References of "Moonen, Gustave"
     in
Bookmark and Share    
Full Text
Peer Reviewed
See detailCerebral resting state fluctuations predict somatosensory perception
Boly, Mélanie ULg; Balteau, Evelyne ULg; Schnakers, Caroline ULg et al

in Journal of Neurology (2007, May), 254(Suppl. 3), 42

Detailed reference viewed: 22 (9 ULg)
Peer Reviewed
See detailLocked-in syndrome et états de conscience altérée: comment détecter la conscience?
Vanhaudenhuyse, Audrey ULg; Bruno, Marie-Aurélie ULg; Schnakers, Caroline ULg et al

in Pellas, Frederique; Kiefer, C; Weiss, JJ (Eds.) et al Eveil de coma et états limites (2007)

Detailed reference viewed: 10 (4 ULg)
Full Text
Peer Reviewed
See detailEvaluation comportementale et par neuroimagerie fonctionnelle des patients en état végétatif
Vanhaudenhuyse, Audrey ULg; Schnakers, Caroline ULg; Boly, Mélanie ULg et al

in Revue Médicale de Liège (2007), 62 Spec No

Currently, there remains a high rate of misdiagnosis of the vegetative state. This should incite clinicians to use the most sensitive "coma scales" to detect signs of consciousness in these patients. The ... [more ▼]

Currently, there remains a high rate of misdiagnosis of the vegetative state. This should incite clinicians to use the most sensitive "coma scales" to detect signs of consciousness in these patients. The gold standard remains the Glasgow Coma Scale (GCS, Teasdale and Jennet, 1974), with the Glasgow Liege Scale (GLS, Born, 1988) adding standardized assessment of brainstem reflexes. New sensible behavioral assessment tools for use in the acute neurocritical care setting include the Full Outline of UnResponsiveness (FOUR, Wijdicks et al., 2005). The Coma Recovery Scale-Revised (CRS-R, Giacino and Kalmar, 2004) specifically tests the diagnostic criteria differentiating vegetative from minimally conscious patients. Detecting signs of consciousness also depends on the employed methodology. We showed that for the assesment of the presence of visual pursuit, using a moving mirror is better suited than using a moving object or person. The clinical diagnosis can be confirmed by cerebral positron emission tomography studies objectively quantifying residual metabolic activity in vegetative and minimally conscious patients. Ongoing studies evaluate the prognostic value of functional magnetic resonance imaging studies in these challenging patient populations. [less ▲]

Detailed reference viewed: 206 (33 ULg)
Full Text
Peer Reviewed
See detailTherapeutic use of high-frequency repetitive transcranial magnetic stimulation in stroke.
Hotermans, Christophe; Peigneux, Philippe ULg; Moonen, Gustave ULg et al

in Stroke (2007), 38(2), 253254

Detailed reference viewed: 18 (5 ULg)
Full Text
Peer Reviewed
See detailTherapeutic armamentarium in neurology: the birth of a new era
Belachew, Shibeshih ULg; Magis, Delphine ULg; Lievens, Isabelle ULg et al

in Revue Médicale de Liège (2007), 62(5-6), 432-448

The field of neurology was long infamous for a lack of therapeutic options. How many of you have once thought: "Neurologists don't cure the disease, they admire it". But those days have passed into ... [more ▼]

The field of neurology was long infamous for a lack of therapeutic options. How many of you have once thought: "Neurologists don't cure the disease, they admire it". But those days have passed into history, and the field is now vibrant with new treatments and hope even for patients with the worst neurodegenerative diseases. We summarized in the present review the latest major advances in therapeutic principles and practice for some of the most frequent chronic neurological disorders such as headaches, epilepsy, multiple sclerosis, dementias, Parkinson's disease, sleep/wake disturbances and peripheral neuropathies. We cannot cure or prevent, but we can now halt or control symptoms and disease progression to provide physical and psychological relief, and a better quality of life for patients who suffer from these otherwise devastating neurological conditions. [less ▲]

