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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 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) : 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)

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See detailNeurology.
Schoenen, Jean ULg; Jansen, An

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

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See detailNeuromodulation of chronic headaches: position statement from the European Headache Federation
Martelletti, P; Jensen, R; Antal, A et al

in Journal of Headache & Pain (2013), 14

The medical treatment of patients with chronic primary headache syndromes (chronic migraine, chronic tension-type headache, chronic cluster headache, hemicrania continua) is challenging as serious side ... [more ▼]

The medical treatment of patients with chronic primary headache syndromes (chronic migraine, chronic tension-type headache, chronic cluster headache, hemicrania continua) is challenging as serious side effects frequently complicate the course of medical treatment and some patients may be even medically intractable. When a definitive lack of responsiveness to conservative treatments is ascertained and medication overuse headache is excluded, neuromodulation options can be considered in selected cases.Here, the various invasive and non-invasive approaches, such as hypothalamic deep brain stimulation, occipital nerve stimulation, stimulation of sphenopalatine ganglion, cervical spinal cord stimulation, vagus nerve stimulation, transcranial direct current stimulation, repetitive transcranial magnetic stimulation, and transcutaneous electrical nerve stimulation are extensively published although proper RCT-based evidence is limited. The European Headache Federation herewith provides a consensus statement on the clinical use of neuromodulation in headache, based on theoretical background, clinical data, and side effect of each method. This international consensus further gives recommendations for future studies on these new approaches.In spite of a growing field of stimulation devices in headaches treatment, further controlled studies to validate, strengthen and disseminate the use of neurostimulation are clearly warranted. Consequently, until these data are available any neurostimulation device should only be used in patients with medically intractable syndromes from tertiary headache centers either as part of a valid study or have shown to be effective in such controlled studies with an acceptable side effect profile. [less ▲]

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See detailNeuromorphic reinforcement learning
Dethier, Julie ULg; Ernst, Damien; Sepulchre, Rodolphe

Conference (2012, March 29)

Living organisms are able to successfully perform challeng- ing tasks such as perception, classification, association, and control. In hope for similar successes in artificial systems, neuromorphic ... [more ▼]

Living organisms are able to successfully perform challeng- ing tasks such as perception, classification, association, and control. In hope for similar successes in artificial systems, neuromorphic engineering uses neurophysiological models of perception and information processing in biological sys- tems to emulate their functions but also resemble their struc- ture [1]. In this abstract, we focus on the basal ganglia (BG), brain region in control of primitive functions of the nervous system, and specifically on their involvement in action selec- tion and reinforcement learning (RL). We hypothesize that neuromorphic-inspired systems will greatly benefit the RL community. [less ▲]

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See detailNeuromuscular transmission in migraine patients with prolonged aura
Ambrosini, Anna; MAERTENS DE NOORDHOUT, Alain ULg; SCHOENEN, Jean ULg

in Acta Neurologica Belgica (2001), 101(3), 166-70

P/Q Ca2+ channels are genetically abnormal in most cases of familial hemiplegic migraine (FHM) and may be involved in other types of migraine. They are also found at the neuromuscular junctions, where ... [more ▼]

P/Q Ca2+ channels are genetically abnormal in most cases of familial hemiplegic migraine (FHM) and may be involved in other types of migraine. They are also found at the neuromuscular junctions, where they control stimulation-induced acetylcholine release. Prolonged aura is a very frequent clinical feature in FHM patients. The objective of this study was thus to explore neuromuscular transmission in migraine with typical and prolonged aura patients. We performed single fiber electromyography (SFEMG) in such patients and compared them to a group of healthy volunteers. Results were expressed as mean jitter (MCD) and percentage of single endplate abnormalities. Mean MCD was on average comparable in controls and migraineurs. By contrast, single endplate abnormalities were only found in patients (p < 0.01), especially in those with prolonged aura (p < 0.001). These results suggest subtle impairment of neuromuscular transmission in a subgroup of migraineurs characterized by prolonged aura, which might be due to dysfunctioning P/Q Ca(2+)-channels. [less ▲]

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See detailNeuromuscular transmission in migraine: a single-fiber EMG study in clinical subgroups.
Ambrosini, Anna; Maertens De Noordhout, Alain ULg; Schoenen, Jean ULg

in Neurology (2001), 56(8), 1038-43

OBJECTIVE: To search for impairment of neuromuscular transmission by single-fiber electromyography (SFEMG) in patients with common forms of migraine. BACKGROUND: P/Q Ca(2+) channels are genetically ... [more ▼]

