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5. Identification of sixteen novel candidate genes for late onset Parkinson's disease

Author

Gialluisi, A, Reccia, MG, Modugno, N, Nutile, T, Lombardi, A, Di Giovannantonio, LG, Pietracupa, S, Ruggiero, D, Scala, S, Gambardella, S, Iacoviello, L, Gianfrancesco, F, Acampora, D, D'Esposito, M, Simeone, A, Ciullo, M, Esposito, T, Kulisevsky J., Pagonabarraga J., and Int Parkinsons Dis Genomics Consor

Subjects
Rare variant burden analysis, Whole exome sequencing, Novel candidate genes for Parkinson's disease, Late onset Parkinson's disease
Abstract

Background Parkinson's disease (PD) is a neurodegenerative movement disorder affecting 1-5% of the general population for which neither effective cure nor early diagnostic tools are available that could tackle the pathology in the early phase. Here we report a multi-stage procedure to identify candidate genes likely involved in the etiopathogenesis of PD. Methods The study includes a discovery stage based on the analysis of whole exome data from 26 dominant late onset PD families, a validation analysis performed on 1542 independent PD patients and 706 controls from different cohorts and the assessment of polygenic variants load in the Italian cohort (394 unrelated patients and 203 controls). Results Family-based approach identified 28 disrupting variants in 26 candidate genes for PD including PARK2, PINK1, DJ-1(PARK7), LRRK2, HTRA2, FBXO7, EIF4G1, DNAJC6, DNAJC13, SNCAIP, AIMP2, CHMP1A, GIPC1, HMOX2, HSPA8, IMMT, KIF21B, KIF24, MAN2C1, RHOT2, SLC25A39, SPTBN1, TMEM175, TOMM22, TVP23A and ZSCAN21. Sixteen of them have not been associated to PD before, were expressed in mesencephalon and were involved in pathways potentially deregulated in PD. Mutation analysis in independent cohorts disclosed a significant excess of highly deleterious variants in cases (p = 0.0001), supporting their role in PD. Moreover, we demonstrated that the co-inheritance of multiple rare variants (>= 2) in the 26 genes may predict PD occurrence in about 20% of patients, both familial and sporadic cases, with high specificity (> 93%; p = 4.4 x 10(- 5)). Moreover, our data highlight the fact that the genetic landmarks of late onset PD does not systematically differ between sporadic and familial forms, especially in the case of small nuclear families and underline the importance of rare variants in the genetics of sporadic PD. Furthermore, patients carrying multiple rare variants showed higher risk of manifesting dyskinesia induced by levodopa treatment. Conclusions Besides confirming the extreme genetic heterogeneity of PD, these data provide novel insights into the genetic of the disease and may be relevant for its prediction, diagnosis and treatment.