Detailed reference viewed: 198 (16 ULg)
Full Text
Peer Reviewed
See detailStudy of the interaction of antiplasmodial strychnine derivatives with the glycine receptor
Philippe, Geneviève ULg; Nguyen, Laurent ULg; Angenot, Luc ULg et al

in European Journal of Pharmacology (2006), 530(1-2), 15-22

Strychnos icaja Baill. (Loganiaccae) is a liana found in Central Africa known to be an arrow and ordeal poison but also used by traditional medicine to treat malaria. Recently, many dimeric or trimeric ... [more ▼]

Strychnos icaja Baill. (Loganiaccae) is a liana found in Central Africa known to be an arrow and ordeal poison but also used by traditional medicine to treat malaria. Recently, many dimeric or trimeric indolomonoterpenic alkaloids with antiplasmodial properties have been isolated from its rootbark. Since these alkaloids are derivatives of strychnine, it was important, in view of their potential use as antimalarial drugs, to assess their possible convulsant strychnine-like properties. In that regard, their interaction with the strychnine-sensitive glycine receptor was investigated by whole-cell patch-clamp recordings on glycine-gated currents in mouse spinal cord neurons in culture and by [H-3]strychnine competition assays on membranes from adult rat spinal cord. These experiments were carried out on sungucine (leading compound of the chemical class) and on the antiplasmodial strychnogucine B (dimeric) and strychnohexamine (trimeric). In comparison with strychnine, all compounds interact with a very poor efficacy and only at concentrations > I mu M with both [H-3]strychnine binding and glycine-gated currents. Furthermore, the effects of strychnine and protostrychnine, a monomeric alkaloid (without antiplasmodial activity) also isolated from S. icaja and differing from strychnine only by a cycle opening, were compared in the same way. The weak interaction of protostrychnine confirms the importance of the G cycle ring structure in strychnine for its binding to the glycine receptor and its antagonist properties. (c) 2005 Elsevier B.V. All rights reserved. [less ▲]

Detailed reference viewed: 142 (12 ULg)
Full Text
See detailL'image du mois. Un cas de leucoencephalopathie rapidement progressive sur angiopathie amyloide
Wauters, Odile ULg; Scholtes, Félix ULg; Dive, Dominique ULg et al

in Revue Médicale de Liège (2006), 61(1), 3-4

Detailed reference viewed: 174 (14 ULg)
Full Text
Peer Reviewed
See detailSudden deafness : a diagnosis can hide another one.
POIRRIER, Anne-Lise ULg; DEMANEZ, Laurent CH P ULg; Zangerle, Pierre François et al

in B-ENT (2006)

Detailed reference viewed: 7 (0 ULg)
See detailRole of Sox 10 in the development of the inner ear
Bodson, M; Breuskin, I; Thelen, Nicolas ULg et al

Poster (2006)

Detailed reference viewed: 12 (2 ULg)
Full Text
Peer Reviewed
See detailEarly boost and slow consolidation in motor skill learning
Hotermans, C.; Peigneux, Philippe ULg; Maertens De Noordhout, Alain ULg et al

in Learning & Memory (Cold Spring Harbor, N.Y.) (2006), 13(5, Sep-Oct), 580-583

Motorskill learning is a dynamic process that continues covertly after training has ended and eventually leads to delayed increments in performance. Current theories Suggest that this off-line improvement ... [more ▼]

Motorskill learning is a dynamic process that continues covertly after training has ended and eventually leads to delayed increments in performance. Current theories Suggest that this off-line improvement takes time and appears only after several hours. Here we show an early transient and short-lived boost in performance, emerging as early as 5-30 min after training but no longer observed 4 h later. This early boost is predictive of the performance achieved 48 h later, Suggesting its functional relevance for memory processes. [less ▲]

Detailed reference viewed: 23 (3 ULg)
Full Text
Peer Reviewed
See detailBrain response to one's own name in vegetative state, minimally conscious state and locked-in syndrome
Perrin, F.; Schnakers, Caroline ULg; Schabus, M. et al

in Archives of Neurology (2006), 63

Detailed reference viewed: 39 (7 ULg)
Full Text
Peer Reviewed
See detailThe Yin and Yang of cell cycle progression and differentiation in the oligodendroglial lineage
Nguyen, Laurent ULg; Borgs, Laurence ULg; Vandenbosch, Renaud ULg et al

in Mental Retardation & Developmental Disabilities Research Reviews (2006), 12(2), 85-96

