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4. Abstracts Second Congress of the European Society for Clinical Neuropharmacology: Würzburg, November 9–11, 1995

Author

Agid, Y., Arendt, T., Gärtner, U., Holzer, M., Fruth, P., Brückner, M. K., Arzberger, T., Weindl, A., Baas, H., Demisch, L., Harder, S., Bürklin, F., Fischer, P. A., Bagli, M., Rao, M. L., Sobanski, T., Laux, G., Barbier, P., Fumagalli, F., Donati, E., Maggio, R., Racagni, G., Corsini, G. U., Riva, M., Berger, J., Löschl, B., Bernheimer, H., Lugowska, A., Tylki-Szymanska, A., Gieselmann, V., Molzer, B., Faé, I., Bernocchi, G., Scherini, E., Necchi, D., Bigl, M., Bleyl, D., Bigl, V., Eschrich, K., Block, F., Schwarz, M., Blum-Degen, D., Müller, Th., Kuhn, W., Gerlach, M., Przuntek, H., Riederer, R., Bonuccelli, U., Ceravolo, R., Nuti, A., D'Avino, C., Placidi, G., Perugi, G., Cassano, G. B., Del Dotto, P., Piccini, P., Colzi, A., Muratorio, A., Braak, H., Braak, E., Yilmazer, D. M., de Vos, R. A. I., Jansen, E. N. H., Bringmann, G., Clement, H. W., Grote, C., Rausch, F., Reichmann, H., Riederer, P., Sontag, K. -H., Wesemann, W., God, R., Feineis, D., Brückner, R., Protzen, J. -A., Fähr, S., Rausch, W. -D., Brunt, E. R. P., Pruim, J., Willemsen, A. J., van Weerden, T. W., Bryan-Lluka, L. J., Bönisch, H., Büttner, Th., Kühn, W., McMonagle, U., Calza, L., Pozza, M., Coraddu, F., Farci, G., Carlsson, A., Napolitano, A., Salvetti, S., Dell'Agnello, G., Renna, M., Conquet, F., Bashir, Z., Daniel, H., Ferraguti, F., Collingridge, G., Crépel, F., Coos Verhoef, J., Merkus, F. W. H. M., Junginger, H. E., Cruz-Sánchez, F. F., Kutschka, T., Beeg, M., Deuschle, M., Weber, B., Körner, A., Standhardt, H., Lammers, C. -H., Motzek-Noé, T., Heuser, I., Earl, C. D., Reum, T., Sautter, J., Xie, J. -X, Kupsch, A., Oertel, W. H., Morgenstern, R., Emilien, G. M., Maloteaux, J. M., Seghers, A., Charles, G., Erdmann, R., Högemann, D., Fichter, N., Lücking, C. H., Landwehrmeyer, G. B., Winter, T., Feuerstein, T. J., Fitzgeral, D., Anderson, M. C., Lawlor, B., Tipton, K. F., Frackowiak, R. S. J., Freo, U., Dam, M., Pizzolato, G., Merico, A., Ori, C., Sale, E., Battistin, L., Fritze, J., Froelich, L., Goetz, M., Gsell, W., Jellinger, K., Beckmann, H., Fünfgeld, E. W., Glinka, Y., Youdim, M. B. H., Götz, M. E., Breithaupt, W., Burger, R., Streifler, M., Simanyi, M., Müller, F., Danielczyk, W., Hirning, T., Sohlbach, M., Nafc, R., Sternadl, H., Winter, M., Nöth, U., Heim, C., Hartmann, J., Künig, G., Niedermeyer, B., Berger, W., Deckert, J., Abel, F., Heinsen, H., Senitz, D., Mayr, J., Ransmayr, G., Hartung, H. -P., Heils, A., Teufel, A., Petri, S., Seemann, M., Bengel, D., Degen, H. J., Lesch, K. P., Sontag, T., Heinen, F., Korinthenberg, R., Heiss, W. -D., Rüb, U., Gangus, B., Jungkunz, G., Bauer, M., Ulmar, G., Böcker, F., Schüler, M., Bethke, B., Lockemann, U., Hermans, E., Vanhoorde, P., Hesse, S., Hüll, M., Fiebich, B., Lieb, K., Strauss, S., Berger, M., Volk, B., Bauer, J., Iversen, L. L., Janetzky, B., Hauck, S., Jeanjean, A. P., Laterre, E. C., Bancher, C., Jost, W. H., Kalus, P., Kanner, B., Khrapova, E. V., Brusov, O. S., Knauber, J., Müller, W. E., Korczyn, A. D., Kornhuber, J., Parsons, C. G., Hartmann, S., Retz, W., Kamolz, S., Thome, J., Koutsilieri, E., Chen, T. -S., Kreutzberg, G. W., Krieglstein, J., Winkel, R., Danielcyk, S., Gerstner, A., Mattern, C., Häcker, R., Labunsky, D., Zhirnova, I., Komelkova, L., Popova, L., Avdiunina, I., Lakke, J. P. W. F., Lange, K. W., Steup, A., Tucha, O., Naumann, M., Lassmann, H., Leszek, J., Gasiorowski, K., Inglot, D., Lohse, M. J., Löschmann, P. -A., Eblen, F., Wüllner, U., Klockgether, T., Dichgans, J., Macrae, I. M., Mimmack, M. L., Emson, P., Norta, M., Borchert, H. -H., Medori, R., Chan, W. W., Heinemann, T., Melzacka, M., Kolasiewicz, W., Sieklucka, M., Jaros, T., Mesec, A., Šega, S., Kiauta, T., Moser, A., Vieregge, P., Siebecker, F., Münch, G., Schinzel, R., Michaelis, J., Cunningham, A., Da Prada, M., Borroni, E., Zürcher, G., Reiners, K., Neveu, P. J., Nitsch, R. M., Pavese, N., Lucetti, C., Rossi, G., Offen, D., Ziv, I., Stein, R., Barzilai, A., Hochman, A., Melamed, E., Ozawa, H., Hashimoto, E., Saito, T., Ymamoto, M., Takahata, N., Frölich, L., Paulus, W., Hermsteiner, E., Haug, B., Bandelow, B., Peckys, D., Gleichauf, O., Jackisch, R., Landwehrmeyer, B., Bloß, H. G., Plaschke, K., Müller, D., Hoyer, S., Avdyuna, L. A., Putzke, J., Spanagel, R., Tolle, T. R., Zieglgänsberger, W., Rabey, J. -M., Orlov, E., von Raison, F., Lehmann, K., Havemann-Reinecke, U., Butà, M., Federspiel, S., Maier, H., Abdel-mohsen, M., Abdel-moneim, M., Reynolds, G. P., Sardar, A. M., Eggett, C. J., Rosario, P., de la Morena, E., José Barro, M., Rossini, P. M., Roth, J., Růžička, E., Svobodová, I., Mečíř, P., Jech, R., Remeš, F., Kleinschroth, A., Schliebs, R., Roßner, S., Heider, M., Schubert, H., König, P., Schuttes, H., HaveIec, L., Schwartz, J. -C., Sendtner, M., Smith, A., Li, M., Griesbeck, O., Parsadanian, A., Holtmann, B., Carroll, P., Toyka, K. V., Thoenen, H., Sharkawy, A. A., Ibrahim, T. A., Pulkowski, U., Siesjö, B. K., Klessaschek, M., Sopper, S., Demuth, M., Dörries, R., Hemm, S., Stahl-Hennig, C., Brinkmann, R., ter Meulen, V., Sperk, G., Schwarzer, C., Stern, G., Storm, G., Strein, I., Struck, M., Stürenburg, H. J., Kunze, K., Svadovsky, A. I., Morgunov, K. V., Peresedov, V. V., Moshkin, A. V., Teherani, D. K., Baumer, A., Rösier, M., Rösler, M., Wiesbeck, G. A., Wodarz, N., Boning, J., Timerbaeva, S. L., Alekseeva, N. S., Toso, A., Barletta, D., Tuulik, V., Lossmann, E., Raja, A., Meister, A., Uitti, R. J., Rajput, A. H., Ahlskog, J. E., Offord, K. P., Schroeder, D. R., O'Brien, P. C., Vaglini, F., Fascetti, F., Pardini, C., Mancino, L., Velbinger, K., Hartmann, H., Eckert, A., Grüter, S., Behrens, S., Niemann, J., Guschelbauer, B., Lauk, M., Wissel, J., Poewe, W., Wurthman, C., Janzen, E. N. H., Goping, G., Adegemo, O. M., Gemma, A., Kuijpers, J., Pollard, H. B., Zielke, B., Ziemann, U., and Bruns, D.

