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13. Markers for neural degeneration and regeneration: novel highly sensitive methods for the measurement of thrombin and activated protein C in human cerebrospinal fluid

Author

Shavit-Stein, Efrat, primary, Gerasimov, Alexandra, additional, Golderman, Valery, additional, Gofrit, ShanyGuly, additional, Aharoni, ShayAnat, additional, Zohar, DanielaNoa, additional, Itsekson-Hayosh, Ze’ev, additional, Fay-Karmon, Tsviya, additional, Hassin-Baer, Sharon, additional, Chapman, Joab, additional, and Maggio, Nicola, additional

Published
2021
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14. Treatment of Diabetic Neuropathy with A Novel PAR1-Targeting Molecule

Author

Shavit-Stein, Efrat, primary, Gofrit, Shany Guly, additional, Gayster, Alexandra, additional, Teldan, Yotam, additional, Ron, Ariel, additional, Abu Bandora, Eiman, additional, Golderman, Valery, additional, Gera, Orna, additional, Harnof, Sagi, additional, Chapman, Joab, additional, and Dori, Amir, additional

Published
2020
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16. Rectracted: Anti-ribosomal-phosphoprotein autoantibodies penetrate to neuronal cells via neuronal growth associated protein, affecting neuronal cells in vitro.

Author

Kivity, Shaye, Shoenfeld, Yehuda, Arango, Maria-Teresa, Cahill, Dolores J., O'Kane, Sara Louise, Zusev, Margalit, Slutsky, Inna, Harel-Meir, Michal, Chapman, Joab, Matthias, Torsten, and Blank, Miri

Abstract

Objective Anti-ribosomal-phosphoprotein antibodies (anti-Ribos.P Abs) are detected in 10–45% of NPSLE patients. Intracerebroventricular administration of anti-ribosomal-P Abs induces depression-like behaviour in mice. We aimed to discern the mechanism by which anti-Ribos.P Abs induce behavioural changes in mice. Methods Anti-Ribos.P Abs were exposed to human and rat neuronal cell cultures, as well as to human umbilical vein endothelial cell cultures for a control. The cellular localization of anti-Ribo.P Abs was found by an immunofluorescent technique using a confocal microscope. Identification of the target molecules was undertaken using a cDNA library. Immunohistochemistry and an inhibition assay were carried out to confirm the identity of the target molecules. Neuronal cell proliferation was measured by bromodeoxyuridine, and Akt and Erk expression by immunoblot. Results Human anti-Ribos.P Abs penetrated into human neuronal cells and rat hippocampal cell cultures in vitro , but not to endothelial cells as examined. Screening a high-content human cDNA-library with anti-Ribos.P Abs identified neuronal growth–associated protein (GAP43) as a target for anti-Ribos.P Abs. Ex vivo anti-Ribos.P Abs bind to mouse brain sections of hippocampus, dentate and amygdala. Anti-Ribos.P Abs brain-binding was prevented by GAP43 protein. Interestingly, GAP43 inhibited in a dose-dependent manner the anti-Ribos.P Abs binding to recombinant-ribosomal-P0, indicating mimicry between the ribosomal-P0 protein and GAP43. Furthermore, anti-Ribos.P Abs reduced neuronal cell proliferation activity in vitro (P < 0.001), whereas GAP43 decreased this inhibitory activity by a factor of 7.6. The last was related to Akt and Erk dephosphorylation. Conclusion Anti-Ribos.P Abs penetrate neuronal cells in vitro by targeting GAP43. Anti -Ribos.P Abs inhibit neuronal-cell proliferation via inhibition of Akt and Erk. Our data contribute to deciphering the mechanism for anti-Ribos.P Abs' pathogenic activity in NPSLE. [ABSTRACT FROM AUTHOR]

Published
2021
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17. Brain Protease Activated Receptor 1 Pathway: A Therapeutic Target in the Superoxide Dismutase 1 (SOD1) Mouse Model of Amyotrophic Lateral Sclerosis