In white matter disorders such as leukodystrophies (LD), periventricular leucomalacia (PVL), or multiple sclerosis (MS), the hypomyelination or the remyelination failure by oligodendrocyte progenitor ... [more ▼]

In white matter disorders such as leukodystrophies (LD), periventricular leucomalacia (PVL), or multiple sclerosis (MS), the hypomyelination or the remyelination failure by oligodendrocyte progenitor cells involves errors in the sequence of events that normally occur during development when progenitors proliferate, migrate through the white matter, contact the axon, and differentiate into myelin-forming oligodendrocytes. Multiple mechanisms underlie the eventual progressive deterioration that typifies the natural history of developmental demyelination in LID and PVL and of adult-onset demyelination in MS. Over the past few years, pathophysiological studies have mostly focused on seeking abnormalities that impede oligodendroglial maturation at the level of migration, myelination, and survival. In contrast, there has been a strikingly lower interest for early proliferative and differentiation events that are likely to be equally critical for white matter development and myelin repair. This review highlights the Yin and Yang principles of interactions between intrinsic factors that coordinately regulate progenitor cell division and the onset of differentiation, i.e. the initial steps of oligodendrocyte lineage progression that are obviously crucial in health and diseases. (C) 2006 Wiley-Liss, Inc. [less ▲]

Detailed reference viewed: 60 (4 ULg)
Full Text
Peer Reviewed
See detailActivation of protein kinase CbetaI constitutes a new neurotrophic pathway for deafferented spiral ganglion neurons
Lallemend, François; Hadjab, Saida; Hans, Grégory ULg et al

in Journal of Cell Science (2005), 118(19), 4511-4525

In mammals, degeneration of peripheral auditory neurons constitutes one of the main causes of sensorineural hearing loss. Unfortunately, to date, pharmacological interventions aimed at counteracting this ... [more ▼]

In mammals, degeneration of peripheral auditory neurons constitutes one of the main causes of sensorineural hearing loss. Unfortunately, to date, pharmacological interventions aimed at counteracting this condition have not presented complete effectiveness in protecting the integrity of cochlear neural elements. In this context, the protein kinase C (PKC) family of enzymes are important signalling molecules that play a role in preventing neurodegeneration after nervous system injury. The present study demonstrates, for the first time, that the PKC signalling pathway is directly neurotrophic to axotomised spiral ganglion neurons (SGNs). We found that PKC beta I was strictly expressed by postnatal and adult SGNs both in situ and in vitro. In cultures of SGNs, we observed that activators of PKC, such as phorbol esters and bryostatin 1, induced neuronal survival and neurite regrowth in a manner dependent on the activation of PKC beta I. The neuroprotective effects of PKC activators were suppressed by pre-treatment with LY294002 (a PI3K inhibitor) and with U0126 (a MEK inhibitor), indicating that PKC activators promote the survival and neurite outgrowth of SGNs by both PI3K/Akt and MEK/ERK-dependent mechanisms. In addition, whereas combining the neurotrophins brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT3) was shown to provide only an additive effect on SGN survival, the interaction between PKC and neurotrophin signalling gave rise to a synergistic increase in SGN survival. Taken together, the data indicate that PKC beta I activation represents a key factor for the protection of the integrity of neural elements in the cochlea. [less ▲]

Detailed reference viewed: 40 (3 ULg)
Full Text
Peer Reviewed
See detailNeuropathie périphérique diabétique
DIVE, Dominique ULg; LIEVENS, Isabelle ULg; Moonen, Gustave ULg et al

in Revue Médicale de Liège (2005)

Detailed reference viewed: 24 (3 ULg)
Full Text
Peer Reviewed
See detailDevelopmental regulation of beta-carboline-induced inhibition of glycine-evoked responses depends on glycine receptor beta subunit expression
Mangin, Jean-Marie; Nguyen, Laurent ULg; Gougnard, Catherine et al

in Molecular Pharmacology (2005), 67(5), 1783-1796

In this work, we show that beta-carbolines, which are known negative allosteric modulators of GABA A receptors, inhibit glycine-induced currents of embryonic mouse spinal cord and hippocampal neurons. In ... [more ▼]