Published
2021

6. Identification of sixteen novel candidate genes for late onset Parkinson's disease

Author

Gialluisi, Alessandro, Reccia, Mafalda Giovanna, Modugno, Nicola, Nutile, Teresa, Lombardi, Alessia, Di Giovannantonio, Luca Giovanni, Pietracupa, Sara, Ruggiero, Daniela, Scala, Simona, Gambardella, Stefano, Noyce, Alastair J., Kaiyrzhanov, Rauan, Middlehurst, Ben, Kia, Demis A., Tan, Manuela, Houlden, Henry, Morris, Huw R., Plun-Favreau, Helen, Holmans, Peter, Hardy, John, Trabzuni, Daniah, Quinn, John, Bubb, Vivien, Mok, Kin Y., Kinghorn, Kerri J., Billingsley, Kimberley, Wood, Nicholas W., Lewis, Patrick, Schreglmann, Sebastian, Lovering, Rruth, R'Bibo, Lea, Manzoni, Claudia, Rizig, Mie, Ryten, Mina, Guelfi, Sebastian, Escott-Price, Valentina, Chelban, Viorica, Foltynie, Thomas, Williams, Nigel, Morrison, Karen E., Clarke, Carl, Brice, Alexis, Danjou, Fabrice, Lesage, Suzanne, Corvol, Jean-Christophe, Martinez, Maria, Schulte, Claudia, Brockmann, Kathrin, Simón-Sánchez, Javier, Heutink, Peter, Rizzu, Patrizia, Sharma, Manu, Gasser, Thomas, Cookson, Mark R., Bandres-Ciga, Sara, Blauwendraat, Cornelis, Craig, David W., Narendra, Derek, Faghri, Faraz, Gibbs, J.Raphael, Hernandez, Dena G., Van Keuren-Jensen, Kendall, Shulman, Joshua M., Iwaki, Hirotaka, Leonard, Hampton L., Nalls, Mike A., Robak, Laurie, Bras, Jose, Guerreiro, Rita, Lubbe, Steven, Finkbeiner, Steven, Mencacci, Niccolo E., Lungu, Codrin, Singleton, Andrew B., Scholz, Sonja W., Reed, Xylena, Alcalay, Roy N., Gan-Or, Zin, Rouleau, Guy A., Krohn, Lynne, van Hilten, Jacobus J., Marinus, Johan, Adarmes-Gómez, A.D, Aguilar Barberà, Miquel, Alvarez, Ignacio, Alvarez, Victoria, Barrero, Francisco Javier, Bergareche Yarza, Jesús Alberto, Bernal-Bernal, Inmaculada, Blazquez, Marta, Bonilla-Toribio, Marta, Botía, Juan A., Boungiorno, María Teresa, Buiza-Rueda, Dolores, Carrillo, Fátima, Carrión-Claro, M, Cerdan, Debora, Clarimón, Jordi, Compta, Yaroslau, Diez-Fairen, Monica, Dols Icardo, Oriol, Duarte, Jacinto, Duran, Raquel, Escamilla Sevilla, Francisco, Ezquerra, Mario, Feliz, Cici, Fernández, Manel, Fernández-Santiago, Rubén, Garcia, Ciara, García-Ruiz, Pedro, Gómez-Garre, Pilar, Gomez Heredia, Maria Jose, Gonzalez-Aramburu, Isabel, Gorostidi Pagola, Ana, Hoenicka, Janet, Infante, Jon, Jesús, Silvia, Jimenez-Escrig, Adriano, Kulisevsky, Jaime, Labrador-Espinosa, Miguel A., Lopez-Sendon, Jose Luis, López de Munain Arregui, Adolfo, Macias, Daniel, Martínez Torres, Irene, Marín, Juan, Marti, Maria Jose, Martínez-Castrillo, Juan Carlos, Méndez-del-Barrio, Carlota, Menéndez González, Manuel, Mata, Marina, Mínguez, Adolfo, Mir, Pablo, Mondragon Rezola, Elisabet, Muñoz, Esteban, Pagonabarraga Mora, Javier, Pastor, Pau, Perez Errazquin, Francisco, Periñán-Tocino, Teresa, Ruiz-Martínez, Javier, Ruz, Clara, Sanchez Rodriguez, Antonio, Sierra, María, Suarez-Sanmartin, Esther, Tabernero, Cesar, Tartari, Juan Pablo, Tejera-Parrado, Cristina, Tolosa, Eduard, Valldeoriola, Francesc, Vargas-González, Laura, Vela, Lydia, Vives, Francisco, Zimprich, Alexander, Pihlstrom, Lasse, Toft, Mathias, Koks, Sulev, Taba, Pille, Hassin-Baer, Sharon, Majamaa, Kari, Siitonen, Ari, Okubadejo, Njideka U., Ojo, Oluwadamilola O., Shashkin, Chingiz, Zharkynbekova, Nazira, Akhmetzhanov, Vadim, Aitkulova, Akbota, Zholdybayeva, Elena, Zharmukhanov, Zharkyn, Kaishybayeva, Gulnaz, Karimova, Altynay, Sadykova, Dinara, Iacoviello, Licia, Gianfrancesco, F., Acampora, D., D'Esposito, M., Simeone, A., Ciullo, M., Esposito, T., and Universidad de Cantabria

Subjects
0301 basic medicine, Male, Aging, Candidate gene, Parkinson's disease, Neurodegenerative, Bioinformatics, 0302 clinical medicine, Late onset Parkinson’s disease, Novel candidate genes for Parkinson’s disease, Rare variant burden analysis, Whole exome sequencing, Adult, Age of Onset, Aged, Female, Genetic Predisposition to Disease, Humans, Middle Aged, Parkinson Disease, Pedigree, Whole Exome Sequencing, 2.1 Biological and endogenous factors, Medicine, Novel candidate genes for Parkinson's disease, Aetiology, Exome, Exome sequencing, screening and diagnosis, education.field_of_study, Parkinson's Disease, LRRK2, International Parkinson’s Disease Genomics Consortium, Detection, Neurological, Late onset Parkinson's disease, 4.2 Evaluation of markers and technologies, Research Article, Clinical Sciences, Population, 03 medical and health sciences, Cellular and Molecular Neuroscience, Clinical Research, Exome Sequencing, Genetics, RC346-429, education, Molecular Biology, Neurology & Neurosurgery, business.industry, Genetic heterogeneity, Prevention, RC952-954.6, Neurosciences, PARK7, medicine.disease, Brain Disorders, 030104 developmental biology, Geriatrics, Neurology. Diseases of the nervous system, Neurology (clinical), business, 030217 neurology & neurosurgery
Abstract

