some delay in neuroinvasion of prion disease but also to evaluate if this percentage of well innervated FDC network contributes to the prion pathogenesis within the spleen. In conclusion, scrapie 139A and ME7 strains don’t modify FDC-SNS neuroimmune interface of secondary lymphoid organs, not allowing explaining the different incubation period observed with equivalent infectious doses. Moreover, following an oral inoculation of prion, neuroinvasion within PP would not involve direct contact between FDC and sympathetic nerves, but rather another process still to be determined or implying other nerve fibres and/or mobile cells such as macrophages or dendritic cells. However, in the spleen, the percentage of FDC networks with close sympathetic neural fibres – rather than the number of sympathetic neural fibres close to the FDC network – observed for a given age, species and Prnp genotype at the time of inoculation could play a role in the different incubation periods observed for the same prion strain. The cellular compounds involved in the specific FDC microenvironment still have to be determined for each cell implied in the neuroinvasion process. [less ▲]

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See detailNeurokinin-1 receptor antagonists in the prevention of postoperative nausea and vomiting
Diemunsch, P.; Joshi, G. P.; Brichant, Jean-François ULg

in British Journal of Anaesthesia (2009), 103(1), 7-13

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See detailNeuroleptiques à longue durée d'action. III. Etude pilote du penfluridol (R16341)
Bobon, Jean; Mélon, Jean; Mormont, Christian ULg et al

in Acta Psychiatrica Belgica (1970), 70

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See detailNeuroleptiques à longue durée d'action: III. Etude pilote du penfluridol (R16341) : données psychométriques
Mormont, Christian ULg

in Acta Psychiatrica Belgica (1972), 72(5), 595-601

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See detailNeurological aspects of developmental oro-linguo-facial disorders
Misson, Jean-Paul ULg; Evrard, Philippe

Conference (1984)

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See detailNeurological complications of acute and persistent Epstein-Barr virus infection in paediatric patients
Häusler, M.; Ramaekers, Vincent ULg; Doenges, M. et al

in Journal of Medical Virology (2002), 68(2), 253-263

Neurological complications of Epstein-Barr virus (EBV) have been reported almost exclusively in the course of acute primary infections. The role of EBV in paediatric neurological disease was investigated ... [more ▼]

Neurological complications of Epstein-Barr virus (EBV) have been reported almost exclusively in the course of acute primary infections. The role of EBV in paediatric neurological disease was investigated prospectively over a 2-year period, searching for acute primary, chronic, and reactivated EBV infections. Active EBV infections were diagnosed in 10/48 patients, including two with acute primary EBV infections (cranial neuritis and cerebellitis), one with chronic active infection (T/NK cell lymphoma with cranial neuritis), and seven with reactivated infections. Among these seven patients, three showed "Alice in Wonderland" syndrome, one facial nerve palsy, one progressive macrocephaly, and two prolonged encephalitic illness. The prognosis was good except for the patient with lethal T/NK cell lymphoma and the two girls with encephalitic illness. Despite steroid treatment, these girls suffered prolonged cognitive impairment and epileptic seizures. Both developed left-sided hippocampal atrophy, and one of them hippocampal sclerosis. Like primary infections, reactivated EBV infections cause neurological complications in a considerable number of paediatric patients, lead to serious long-term complications, and may contribute to the pathogenesis of hippocampal lesions. © 2002 Wiley-Liss, Inc. [less ▲]

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See detailNeurological picture. Extreme unilateral widening of Virchow-Robin spaces
Fumal, Arnaud ULg; Maertens De Noordhout, Alain ULg; Collignon, Laurent

in Journal of Neurology, Neurosurgery & Psychiatry (2009), 80(1), 64-65

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See detailNeurologie des équidés
Amory, Hélène ULg

Learning material (2011)

Detailed reference viewed: 34 (3 ULg)
See detailNeurology.
Schoenen, Jean ULg; Jansen, An

in Acta neurologica Belgica (2010), 110(4), -

Detailed reference viewed: 18 (6 ULg)