In this work, we show that beta-carbolines, which are known negative allosteric modulators of GABA A receptors, inhibit glycine-induced currents of embryonic mouse spinal cord and hippocampal neurons. In both cell types, beta-carboline-induced inhibition of glycine receptor (GlyR)-mediated responses decreases with time in culture. Single-channel recordings show that the major conductance levels of GlyR unitary currents shifts from high levels (>= 50 pS) in 2 to 3 days in vitro (DIV) neurons to low levels (< 50 pS) in 11 to 14 DIV neurons, assessing the replacement of functional homomeric GlyR by heteromeric GlyR. In cultured spinal cord neurons, the disappearance of beta-carboline inhibition of glycine responses and high conductance levels is almost complete in mature neurons, whereas a weaker decrease in beta-carboline-evoked glycine response inhibition and high conductance level proportion is observed in hippocampal neurons. To confirm the hypothesis that the decreased sensitivity of GlyR to beta-carbolines depends on beta subunit expression, Chinese hamster ovary cells were permanently transfected either with GlyR alpha 2 subunit alone or in combination with GlyR beta subunit. Single-channel recordings revealed that the major conductance levels shifted from high levels (>= 50 pS) in GlyR-alpha 2-transfected cells to low levels (< 50 pS) in GlyR-alpha 2-containing cells. Consistently, both picrotoxinand beta-carboline-induced inhibition of glycine-gated currents were significantly decreased in GlyR-alpha 2-transfected cells compared with GlyR-alpha 2-containing cells. In summary, we demonstrate that the incorporation of beta subunits in GlyRs confers resistance not only to picrotoxin but also to beta-carbolineinduced inhibition. Furthermore, we also provide evidence that hippocampal neurons undergo in vitro a partial maturation process of their GlyR-mediated responses. [less ▲]

Detailed reference viewed: 64 (3 ULg)
Full Text
Peer Reviewed
See detailPeripheral benzodiazepine receptor (PBR) ligand cytotoxicity unrelated to PBR expression
Hans, Grégory ULg; Wislet, Sabine ULg; Lallemend, François et al

in Biochemical Pharmacology (2005), 69(5), 819-830

Some synthetic ligands of the peripheral-type benzodiazepine receptor (PBR), an 18 kDa protein of the outer mitochondrial membrane, are cytotoxic for several tumor cell lines and arise as promising ... [more ▼]

Some synthetic ligands of the peripheral-type benzodiazepine receptor (PBR), an 18 kDa protein of the outer mitochondrial membrane, are cytotoxic for several tumor cell lines and arise as promising chemotherapeutic candidates. However, conflicting results were reported regarding the actual effect of these drugs on cellular survival ranging from protection to toxicity. Moreover, the concentrations needed to observe such a toxicity were usually high, far above the affinity range for their receptor, hence questioning its specificity. In the present study, we have shown that micromolar concentrations of FGIN-1-27 And Ro 5-4864, two chemically unrelated PBR ligands are toxic for both PBR-expressing SK-N-BE neuroblastoma cells and PBR-deficient Jurkat lymphoma cells. We have thereby demonstrated that the cytotoxicity of these drugs is unrelated to their PBR-binding activity. Moreover, Ro 54864-induced cell death differed strikingly between both cell types, being apoptotic in Jurkat cells while necrotic in SK-N-BE cells. Again, this did not seem to be related to PBR expression since Ro 5-4864-induced death of PBR-transfected Jurkat cells remained apoptotic. Taken together, our results show that PBR is unlikely to mediate all the effects of these PBR ligands. They however confirm that some of these ligands are very effective cytotoxic drugs towards various cancer cells, even for reputed chemoresistant tumors such as neuroblastoma, and, surprisingly, also for PBR-lacking tumor cells. (C) 2004 Elsevier Inc. All rights reserved. [less ▲]