Background Parkinson’s disease (PD) is a neurodegenerative movement disorder affecting 1–5% of the general population for which neither effective cure nor early diagnostic tools are available that could tackle the pathology in the early phase. Here we report a multi-stage procedure to identify candidate genes likely involved in the etiopathogenesis of PD. Methods The study includes a discovery stage based on the analysis of whole exome data from 26 dominant late onset PD families, a validation analysis performed on 1542 independent PD patients and 706 controls from different cohorts and the assessment of polygenic variants load in the Italian cohort (394 unrelated patients and 203 controls). Results Family-based approach identified 28 disrupting variants in 26 candidate genes for PD including PARK2, PINK1, DJ-1(PARK7), LRRK2, HTRA2, FBXO7, EIF4G1, DNAJC6, DNAJC13, SNCAIP, AIMP2, CHMP1A, GIPC1, HMOX2, HSPA8, IMMT, KIF21B, KIF24, MAN2C1, RHOT2, SLC25A39, SPTBN1, TMEM175, TOMM22, TVP23A and ZSCAN21. Sixteen of them have not been associated to PD before, were expressed in mesencephalon and were involved in pathways potentially deregulated in PD. Mutation analysis in independent cohorts disclosed a significant excess of highly deleterious variants in cases (p = 0.0001), supporting their role in PD. Moreover, we demonstrated that the co-inheritance of multiple rare variants (≥ 2) in the 26 genes may predict PD occurrence in about 20% of patients, both familial and sporadic cases, with high specificity (> 93%; p = 4.4 × 10− 5). Moreover, our data highlight the fact that the genetic landmarks of late onset PD does not systematically differ between sporadic and familial forms, especially in the case of small nuclear families and underline the importance of rare variants in the genetics of sporadic PD. Furthermore, patients carrying multiple rare variants showed higher risk of manifesting dyskinesia induced by levodopa treatment. Conclusions Besides confirming the extreme genetic heterogeneity of PD, these data provide novel insights into the genetic of the disease and may be relevant for its prediction, diagnosis and treatment.

Published
2021
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8. Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