Author

Shavit-Stein, Efrat, primary, Abu Rahal, Ihab, additional, Bushi, Doron, additional, Gera, Orna, additional, Sharon, Roni, additional, Gofrit, Shany G., additional, Pollak, Lea, additional, Mindel, Kate, additional, Maggio, Nicola, additional, Kloog, Yoel, additional, Chapman, Joab, additional, and Dori, Amir, additional

Published
2020
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20. Ancestral origins and worldwide distribution of the PRNP 200K mutation causing familial Creutzfeldt-Jakob disease

Author

Lee, Hee Suk, Sambuughin, Nyamkhishig, Cervenakova, Larisa, Chapman, Joab, Pocchiari, Maurizio, Litvak, Svetlana, Qi, Hai Yan, Budka, Herbert, Ser, Teodoro del, Furukawa, Hisako, Brown, Paul, American football coach, Gajdusek, D. Carleton, Long, Jeffrey C., Korczyn, Amos D., and Goldfarb, Lev G.

Subjects
Creutzfeldt-Jakob disease -- Genetic aspects, Central nervous system diseases -- Genetic aspects, Genetic disorders -- Research, Biological sciences
Abstract

Researchers have determined that independent mutational events and founder effect are responsible for the geographically based distribution of the hereditary form of Creutzfeldt-Jakob disease. Studies targeting the PRNP gene's 200K mutation and selected microsatellite markers revealed that haplotypes in different regions are unique, but follow the migratory patterns of ancestral carriers.

Published
1999

24. Decreased hippocampal cell proliferation in mice with experimental antiphospholipid syndrome

Author

Frauenknecht, Katrin, Leukel, Petra, Weiss, Ronen, von Pein, Harald D, Katzav, Aviva, Chapman, Joab, Sommer, Clemens J, University of Zurich, and Frauenknecht, Katrin

Subjects
Histology, General Neuroscience, 10208 Institute of Neuropathology, 570 Life sciences, biology, 2800 General Neuroscience, 610 Medicine & health, Anatomy, 2702 Anatomy, 2722 Histology
Published
2018

29. Pros and cons of a prion-like pathogenesis in Parkinson's disease

Author

Brotchie Jonathan M, Hilker Ruediger, and Chapman Joab

Subjects
Neurology. Diseases of the nervous system, RC346-429
Abstract

Abstract Background Parkinson's disease (PD) is a slowly progressive neurodegenerative disorder which affects widespread areas of the brainstem, basal ganglia and cerebral cortex. A number of proteins are known to accumulate in parkinsonian brains including ubiquitin and α-synuclein. Prion diseases are sporadic, genetic or infectious disorders with various clinical and histopathological features caused by prion proteins as infectious proteinaceous particles transmitting a misfolded protein configuration through brain tissue. The most important form is Creutzfeldt-Jakob disease which is associated with a self-propagating pathological precursor form of the prion protein that is physiologically widely distributed in the central nervous system. Discussion It has recently been found that α-synuclein may behave similarly to the prion precursor and propagate between cells. The post-mortem proof of α-synuclein containing Lewy bodies in embryonic dopamine cells transplants in PD patient suggests that the misfolded protein might be transmitted from the diseased host to donor neurons reminiscent of prion behavior. The involvement of the basal ganglia and brainstem in the degenerative process are other congruencies between Parkinson's and Creutzfeldt-Jakob disease. However, a number of issues advise caution before categorizing Parkinson's disease as a prion disorder, because clinical appearance, brain imaging, cerebrospinal fluid and neuropathological findings exhibit fundamental differences between both disease entities. Most of all, infectiousness, a crucial hallmark of prion diseases, has never been observed in PD so far. Moreover, the cellular propagation of the prion protein has not been clearly defined and it is, therefore, difficult to assess the molecular similarities between the two disease entities. Summary At the current state of knowledge, the molecular pathways of transmissible pathogenic proteins are not yet fully understood. Their exact involvement in the pathophysiology of prion disorders and neurodegenerative diseases has to be further investigated in order to elucidate a possible overlap between both disease categories that are currently regarded as distinct entities.