OBJECTIVE: To search for impairment of neuromuscular transmission by single-fiber electromyography (SFEMG) in patients with common forms of migraine. BACKGROUND: P/Q Ca(2+) channels are genetically abnormal in most cases of familial hemiplegic migraine (International Headache Society [IHS] code 1.2.3) and may be involved in other types of migraine. Besides in the brain, these channels are found in motor nerve endings, where they control stimulation-induced acetylcholine release. If they are functionally abnormal, the neuromuscular transmission might be impaired. METHODS: Sixty-two migraineurs (18 without aura, IHS code 1.1; 19 with typical aura, IHS code 1.2.1; 10 with prolonged aura, IHS code 1.2.2; 15 with and without aura) and 16 healthy control subjects underwent stimulation SFEMG. Results were expressed as the mean value of consecutive differences (MCD) and percentage of single-fiber abnormalities (abnormal jitter or impulse blocking). RESULTS: Average MCD was comparable in control subjects and migraineurs (17.1 +/- 2.6 versus 17.5 +/- 4.7 microsec). By contrast, single-fiber abnormalities were found in 17 patients but in none of the control subjects (p = 0.036). Most of these patients had unilateral sensorimotor symptoms and/or aphasia and/or loss of balance during the aura. SFEMG abnormalities were significantly correlated with the occurrence of these clinical features and with a diagnosis of migraine with prolonged aura. CONCLUSIONS: Stimulation SFEMG shows mild abnormalities of neuromuscular transmission in a subgroup of migraineurs with aura, characterized by clinical features frequently found in human P/Q Ca(2+) channelopathies. These abnormalities might thus be due to genetically modified P/Q Ca(2+) channels. [less ▲]

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See detailNeuronal and glial expression of the inducible HSP70 in forebrain ischemia
Xu, D.; Plumier, Jean-Christophe ULg; Robertson, Harold A. et al

Poster (1995)

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See detailNeuronal and psychological underpinnings of pathological gambling
Singer, Bryan F.; Anselme, Patrick ULg; Robinson, Mike J.F. et al

in Frontiers in Behavioral Neuroscience (2014), 8, 230

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See detailNeuronal Control of Astrocytes Proliferation
Rogister, Bernard ULg; Leprince, Pierre ULg; Martin, Didier ULg et al

in Fedoroff, S.; Juurlink, B. H. J.; Doucette, R. (Eds.) Biology and pathology of astrocyte-neuron interactions (1993)

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See detailNeuronal Differentiation in the Adult Brain: Cdk6 as the Molecular Regulator
Caron, Nicolas ULg; Genin, Emmanuelle ULg; Vandenbosch, Renaud ULg et al

in Hayat, Eric (Ed.) TUMORS OF THE CENTRAL NERVOUS SYSTEM (2013)

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See detailNeuronal injury in NCX3 knockout mice following permanent focal cerebral ischemia and in NCX3 knockout cortical neuronal cultures following oxygen-glucose deprivation and glutamate exposure
Cross, J. L.; Meloni, B. P.; Bakker, A. J. et al

in Journal of Experimental Stroke & Translational Medicine (2009), 2(1), 3-9

In this study we subjected NCX3 knockout and wildtype mice to permanent focal cerebral ischemia by intraluminal middle cerebral artery occlusion. Analysis of brain sections by 2,3,5-Triphenyl-2H ... [more ▼]

In this study we subjected NCX3 knockout and wildtype mice to permanent focal cerebral ischemia by intraluminal middle cerebral artery occlusion. Analysis of brain sections by 2,3,5-Triphenyl-2H-tetrazolium chloride staining, 12 hours after middle cerebral artery occlusion revealed no difference in infarct volume between NCX3 knockout and wildtype mice. In addition, we evaluated the effect of NCX3 protein knockdowri on neuronal viability in primary cortical neuronal cultures following in vitro ischemia (oxygen-glucose deprivation) and L-glutamate (glutamate) exposure. In vitro experiments revealed that neuronal viability was higher in NCX3 knockout neuronal cultures than in the wildtype cultures following ischemic and glutamate insults. The reduced sensitivity of neurons from NCX3 knockout mice to in vitro ischemia and excitotoxicity indicates that NCX3 calcium entry mode activity contributes to calcium overload and neuronal death. However our in vivo finding of e lack of differential sensitivity on infarct volume in NCX3 knockout and wildtype mice suggests that any benefit of reduced NCX3 activity is overridden following permanent focal cerebral ischemia. Taken together, these f]ndings suggest that reduced NXC3 activity limits calcium neurotoxicity during severe transient, but not during severe sustained ischemic insults. These results have important implications for the development of the NCX3 protein as a therapeutic target to reduce ischemic brain injury [less ▲]

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