Published
1995
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18. Cloning of the Beta Amyloid Peptide Gene in Alzheimer’s Disease

Author

Octave, J. N., primary, de Sauvage, F., additional, Macq, A. F., additional, Maloteaux, J. M., additional, Rasool, C. G., additional, Vitek, M. P., additional, Blume, A. J., additional, Brucher, J. M., additional, de Barsy, T., additional, Trouet, A., additional, and Laterre, E. C., additional

Published
1988
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41. The elution of IgG from subacute sclerosing panencephalitis and multiple sclerosis brains.

Author

Sindic, C. J. M., Cambiaso, C. L., Masson, P. L., and Laterre, E. C.

Subjects
IMMUNOGLOBULIN G, MULTIPLE sclerosis, VIRUS diseases, SUBACUTE sclerosing panencephalitis, ENCEPHALITIS, MEASLES complications
Abstract

IgG was extracted from sections of a multiple sclerosis brain by repeated washing with phosphate-buffered saline. After this extraction, no IgG was recovered by further washing at pH 2.2. This indicates that the IgG of the plaques has no strong affinity for insoluble constituents of the brain. Sections of a subacute sclerosing panencephalitis brain were used as positive controls: after repeated extraction with phosphate-buffered saline, IgG with anti-measles antibody activity was eluted at acid pH. [ABSTRACT FROM AUTHOR]

Published
1980

42. The binding of myelin basic protein to the Fc region of aggregated IgG and to immune complexes.

Author

Sindic, C. J. M., Cambiaso, C. L., Masson, P. L., and Laterre, E. C.

Subjects
MYELIN proteins, IMMUNOGLOBULINS, NERVE tissue proteins, AGGLUTINATION, ANTIGEN-antibody reactions, ALKYLATION
Abstract

Bovine myelin basic protein was found to agglutinate polystyrene particles coated with human polyclonal IgG, monoclonal IgG1, or IgG Fc fragments, but not those coated with IgG F(ab′)2 fragments, IgA, or IgM. The agglutination of Fc-coated particles was inhibited by heat-aggregated polyclonal IgG or monoclonal IgG2, IgG3 and IgG4, but not by native IgG. Reduction and alkylation of aggregated IgG did not affect their inhibitory activities. Soluble immune complexes displayed the highest inhibitory activity at a two-fold antigen excess. The interaction between myelin basic protein and aggregated IgG was confirmed by gel exclusion experiments on Sephadex G-200, The possible consequence of these findings could be significant in the interpretation of IgG deposits in brain plaques of multiple sclerosis patients and of the results of immunohistochemical studies, titration of anti-myelin basic protein antibodies and immunoassay of myelin basic protein. [ABSTRACT FROM AUTHOR]

Published
1980

43. Assessment of damage to the central nervous system by determination of S-100 protein in the cerebrospinal fluid.

Author

Sindic, C J, Chalon, M P, Cambiaso, C L, Laterre, E C, and Masson, P L

Subjects
DIAGNOSIS of brain damage, BRAIN damage, CALCIUM-binding proteins, CENTRAL nervous system diseases, COMPARATIVE studies, ELECTROPHORESIS, RESEARCH methodology, MEDICAL cooperation, NERVE tissue proteins, PROGNOSIS, RESEARCH, EVALUATION research, DIAGNOSIS
Abstract