Published
2011
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30. A Novel Compound Targeting Protease Receptor 1 Activators for the Treatment of Glioblastoma

Author

Shavit-Stein, Efrat, primary, Sheinberg, Ehud, additional, Golderman, Valery, additional, Sharabi, Shirley, additional, Wohl, Anton, additional, Gofrit, Shany Guly, additional, Zivli, Zion, additional, Shelestovich, Natalia, additional, Last, David, additional, Guez, David, additional, Daniels, Dianne, additional, Gera, Orna, additional, Feingold, Kate, additional, Itsekson-Hayosh, Zeev, additional, Rosenberg, Nurit, additional, Tamarin, Ilia, additional, Dori, Amir, additional, Maggio, Nicola, additional, Mardor, Yael, additional, Chapman, Joab, additional, and Harnof, Sagi, additional

Published
2018
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32. Ocrelizumab versus Interferon Beta-1a in Relapsing Multiple Sclerosis

Author

Hauser, Stephen L., Bar-Or, Amit, Comi, Giancarlo, Giovannoni, Gavin, Hartung, Hans-Peter, Hemmer, Bernhard, Lublin, Fred, Montalban, Xavier, Rammohan, Kottil W., Selmaj, Krzysztof, Traboulsee, Anthony, Wolinsky, Jerry S., Arnold, Douglas L., Klingelschmitt, Gaelle, Masterman, Donna, Fontoura, Paulo, Belachew, Shibeshih, Chin, Peter, Mairon, Nicole, Garren, Hideki, Kappos, Ludwig, And Opera Ii Clinical Investigators, Opera I., Reingold, Stephen C., Sandberg-Wollheim, Magnhild, Barkhof, Frederik, Dörmer, Thomas, Evans, Scott, Mcfarland, Henry F., Steiner, Israel, Yaldizli, Özgür, D Souza, Marcus, Andelova, Michaela, Rust, Heiko, Ballario, Carlos, Giannaula, Rolando, Reich, Edgardo Gabriel, Parratt, John, Eggers, Christian, Buyle, Maarten, Pesch, Vincent, Vanopdenbosch, Ludo, Carneiro, Denise, Friedrich, Mauricio, Longo, Alexandre Luiz, Genov, Krasimir, Ivanova, Sonya, Maslarov, Dimitar, Lilovski, Hristo, Staikov, Ivan, Cueto, German, Dufek, Michal, Havrdova, Eva, Novotna, Alena, Skoda, Ondrej, Talabova, Marika, Vachova, Marta, Gross-Paju, Katrin, Haldre, Sulev, Elovaara, Irina, Brochet, Bruno, Castelnovo, Giovanni, Clavelou, Pierre, Seze, Jerome, Debouverie, Marc, Braune, Stefan, Haas, Judith, Heidenreich, Fedor, Schwarz, Wolfgang, Siever, Arno, Urban, Peter Paul, Zettl, Uwe, Ziemann, Ulf, Ziemssen, Tjalf, Zipp, Frauke, Debreczeni, Robert, Rozsa, Csilla, Satori, Maria, Chapman, Joab, Ghezzi, Angelo, Perini, Paola, Pozzilli, Carlo, Kalnina, Jolanta, Millers, Andrejs, Budrys, Valmantas, Kizlaitiene, Rasa, Malciene, Lina, Vaitkus, Antanas, Castro Farfan, Guillermo, Gongora Rivera, Juan Fernando, Frequin, S. T. F. M., Gavidia Chucan, Jorge Martin, Perez Villegas, Julio, Pretell, Edwin Javier, Rodriguez Kadota, Liliana Elizabe, Fryze, Waldemar, Hertmanowska, Hanka, Maciejowski, Maciej, Opala, Grzegorz, Cerqueira, João, Arefieva, Elena, Maslova, Natalia, Odinak, Miroslav, Pankratov, Evgeny, Perfiliev, Semen, Poverennova, Irina, Sazonov, Denis, Shirshova, Elena, Sivertseva, Stella, Volkova, Larisa, Vorobyova, Olga, Knezevic, Zorica, Raicevic, Ranko, Vojinovic, Slobodan, Hancinova, Viera, Saffova, Patricia, Turcani, Peter, Vyletelka, Juraj, Coetzee, Christo C., Garcia-Merino, Antonio, Hernandez, Miguel A., Izquierdo Ayuso, Guillermo, Rodriguez Antigüedad, Alfredo, Gobbi, Claudio, Belal, Samir, Frih-Ayed, Mahbouba, Gouider, Riadh, Mrissa, Ridha, Sergii Moskovko, Sanotskyy, Yanosh, Sokolova, Larysa, Statinova, Olena, Voloshyna, Nataliya, Turner, Benjamin, Wilson, Martin, Applebee, Angela, Bandari, Daniel, Belkin, Martin, Birnbaum, Gary, Borresen, Thor, Boyd, James, Cascione, Mark, Cohan, Stanley, Cohen, Bruce, Conway, Jill, Cree, Bruce, Dihenia, Bhupesh, Dissin, Jonathan, Flitman, Stephen, Ford, Corey, Giancarlo, Thomas, Gold, Scott, Green, Barbara, Gwynn, Matthews, Honeycutt, David, Huddlestone, John, Klawiter, Eric, Kohrman, Bruce, Langer-Gould, Annette, Lava, Neil, Lindsey, William, Mitchell, Galen, Naismith, Robert, Nicolas, Joseph, Pardo, Gabriel, Patel, Malti, Porter, John