Author

Ridker PM, Everett BM, Thuren T, MacFadyen JG, Chang WH, Ballantyne C, Fonseca F, Nicolau J, Koenig W, Anker SD, Kastelein JJP, Cornel JH, Pais P, Pella D, Genest J, Cifkova R, Lorenzatti A, Forster T, Kobalava Z, Vida-Simiti L, Flather M, Shimokawa H, Ogawa H, Dellborg M, Rossi PRF, Troquay RPT, Libby P, Glynn RJ, Novo S, Krum H, Varigos J, Siostrzonek P, Sinnaeve P, Gotcheva N, Yong H, Urina-Triana M, Milicic D, Vettus R, Manolis AJ, Wyss F, Sigurdsson A, Fucili A, Veze I, Petrauskiene B, Salvador L, Klemsdal TO, Medina F, Budaj A, Otasevic P, Lainscak M, Seung KB, Commerford P, Donath M, Hwang JJ, Kultursay H, Bilazarian S, East C, Forgosh L, Harris B, Ligueros M, Bohula E, Charmarthi B, Cheng S, Chou S, Danik J, McMahon G, Maron B, Ning M, Olenchock B, Pande R, Perlstein T, Pradhan A, Rost N, Singhal A, Taqueti V, Wei N, Burris H, Cioffi A, Dalseg AM, Ghosh N, Gralow J, Mayer T, Rugo H, Fowler V, Limaye AP, Cosgrove S, Levine D, Lopes R, Scott J, Hilkert R, Tamesby G, Mickel C, Manning B, Woelcke J, Tan M, Manfreda S, Ponce T, Kam J, Saini R, Banker K, Salko T, Nandy P, Tawfik R, O’Neil G, Manne S, Jirvankar P, Lal S, Nema D, Jose J, Collins R, Bailey K, Blumenthal R, Colhoun H, Gersh B, Abreu M, Actis MV, Aiub J, Aiub F, Albisu J, Alvarisqueta A, Avalos V, Barreto M, Berli MA, Blumberg C, Bocanera M, Botta C, Bowen L, Budassi N, Buhlman S, Westberg JC, Carabajal T, Caruso G, Casala J, Cendali G, Coloma G, Berra FC, Cuneo C, Degennaro N, Dellasa M, Diaz M, Dos Santos P, Espinosa V, Facello A, Facello M, Farias E, Fernandez AA, Ferrari V, Pacora FF, Flores GS, Franco M, Gabito A, Viola HG, Garcia F, Garcia Duran R, Garcia Pinna J, Glenny J, Godoy Sanchez M, Grosse A, Guzman P, Hasbani E, Hominal M, Ibañez J, Jure H, Jure D, Vico ML, Liniado G, Luciardi H, Luquez H, Maehara G, Maffei L, Majul C, Mallagray M, Marinaro S, Martinez J, Massaccesi R, De Los Milagros Had M, Azize GM, Montana O, Montenegro E, Morell Y, Muntaner J, Navarrete S, Olmedo M, Paganini M, Paz S, Perez Manghi F, Piskorz D, Polato C, Recoaro R, Romano A, Salinger M, Sanchez A, Saravia MA, Sarjanovich R, Scaro G, Schiavi LB, Soler J, Tinnirello V, Tomassi A, Valle M, Vallejo MA, Venturini C, Marcela Wenetz LM, Yossen M, Zaidman C, Zalazar L, Zangroniz P, Amerena J, Brady L, Colquhoun D, Eccleston D, Ferreira-Jardim A, French J, Jayasinghe R, Mcintosh C, Ord M, Plotz M, Purnell P, Roberts-Thomson P, Schultz C, Shanahan T, Tan R, Taverner P, Turner F, Vibert J, Vorster M, William M, Youssef G, Bergler-Klein J, Brath H, Brodmann M, Fliesser-Goerzer E, Haider K, Heeren G, Hiden C, Mandic L, Paulweber B, Ploechl A, Prenner A, Steringer-Mascherbauer R, Strohner-Kaestenbauer H, Barbato E, Bouvy C, Briké C, Charlier F, Cools F, De Knijf K, De Wolf L, Delforge M, Deweerdt N, Gits F, Goffinet C, Hermans K, Hollanders G, Mestdagh I, Pirenne B, Servaes V, Simons N, Tahon S, Theunissen E, Van Genechten G, Vervoort G, Vissers C, Vranckx P, Vrolix M, Abib E Jr, Abrantes J, Araujo Fonseca M, Barbosa E, Barroso W, Barroso A, Bodanese L, Botelho R, Costa Amorim R, Da Costa F, Da Silva A, Da Silva O Jr, Da Silva D Jr, Ferreira Dos Santos T, Dos Santos F, Dos Santos A, Duda N, Feitosa G, Felario Junior GA, Ferraz R, Filho P, Fonseca A, Wanderley FF, Freitas E, Fucci F, Marengo Garcia De Carvalho L, Hernandez M, Hettwer Magedanz E, Julião K, Kormann A, Lameira A, Lima F, Lino E, Maia L, Manenti E, Marchi AL, Fischer SM, Michalaros Y, Moraes J Jr, Moreira L, Pagnan M, Pesce F, Pinheiro L, Rassi S, Reis G, Reis H, Resende I, Roel A, Ruschel K, Saporito W, Saraiva JF, Seroqui M, Silva R, Unterkircher B, Vicente C, Vieira N, Xavier JP, Zucchetti C, Angelova I, Dimitrov G, Genova D, Gospodinov K, Goudev A, Grigorova V, Hristova K, Makedonska JJ, Katova T, Kostov K, Lazov P, Manov E, Manukov I, Manukov D, Milanova M, Kabakchieva VM, Petrov D, Petrusheva T, Pramatarova I, Raev D, Runev N, Sirakova-Taseva A, Tisheva-Gospodinova S, Todorova A, Tzekova M, Yakovova S, Yanev T, 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L, Sang X, Song M, Sun Z, Wang J, Wang Y, Wei J, Wu W, Wu J, Xu H, Yan J, Yang P, Yang K, Yao Z, Yaoqing H, Yuan Z, Zhai Z, Zhang J, Zhang Y, Zhao R, Zhou H, Accini Mendoza JL, Aparicio CV, Castillo T, Chaverra I, Conrado Y, Coronel J, Cotes C, Cuentas I, Cuervo A, Dussan MA, Echeverria L, Hernandez E, Ibarra J, Isaza