S-100 protein was determined by Particle Counting ImmunoAssay in the CSF of patients with various neurological disorders. With a limit of sensitivity of 2.5 micrograms/l this brain-specific protein was detected only in samples from patients with acute damage of the central nervous system, particularly in compression of the spinal cord by tumour, ischaemic disorders, subarachnoïd bleeding and haematoma, and viral or suspected viral infections. Our results support the assumption that S-100 is a reliable index of central nervous system damage and that changes in its concentration could have a prognostic value. [ABSTRACT FROM AUTHOR]

Published
1982

44. The clinical relevance of ferritin concentration in the cerebrospinal fluid.

Author

Sindic, C J, Collet-Cassart, D, Cambiaso, C L, Masson, P L, and Laterre, E C

Subjects
BACTERIAL diseases, CEREBRAL hemorrhage, BRAIN tumors, CEREBROVASCULAR disease, COMPARATIVE studies, DEMENTIA, ENCEPHALITIS, FERRITIN, HEMATOMA, RESEARCH methodology, MEDICAL cooperation, NEUROLOGICAL disorders, RESEARCH, VIRUS diseases, EVALUATION research, VIRAL meningitis
Abstract

By means of a new technique (Particle Counting Immunoassay), we have determined the level of ferritin in 470 samples of cerebrospinal fluid of patients with various neurological disorders. The median value obtained in a control group was 2.3 ng/ml with an upper limit at 5.5 ng/ml. the concentrations in the serum and cerebrospinal fluid were independent, but that in cerebrospinal fluid correlated with its total protein content. High values of ferritin were found in infectious meningo-encephalitis, in vascular diseases of the central nervous system, and, unexpectedly, in several cases of dementia without obvious vascular pathology. [ABSTRACT FROM AUTHOR]

Published
1981

45. Down-regulation of H-lofentanil binding to opiate receptors in different cultured neuronal cells.

Author

Maloteaux, J., Octave, J., Laterre, E., and Laduron, P.

Abstract

There was stereospecific binding of H-lofentanil ( K value = 1.53 nM) to membranes of neuroblastoma-glioma NG 108-15 cells which are known to bear high affinity binding sites for enkephalin derivatives (δ-opiate receptor subtype). There was no high affinity specific binding of the μ-opiate specific ligand H-sufentanil. The specific binding of H-lofentanil to δ-opiate receptor subtype was down-regulated (decrease in B value without change in the K value) after prolonged incubation of the cells in the presence of leu- and met- enkephalin (0.1 μM). There was no down-regulation of the opiate receptors (H-lofentanil and H- d-ala- d-leu-enkephalin specific binding) after incubation of NG 108-15 cells with drugs from the fentanyl series (alfentanil or sufentanil). In cultured neurones from rat forebrain (15 day old embryos), the H-lofentanil binding was specific with high affinity ( K: 0.048 nM) and a slow dissociation rate similar to that in adult rat cortex. Drugs of the fentanyl series (4-anilino-piperidines) were potent displacers whereas agonists of the δ- (enkephalin derivatives), σ (phencyclidine, haloperidol, 3-hydroxyphenyl-propylpiperidine) or K- (U 50488) opiate sites had a low affinity ( K > 0.5 μM) for H-lofentanil specific binding sites. Since there was also specific binding of H-sufentanil, the opiate receptors in cultured neurones seem to be mainly of the μ-subtype and this is consistent with the ontogeny of opiate receptors subtypes. These receptors were down-regulated after incubation in the presence of etorphine, sufentanil and alfentanil but not enkephalin derivatives. These results strongly suggest specific binding of H-sufentanil and H-lofentanil mainly to the so-called μ-opiate receptors in cultured neurones and a specific binding of H-lofentanil to lower affinity δ-opiate receptors in neuroblastoma-glioma cells. The down-regulation of the μ-opiate binding sites in cultured neurones and that of the δ-site in neuroblastoma × glioma hybrid cells were dose-and temperature-dependent, induced by the corresponding high affinity agonists and prevented by naloxone. Morphine did not induce down-regulation of μ or δ receptor sites, possibly because of a partial antagonist effect on both receptor subtypes. [ABSTRACT FROM AUTHOR]