A. H., Racke, Michael, Robertson, Derrick, Rossman, Howard, Schafer, John, Shubin, Richard, Singer, Barry, Smith, Charles, Suski, Valerie, Thrower, Ben, Wilson, Christopher, Wynn, Daniel, Zabad, Rana, Estol, Conrado J., Scarlatti, Annita, Alekseenko, Yuri, Fedulau, Aliaksandr, Kulesh, Sergey, Navumava, Halina, Willekens, Barbara, Alajbegovic, Azra, Sinanovic, Osman, Christo, Paulo, Papais Alvarenga, Regina Maria, Pereira Damasceno, Benito, Baldaranov, Dimo, Grigorova, Olga, Haralanov, Lyubomir, Milanova, Milena, Ayotte, Charles, Blevins, Gregg, Freedman, Mark, Grand Maison, François, Jacques, François, Yeung, Michael, Basic, Silvio, Hajnsek, Sanja, Janko-Labinac, Dolores, Kidjemet Piskac, Spomenka, Benesova, Yvonne, Hradilek, Pavel, Brassat, David, Edan, Gilles, Hautecoeur, Patrick, Moreau, Thibault, Papeix, Caroline, Tourbah, Ayman, Vukusic, Sandra, Aktas, Orhan, Berthele, Achim, Bodenschatz, Ralf, Foerch, Christian, Hohlfeld, Reinhard, Landefeld, Harald, Lang, Michael, Platten, Michael, Puzich, Reinhard, Schmidt, Stephan, Tubridy, Niall, Ardito, Bonaventura, Capra, Ruggero, Centonze, Diego, Crociani, Paola, Danni, Maura, Grimaldi, Luigi, Gusmaroli, Graziano, Mantegazza, Renato, Mirabella, Massimiliano, Uccelli, Antonio, Carbajal Ramirez, Angelica, Lopez Meza, Elmer Guillermo, Lopez Prieto, Juan Jose, Oropeza Alba, Jose Luis, Reyes-Morales, Sarug, San Juan Orta, Daniel, Myhr, Kjell Morten, Binek, Maciej, Czarnecki, Maciej, Klodowska-Duda, Gabriela, Stelmasiak, Zbigniew, Szczudlik, Andrzej, Tutaj, Andrzej, Belova, Anna, Dorogov, Nikolay, Fedyanin, Alexander, Khasanova, Dina, Makarov, Nikolay, Mishin, Gennadiy, Sherman, Mikhail, Skoromets, Alexander, Trushnikova, Tatiana, Donath, Vladimir, Dupejova, Beata, Gurcik, Ladislav, Arroyo, Rafael, Andres, Clara, Fernandez Fernandez, Oscar, Lainez Andrep, Jose Miguel, Martinez Gines, Maria Luisa, Martinez Rodriguez, Jose Enrique, Martinez Yelamos, Sergio, Oreja Guevara, Celia, Perez Sempere, Angel, Ramio, Luis, Ramo Tello, Cristina, Lycke, Jan, Olsson, Tomas, Roshanisefat, Homayoun, Sundström, Peter, Svenningsson, Anders, Akman Demir, Gulsen, Petek Balci, Belgin, Boz, Cavit, Efendi, Husnu, Karabudak, Rana, Siva, Aksel, Terzi, Murat, Yuceyar, Ayse Nur, Chmyr, Galyna, Goncharova, Yana, Kareta, Serhiy, Lutskiy, Igor, Harrower, Timothy, Hawkins, Clive, Pearson, Owen, Silber, Eli, Absher, John, Arnold, Thomas, Bass, Ann, Bernitsas, Evanthia, Braley, Tiffany, Calkwood, Jonathan, Carnes, Kenneth, Coyle, Patricia, Dunn, Jeffrey, Edwards, Keith, English, Jeffrey, Ferencz, Gerald, Fox, Edward, Frohman, Elliott, Gazda, Suzanne, Gitt, Jeffrey, Goodman, Andrew, Gross, Jeffrey, Hendin, Barry, Herrman, Craig, Hillen, Machteld, Huang, Deren, Hunter, Samuel, Hutton, George, Jacobs, Daniel, Keller, Bridget, Khan, Omar, Kister, Ilya, Krupp, Lauren, Lathi, Ellen, Lynch, Sharon, Miller, Tamara, Miravalle, Augusto, Omidvar, Omid, Perumal, Jai, Picone, Maryann, Rao, T. Hemanth, Repovic, Pavle, Riskind, Peter, Rowe, Vernon, Sheremata, William, Steingo, Brian, Twyman, Cary, Weisman, David, Wendt, Jeanette, Wray, Sibyl, Yapundich, Robert, Zarif, Myassar, Lääketieteen ja biotieteiden tiedekunta - Faculty of Medicine and Life Sciences, Tampere University, Hauser, S. L., Bar or, A., Comi, Giancarlo, Giovannoni, G., Hartung, H. . P., Hemmer, B., Lublin, F., Montalban, X., Rammohan, K. W., Selmaj, K., Traboulsee, A., Wolinsky, J. S., Arnold, D. L., Klingelschmitt, G., Masterman, D., Fontoura, P., Belachew, S., Chin, P., Mairon, N., Garren, H., Kappos, L., Universidade do Minho, Willekens, Barbara, and OPERA I and OPERA II Clinical Investigators