D, Jimenez D, Lopez P, Manzur F, Mejia I, Mendoza Y, Molina DI, Patino JM, Rodriguez D, Rodriguez LM, Rodriguez SM, Sanchez Vallejo G, Luz Serrano H, Sotomayor A, Urina M, Vesga B, Yupanqui H, Akrap B, Busic N, Ciglenecki N, Cmrecnjak J, Fucak E, Gabor M, Jeric M, Jutrisa N, Kordic K, Planinc I, Popovic Z, Radeljic V, Sesto I, Sutalo K, Tusek S, Belohlavek J, Budkova J, Busak L, Capova L, Cech V, Cermak O, Coufalova Z, Cyprian R, Dedek V, Dedkova S, Ferkl R, Hanak P, Hanustiakova A, Homza M, Horackova K, Houra M, Iveta H, Kaiserova L, Kala P, Karel I, Kellnerova I, Koleckar P, Kreckova M, Krupicka J, Lorenc Z, Machova V, Malik J, Masarikova L, Matyasek I, Mikus M, 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Korth-Wiemann B, Krapivsky A, Kuenzler J, Kuntzsch A, Landers B, Lappo M, Laube S, Leggewie S, Lehmann D, Lepp H, Lierse T, Lindner C, Luecke-Uzar M, Luedemann J, Marschke T, Maruzzo S, Mauersberger K, Maus O, Meinrich M, Meissner A, Moehring B, Muehlhaus J, Mueller S, Muenter KC, Muenzel T, Naumann R, Nebel J, Neumann J, Nuding S, Overhoff U, Papke B, Pencz I, Peter Y, Peukert AM, Radde I, Rau T, Regner S, Reichenbach D, Reimer D, Rinke A, Roettges R, Romanski A, Rummel R, Samer H, Sanuri M, Sarnighausen HE, Schäfer B, Scheibner T, Schermaul KH, Schindler A, Schlundt C, Schmidt E, Schmidt K, Schnabel A, Schoen N, Schorn K, Schroeder T, Schulenburg D, Schulz M, Schulze U, Schulze J, Schumacher M, Schwerin G, Schwerin M, Stadelmeier S, Stahl HD, Stahl A, Stockhausen J, Stockhausen G, Stoessel J, Stolze K, Stratmann M, Szymanowski N, Teschner AB, Teske A, Uecker C, Veit S, Voeller H, Walter I, Walter J, Walther I, Weber HG, Weimer J, Wichterich K, Wiebusch A, Willmerdinger M, Willner C, Winkelmann B, Winkler J, Wistuba T, Woehrle J, Wohnlich T, Wolf S, Woyczak D, Wrage P, Zirlik A, Anadiotis A, Chachalis G, Dermitzakis A, Kafarakis P, Kaldara E, Kolokathis F, Kostakou P, Lekakis J, Manolis A, Mantas I, Megalou A, Milkas A, Nanas J, Olympios CD, Patsilinakos S, Perperis A, Poulimenos L, Saloustros I, Tsioufis K, Tsorbatzoglou K, Vardas P, Zarifis I, Aguilar M, Arango JL, Borrayo NA, Corona V, Guerrero A, Guzman I, Haase F, De Krumbach L, Montenegro P, Munoz R, Munoz N, Paniagua A, Solares A, Vogel M, Anita S, Blazsek Z, Decsi K, Fulop T, Hangyal T, Hegedus V, Kalina A, Karakai H, Katona A, Kiss RG, Kovacs A, Laszlo Z, Lupkovics G, Medvegy M, Merkely B, Mihaly N, Nagy AC, Dékány JN, Nikoletta P, Noori E, Penzes J, Poor F, Sarszegi Z, Simay A, Simon J, Szakal I, Szatmarine V, Szocs A, Zilahi Z, Karsai XZ, Andersen K, Sigurdadottir E, Skuladottir F, Abdullakutty J, Abhaichand R, Abhyankar A, Agarwal DK, Aggarwal RK, Ahire N, Awasthi AK, Babu R, Bai A, Bali HK, Banker D, Bhadade S, Bisne V, Bohra P, Raghu C, Chauhan D, Chauhan H, Chavada J, Chaware G, Chella S, Chintala P, Dash D, Desai D, Devasia T, Dhanak R, Dobariya H, Dudhatra N, Duhan S, Fulwani M, Ghondale N, Ghosh S, Gohel P, Govindaraj D, Goyal B, Goyal S, Gundala AK, Gupta M, Hardas S, Iby M, Jagtap P, Jain A, Joshi U, Karpuram M, Kaur H, Khan A, Khan R, Kodem DR, Koeitti P, Kulkarni L, Kullal P, Kumar KS, Kumbla M, Latheef K, Lohkare M, Santosh MJ, Makhe B, Mandati M, Mehta A, Minocha G, Mittal A, Modi R, Mohan K, Oomman A, Pai R, Pai V, Palaniswami N, Pansheriya A, Parekh N, Patel J, Patel R, Patole T, Praveen M, Radhakrishnan V, Rajan B A, Rajasekhar D, Rao M, Rao MB, Rao NM, Rathnavel S, Rathore A, Rathore SRS, Rawat S, Reddy NC, Sarma R, Sathe S, Shah J, Shaikh P, Sharma K, Sharma S, Sharma T, Shetty P, Sidhu G, Singh V, Sohi GS, Srinath VS, Raju SS, Taran A, Thakkar B, Velusamy K, Vijan V, Vora V, Vuriya AK, Agosta GF, Antonicelli R, Ardissino D, Argiolas G, Baldin MG, Benedetti G, Berti 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M., Everett, B. M., Thuren, T., Macfadyen, J. G., Chang, W. H., Ballantyne, C., FONSECA E PIRES, CARLOS EDUARDO, Nicolau, J., Koenig, W., Anker, S. D., Kastelein, J. J. P., Cornel, J. H., Pais, P., Pella, D., Genest, J., Cifkova, R., Lorenzatti, A., Forster, T., Kobalava, Z., Vida-Simiti, L., Flather, M., Shimokawa, H., Ogawa, H., Dellborg, M., Rossi, P. R. F., Troquay, R. P. T., Libby, P., Glynn R., J, CANTOS Trial, Group, Perrone, Filardi, P, ACS - Amsterdam Cardiovascular Sciences, Vascular Medicine, ACS - Pulmonary hypertension & thrombosis, and ACS - Atherosclerosis & ischemic syndromes