Detailed reference viewed: 84 (9 ULg)
Full Text
Peer Reviewed
See detailDiffuse cortical atrophy in a patient with Turner syndrome and Leber hereditary optic neuropathy
Blaise, Pierre ULg; Fumal, Arnaud ULg; Janin, Nicolas ULg et al

in Journal of Neurology (2005), 252(2), 232-233

Detailed reference viewed: 72 (3 ULg)
Full Text
Peer Reviewed
See detailbeta-carbolines induce apoptosis in cultured cerebellar granule neurons via the mitochondrial pathway
Hans, Grégory ULg; Malgrange, Brigitte ULg; Lallemend, François et al

in Neuropharmacology (2005), 48(1), 105-117

N-Butyl-beta-carboline-3-carboxylate (betaCCB) is, together with 2-methyl-norharmanium and 2,9-dimethylnorharmanium ions, an endogenously occurring beta-carboline. Due to their structural similarities ... [more ▼]

N-Butyl-beta-carboline-3-carboxylate (betaCCB) is, together with 2-methyl-norharmanium and 2,9-dimethylnorharmanium ions, an endogenously occurring beta-carboline. Due to their structural similarities with the synthetic neurotoxin 1-methy14-phenyl-1,2,3,6-tetrahydropyridine (MPTP), harman and norharman compounds have been proposed to be involved in the pathogenesis of Parkinson's disease. While also structurally related, betaCCB has received much less interest in that respect although we had previously demonstrated that it induces the apoptotic cell death of cultured cerebellar granule neurons (CGNs). Herein, we have investigated the molecular events leading to CGN apoptosis upon betaCCB treatment. We first demonstrated that betaCCB-induced apoptosis occurs in neurons only, most likely as a consequence of a specific neuronal uptake as shown using binding/uptake experiments. Then we observed that, in betaCCB-treated CGNs, caspases 9, 3 and 8 were successively activated, suegesing an activation of the mitochondrial pathway. Consistently, betaCCB also induced the release from the mitochondrial intermembrane space of two pro-apoptotic factors. i.e. cytochrome c and apotptosis inducing factor (AIF). Interestingly, no mitochondrial membrane depolarisation was associated with this release. suggesting a mitochondrial permeability transition pore-independent mechanism. The absence of any neuroprotective effect provided by two mPTP inhibitors. i.e. cyclosporine A and bongkrekic acid. further supported this hypothesis. Together. these results show that betaCCB is specifically taken up by neuronal cells where it triggers a specific permeabilization of the outer mitochondrial membrane and a subsequent apoptotic cell death. (C) 2004 Elsevier Ltd. All rights reserved. [less ▲]

Detailed reference viewed: 80 (14 ULg)
Full Text
Peer Reviewed
See detailActivation of protein kinase C$\beta$I constitutes a new neurotrophic pathway for deafferented spiral ganglion neurons
Lallemend, François; Hadjab, Sa Ida; HANS, Grégory ULg et al

in Journal of cell science (2005), 118(19), 4511--4525

Detailed reference viewed: 15 (4 ULg)
Full Text
Peer Reviewed
See detailMolecular pathways involved in apoptotic cell death in the injured cochlea: Cues to novel therapeutic strategies
Lallemend, François; Lefèbvre, Philippe ULg; Hans, Grégory ULg et al

in Current Pharmaceutical Design (2005), 11(17), 2257-2275

Most hearing loss results from lesions of the sensory cells and/or neurons of the auditory portion of the inner ear. To date, only the cochlear implantation offers long-term hearing-aid benefit, but still ... [more ▼]

Most hearing loss results from lesions of the sensory cells and/or neurons of the auditory portion of the inner ear. To date, only the cochlear implantation offers long-term hearing-aid benefit, but still with limited performance and expensive cost. While the underlying causes of deafness are not clear, the death or hair cells and/or neurons and the loss of neuronal contacts are key pathological features. Pinpointing molecular events that control cell death in the cochlea is critical for the development of new strategies to prevent and treat deafness, whether in combination or not with cochlear implant therapy. [less ▲]

Detailed reference viewed: 31 (1 ULg)