Subjects
0301 basic medicine, Male, Esclerosi múltiple, Adult, Antibodies, Monoclonal, Humanized, Antigens, CD20, B-Lymphocytes, Brain, Disease Progression, Female, Humans, Immunologic Factors, Infusions, Intravenous, Interferon-beta, Magnetic Resonance Imaging, Middle Aged, Multiple Sclerosis, Relapsing-Remitting, Recurrence, Medicine (all), Relapsing-Remitting, Gastroenterology, Medicina Clínica [Ciências Médicas], law.invention, 0302 clinical medicine, Immunologic Factor, Randomized controlled trial, law, Monoclonal, Clinical endpoint, Infusions, Intravenou, Immunologia, Humanized, Hazard ratio, B-Lymphocyte, General Medicine, Settore MED/26 - Neurologia, Intravenous, Neurotieteet - Neurosciences, medicine.drug, Human, medicine.medical_specialty, Infusions, Multiple Sclerosis, Immunology, Antibodies, Multiple sclerosis, 03 medical and health sciences, Internal medicine, medicine, CD20, Antigens, Ciências Médicas::Medicina Clínica, business.industry, Interferon beta-1a, medicine.disease, Confidence interval, Ocrelizumab, Interferon Beta-1a, Relapsing Multiple Sclerosis, 030104 developmental biology, Monoclonal antibodies, Human medicine, business, Anticossos monoclonals, 030217 neurology & neurosurgery
Abstract