Subjects
0301 basic medicine, 030204 cardiovascular system & hematology, law.invention, 0302 clinical medicine, c-reactive protein, Randomized controlled trial, law, Cardiovascular Disease, middle aged, double-blind method, antibodies, Myocardial infarction, humans, Stroke, interleukin-1beta, biology, Antibodies, Monoclonal, drug, General Medicine, Lipid, Aged, anti-inflammatory agents, monoclonal, humanized, atherosclerosis, cardiovascular diseases, dose-response relationship, female, incidence, infections, lipids, male, myocardial infarction, neutropenia, secondary prevention, stroke, Anti-Inflammatory Agent, aged, Editorial, Atherosclerosi, Monoclonal, Human, medicine.drug, medicine.medical_specialty, Neutropenia, Antibodies, Monoclonal, Humanized, Infections, Placebo, antibodies, monoclonal, dose-response relationship, drug, infection, medicine (all), 03 medical and health sciences, Internal medicine, medicine, Dose-Response Relationship, Drug, business.industry, Antiinflammatory Therapy, Canakinumab, for Atherosclerotic Disease, C-reactive protein, medicine.disease, Surgery, Canakinumab, 030104 developmental biology, biology.protein, business
Abstract

Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.)

Published
2017
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13. The brain transcription factor OTX1 is activated in specific non-hodgkin lymphoma subtypes and normally expressed in a germinal center-restricted small subpopulation of CD138(+) plasmacell-like cells

Author

Russo F, Omodiei D, Acampora D, De Filippi R, Severino V, Di Francia R, Frigeri F, Mancuso P, De Chiafa A, Casola S, Pinto A, Simeone A, Casola S., FRANCO, Renato, Russo, F, Omodiei, D, Acampora, D, De Filippi, R, Severino, V, Di Francia, R, Frigeri, F, Mancuso, P, De Chiafa, A, Franco, Renato, Casola, S, Pinto, A, Simeone, A, and Casola, S.

Published
2007

15. The role of Otx genes in progenitor domains of ventral midbrain

Author

Simeone A, Puelles E, Acampora D, Omodei D, Mancuso P, and Giovanni Di Giovannantonio L

Subjects
OTX2
Abstract

The mesencephalic dopaminergic (mesDA) neurons play a relevant role in the control of movement, behaviour and cognition. Indeed loss and/or abnormal development of mesDA neurons is responsible for Parkinson's disease as well as for addictive and psychiatric disorders. A wealth of information has been provided on gene functions involved in the molecular mechanism controlling identity, face and survival of mesDA neurons. Collectively, these studies are contributing to a growing knowledge of the genetic networks required for proper mesDA development, thus disclosing new perspectives for therapeutic approaches of mesDA disorders. Here we will focus on the control exerted by Otx genes in early decisions regulating the differentiation of progenitors located in the ventral midbrain. In this context, the regulatory network involving Otx functional interactions with signalling molecules and transcription factors required to promote or prevent the development of mesDA neurons will be analyzed in derail.