Published
1989
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48. Chronic demyelinating hypertrophic brachial plexus neuropathy

Author

Bergh, Peter Y.K. van den, Thonnard, Jean-Louis, Duprez, Thierry, and Laterre, E. Christian

Abstract

A patient with unilateral, painless, chronic progressive upper limb sensorimotor deficit showed electrophysiological evidence of a focal demyelinating neuropathy with almost complete conduction block across the brachial plexus. Magnetic resonance imaging disclosed marked brachial plexus hypertrophy. Intravenous immunoglobulin led to fast and complete recovery, maintained by intermittent perfusions. Hypertrophic brachial plexus neuropathy can be a presentation of focal chronic inflammatory demyelinating polyradiculoneuropathy. Objective and quantitative assessment of hand function is useful to evaluate treatment results and to optimize treatment regimens. © 2000 John Wiley & Sons, Inc. Muscle Nerve 23: 283–288, 2000.

Published
2000
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49. Cholinergic Neurotransmission Has Different Effects on Cerebral Glucose Consumption and Blood Flow in Young Normals, Aged Normals, and Alzheimer's Disease Patients

Author

Blin, J., Ivanoiu, A., Coppens, A., De Volder, A., Labar, D., Michel, C., and Laterre, E. C.

Abstract

Cerebral blood flow (CBF) and glucose consumption (GC) are both tracers of brain metabolic activity used to image the human brainin vivo.To know if both tracers reacted in the same manner when brain cholinergic neurotransmission was activated, CBF and GC were measured in young normals (YN), aged normals (AN), and Alzheimer's Disease patients (AD) using positron emission tomography (PET), H215O, and18F-FDG. Each subject was studied twice, under placebo and physostigmine, in randomized order and blind fashion using the maximal tolerated dose of physostigmine individually determined. Under physostigmine CBF increased significantly (P=0.0007) in posterior regions of the cerebral cortex and in the subcortical structures. Inversely, GC was decreased significantly in most regions. The largest decrease was seen in the prefrontal region of the cerebral cortex (P<0.0001). Significant regional decreases were registered in all three groups of subjects, but were larger in AD than in controls. Looking at the absolute values of prefrontal cortex metabolism we found no correlation (r=0.04) between the responses of CBF and GC. After normalization of the regional values for the mean we found a significant positive correlation between the responses of CBF and GC (r=0.71,P<0.0001). These findings suggest two components in the CBF response to physostigmine: one metabolic, depressive, and regional which follows the GC response; and one vascular, larger, diffuse, and opposite in direction to the metabolic component. These results have implications for the interpretation of CBF values as tracer of brain metabolic activity when brain cholinergic neurotransmission is manipulated.

Published
1997
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50. Down-regulation of 3H-lofentanil binding to opiate receptors in different cultured neuronal cells

Author

Maloteaux, J. M., Octave, J. N., Laterre, E. C., and Laduron, P. M.

Abstract

There was stereospecific binding of 3H-lofentanil (KD value = 1.53 nM) to membranes of neuroblastoma-glioma NG 108-15 cells which are known to bear high affinity binding sites for enkephalin derivatives (d-opiate receptor subtype). There was no high affinity specific binding of the µ-opiate specific ligand 3H-sufentanil. The specific binding of 3H-lofentanil to d-opiate receptor subtype was down-regulated (decrease in Bmax value without change in the KD value) after prolonged incubation of the cells in the presence of leu- and met- enkephalin (0.1 µM). There was no down-regulation of the opiate receptors (3H-lofentanil and 3H-d-ala-d-leu-enkephalin specific binding) after incubation of NG 108-15 cells with drugs from the fentanyl series (alfentanil or sufentanil).

Published
1989
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