BACKGROUND B cells influence the pathogenesis of multiple sclerosis. Ocrelizumab is a humanized monoclonal antibody that selectively depletes CD20+ B cells. METHODS In two identical phase 3 trials, we randomly assigned 821 and 835 patients with relapsing multiple sclerosis to receive intravenous ocrelizumab at a dose of 600 mg every 24 weeks or subcutaneous interferon beta-1a at a dose of 44 mu g three times weekly for 96 weeks. The primary end point was the annualized relapse rate. RESULTS The annualized relapse rate was lower with ocrelizumab than with interferon beta-1a in trial 1 (0.16 vs. 0.29; 46% lower rate with ocrelizumab; P, info:eu-repo/semantics/publishedVersion

Published
2017

40. Anti-ribosomal-phosphoprotein autoantibodies penetrate to neuronal cells via neuronal growth associated protein, affecting neuronal cells in vitro

Author

Kivity, Shaye, primary, Shoenfeld, Yehuda, additional, Arango, Maria-Teresa, additional, Cahill, Dolores J., additional, O’Kane, Sara Louise, additional, Zusev, Margalit, additional, Slutsky, Inna, additional, Harel-Meir, Michal, additional, Chapman, Joab, additional, Matthias, Torsten, additional, and Blank, Miri, additional

Published
2016
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41. Neurological Impairment in Experimental Antiphospholipid Syndrome is Associated with increased Ligand Binding to Serotonergic 5-HT1A Receptors

Author

Frauenknecht, Katrin, Grimm, Christina, Katzav, Aviva, Chapman, Joab, and Sommer, Clemens

Subjects
ddc: 610, 610 Medical sciences, Medicine
Abstract

The antiphospholipid syndrome (APS) is an autoimmune disease where the presence of high titers of circulating autoantibodies may cause thrombosis with consecutive infarcts. In mouse models of experimental APS (eAPS), mice develop characteristic clinical manifestations which are very similar to those[for full text, please go to the a.m. URL], 57th Annual Meeting of the German Society for Neuropathology and Neuroanatomy (DGNN)

Published
2012

42. The CJD Neurological Status Scale: A New Tool for Evaluation of Disease Severity and Progression in Creutzfeldt - Jakob disease

Author

Cohen, Oren S., Prohovnik, Isak, Korczyn, Amos D., Ephraty, Lilach, Nitsan, Zeev, Tsabari, Rakefet, Appel, Shmuel, Rosenmann, Hanna, Kahana, Ester, and Chapman, Joab

Subjects
Male, Neurologic Examination, Disease Progression, Diagnostic Techniques, Neurological, Humans, Female, Middle Aged, Neuropsychological Tests, Sensitivity and Specificity, Article, Creutzfeldt-Jakob Syndrome, Aged
Abstract

To develop a scale sensitive for the neurological manifestations of Creutzfeldt-Jakob disease (CJD).A 26-item CJD neurological status scale (CJD-NS) was created based on characteristic disease manifestations. Each sign was assigned to one of eight neurological systems to calculate a total scale score (TSS) and a system involvement score (SIS). The scale was administered to 37 CJD patients, 101 healthy first-degree relatives of the patients and 14 elderly patients with Parkinson's disease (PD).The mean TSS (±SD) was significantly higher in patients with CJD (13.19 ± 5.63) compared with normal controls (0.41 ± 0.78) and PD patients (9.71 ± 3.05). The mean SIS was also significantly different between the CJD (5.19 ± 1.22) and PD (2.78 ± 1.18 P ≤ 0.01) groups reflecting the disseminated nature of neurological involvement in CJD. Using a cutoff of TSS4 yielded a sensitivity of 97% for CJD, and specificity of 100% against healthy controls. All individual items showed excellent specificity against healthy subjects, but sensitivity was highly variable. Repeat assessments of CJD patients over 3-9 months revealed a time-dependent increase in both the TSS and the SIS reflecting the scale's ability to track disease progression.The CJD-NS scale is sensitive to neurological signs and their progression in CJD patients.