Published
2009

16. Unsuspected role of the brain morphogenetic gene Otx1 in hematopoiesis

Author

Levantini, E., Giorgetti, A., Cerisoli, F., Traggiai, E., Alessandra Guidi, Martin, R., Acampora, D., Aplan, Pd, Keller, G., Simeone, A., Iscove, Nn, Hoang, T., and Magli, M. C.

Subjects
ematopoiesi, Physiology, hemic and lymphatic diseases, Hematopoesi, Factors de transcripció, cellule staminali, Transcription factors, Fisiologia, omeogeni, Hematopoiesis
Abstract

Otx1 belongs to the paired class of homeobox genes and plays a pivotal role in brain development. Here, we show that Otx1 is expressed in hematopoietic pluripotent and erythroid progenitor cells. Moreover, bone marrow cells from mice lacking Otx1 exhibit a cell-autonomous impairment of the erythroid compartment. In agreement with these results, molecular analysis revealed decreased levels of erythroid genes that include the SCL and GATA-1 transcription factors. Accordingly, a gain of function of SCL rescues the erythroid deficiency in Otx1-/- mice. Taken together, our findings indicate a function for Otx1 in the regulation of blood cell production. There is growing evidence suggesting that common cellular and molecular mechanisms orchestrate differentiation in various tissues. Homeobox-containing genes seem to be strong candidate genes to regulate a number of developmental processes, including neurogenesis and hematopoiesis. Members of the Otx family (Otx1, Otx2, Otx3, and Crx) are the vertebrate homologues of the Drosophila head gap gene orthodenticle and encode transcription factors containing a bicoid-like homeodomain. They are temporally and spatially regulated during development and seem to be required for proper head and sense organ patterning. Otx1, Otx2, and Otx3 show partially overlapping, but distinct expression patterns, and Otx2, the first to be activated during development, plays a major role in gastrulation and in the early specification of the anterior neural plate. In contrast, Otx1 shows a later onset and is involved in corticogenesis, sense organ development, and pituitary function. Mice bearing targeted deletion of Otx1 are affected by a permanent epileptic phenotype and show multiple brain abnormalities and morphological defects of the acoustic and visual sense organs. In addition, at the prepubescent stage, they exhibit transient dwarfism and hypogonadism because of low levels of pituitary hormones. In the present study, we have investigated whether Otx1 also plays a role in blood cell production, as several homeobox genes of different families are involved in normal and/or malignant hematopoiesis.

Published
2003

17. OTX1 compensates for OTX2 requirement in regionalisation of anterior neuroectoderm

Author

Acampora D, Annino A, Puelles E, Alfano I, Tuorto F, and Simeone A

Abstract

Otx genes play a relevant role in specification, maintenance and patterning of anterior neuroectoderm. OTX1 and OTX2 proteins share extensive codogenic similarity even though in OTX1 these regions of homology are separated by stretches of amino acid insertions. From 1 to 3 somites stage onwards, Otx1 and Otx2 are largely coexpressed, but only Otx2 is expressed during gastrulation. To determine whether OTX1 and OTX2 gene products share common biochemical properties, mouse models replacing Otx1 with Otx2 and vice versa have been generated. These studies have indicated a remarkable functional equivalence between the two proteins. Nevertheless, it was still debated whether OTX1 is functionally equivalent to OTX2 in early anterior neuroectoderm. To address this issue we generated a new mouse model (hOtx1 2FL) replacing only the coding sequence and introns of Otx2 with the human Otx1 codogenic sequence. hOtx1 2FL/2FL and hOtx1 2FL/2 mice were viable, fertile and exhibited an apparently normal behaviour. hOtx1 mRNA was correctly transcribed under the Otx2 transcriptional control and, similarly, the hOTX1 protein was properly distributed and quantitatively very similar if not identical to that of OTX2. Patterning and regionalisation of forebrain and midbrain were unaffected as revealed by the expression of diagnostic genes which are highly sensitive to reduction of OTX proteins, such as Fgf8, Pax2 and Gbx2.

Published
2003

19. The paired-type homeobox gene Dmbx1 marks the midbrain and pretectum

Author

Gogoi R., Schubert F., Martinez-Barbera J., Acampora D, Simeone A., and Lumsden A.