Published
2011

46. Rapidly progressive Creutzfeldt-Jakob disease in patients with Familial Mediterranean Fever

Author

Appel, Shmuel A, Chapman, Joab, Kahana, Ester, Rosenmann, Hanna, Prohovnik, Isak, Pras, Elon, Reznik-Wolf, Haike, and Cohen, Oren S.

Subjects
Adult, Male, Heterozygote, Homozygote, Comorbidity, Libya, Middle Aged, Pyrin, Polymerase Chain Reaction, Article, Creutzfeldt-Jakob Syndrome, Familial Mediterranean Fever, Cytoskeletal Proteins, Jews, Mutation, Disease Progression, Humans, Female, Age of Onset
Abstract

The largest cluster of familial Creutzfeldt-Jakob disease (fCJD) exists in Jews of Libyan origin. Familial Mediterranean fever (FMF) is an inflammatory disease also common in this population.We hypothesized that FMF, as a pro-inflammatory condition, may affect the course of CJD.Three hundred and seventy-two consecutive patients diagnosed clinically and genetically as CJD were included in the study. Two hundred and thirty-six had fCJD, and 136 had sporadic disease (sCJD). Review of the patient's records revealed three patients with FMF-CJD co-morbidity. In addition, 50 DNA samples of patients with CJD were genotyped as homozygote, heterozygote, and non-carriers of the FMF mutation. The demographic and clinical variables of the groups were compared.The three patients with FMF had an earlier age of onset and significantly shorter disease duration than the patients without FMF. Heterozygote carriers did not differ in disease onset and duration from patients without FMF.The shorter disease duration of CJD patients with FMF may indicate the importance of pro-inflammatory factors in the disease.

Published
2010

47. Modeling of Cognitive Impairment by Disease Duration in Multiple Sclerosis: A Cross-Sectional Study

Author

Achiron, Anat, primary, Chapman, Joab, additional, Magalashvili, David, additional, Dolev, Mark, additional, Lavie, Mor, additional, Bercovich, Eran, additional, Polliack, Michael, additional, Doniger, Glen M., additional, Stern, Yael, additional, Khilkevich, Olga, additional, Menascu, Shay, additional, Hararai, Gil, additional, Gurevich, Micharel, additional, and Barak, Yoram, additional

Published
2013
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49. 16/6-idiotype expressing antibodies induce brain inflammation and cognitive impairment in mice: the mosaic of central nervous system involvement in lupus

Author

Kivity, Shaye, primary, Katzav, Aviva, additional, Arango, Maria Teresa, additional, Landau-Rabi, Moran, additional, Zafrir, Yaron, additional, Agmon-Levin, Nancy, additional, Blank, Miri, additional, Anaya, Juan-Manuel, additional, Mozes, Edna, additional, Chapman, Joab, additional, and Shoenfeld, Yehuda, additional

Published
2013
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50. Snord 3A: A Molecular Marker and Modulator of Prion Disease Progression

Author

Cohen, Eran, primary, Avrahami, Dana, additional, Frid, Kati, additional, Canello, Tamar, additional, Levy Lahad, Ephrat, additional, Zeligson, Sharon, additional, Perlberg, Shira, additional, Chapman, Joab, additional, Cohen, Oren S., additional, Kahana, Esther, additional, Lavon, Iris, additional, and Gabizon, Ruth, additional

Published
2013
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