Subjects
animal structures, embryonic structures
Abstract

We have isolated a paired-type homeobox gene Dmbx1, previously known as Atx (Development 128 (2001) 4789), from chick and mouse. Sequence similarity reveals that this gene is highly related to the Otx genes. Expression of Dmbx1 commences during gastrulation, when transcripts are detected in a crescent around the anterior neural plate. As development progresses, Dmbx1 marks the prospective midbrain and pretectum. Dmbx1 shares its caudal border of expression with Otx2, while expression is sharply delimited rostrally by the synencephalic-parencephalic boundary, later becoming restricted to the posterior synencephalon. At later stages, Dmbx1 is expressed in dynamic domains of the hindbrain and spinal cord. Additional sites of expression comprise stomodeal ectoderm and foregut endoderm, presomitic mesoderm, and the nasal pit.

Published
2002

20. The Otx family

Author

Simeone A., Puelles E., and Acampora D

Subjects
brain evolution, IsO positioning, brain patterning, gastrulation, Otx regulatory contro
Abstract

Otx1 and Otx2, the murine homologs of the Drosophila orthodenticle gene, play a remarkable role in specification and regionalization of forebrain and midbrain. Recently, genetic approaches have indicated that OTD, OTX1 and OTX2 have retained reciprocal functional equivalence in evolution, whereas their regulatory control has been remarkably modified. This suggests that during the evolution of the vertebrate brain, regulatory changes modulating the transcriptional and translational control of pre-existing gene functions might have favored the establishment of new morphogenetic pathways.

Published
2002

21. The role of Otx2 in organizing the anterior patterning in mouse

Author

Simeone A and Acampora D.

Subjects
Embryonic Induction, Homeodomain Proteins, Mice, Knockout, animal structures, Otx Transcription Factors, Brain, Gene Expression Regulation, Developmental, Nerve Tissue Proteins, Biological Evolution, Mice, embryonic structures, Trans-Activators, Animals, Drosophila, RNA, Messenger, Body Patterning
Abstract

Understanding the molecular mechanism controlling induction and maintenance of signals required for specifying anterior territory (forebrain and midbrain) of the central nervous system is a major task of molecular embryology. The current view indicates that in mouse, early specification of the anterior patterning is established at the beginning of gastrulation by the anterior visceral endoderm, while maintenance and refinement of the early specification is under the control of epiblast-derived tissues corresponding to the axial mesendoderm and rostral neuroectoderm. In vertebrates a remarkable amount of data has been collected on the role of genes contributing to brain morphogenesis. Among these genes,the orthodenticle group is defined by the Drosophila orthodenticle and the vertebrate Otx1 and Otx2 genes, which contain a bicoid-like homeodomain. Mouse models and chimera experiments have provided strong evidence that Otx2 plays an important role in the specification and maintenance of the rostral neuroectoderm destined to become forebrain and midbrain. in evolutionary terms, some of these findings lead us to hypothesize a fascinating and crucial contribution of the Otx genes to the genetic program underlying the establishment of the mammalian brain.

Published
2001

22. Mutant p63 causes defective expansion of ectodermal progenitor cells and impaired FGF signalling in AEC syndrome

Author

Ferone, G., Thomason, H.A., Antonini, D., Rosa, L. De, Hu, B., Gemei, M., Zhou, Huiqing, Ambrosio, R., Rice, D.P., Acampora, D., Bokhoven, H. van, Vecchio, L. Del, Koster, M.I., Tadini, G., Spencer-Dene, B., Dixon, M., Dixon, J., Missero, C., Ferone, G., Thomason, H.A., Antonini, D., Rosa, L. De, Hu, B., Gemei, M., Zhou, Huiqing, Ambrosio, R., Rice, D.P., Acampora, D., Bokhoven, H. van, Vecchio, L. Del, Koster, M.I., Tadini, G., Spencer-Dene, B., Dixon, M., Dixon, J., and Missero, C.

Abstract

Contains fulltext : 93977.pdf (publisher's version ) (Open Access)

Published
2012

30. The proto-oncogene RON is involved in development of epithelial, bone and neuro-endocrine tissues

Author

Gaudino, G., Avantaggiato, V., Follenzi, A., Acampora, D., Antonio Simeone, and Comoglio, P. M.

Subjects
Bone Development, Base Sequence, Transcription, Genetic, Molecular Sequence Data, Receptor Protein-Tyrosine Kinases, Receptors, Cell Surface, Proto-Oncogene Proteins c-met, Neurosecretory Systems, Proto-Oncogene Mas, Epithelium, Mice, Inbred C57BL, Mice, Proto-Oncogenes, Animals, Humans, Female, RNA, Messenger, Cloning, Molecular
Abstract

We previously showed that the proto-oncogene RON encodes the tyrosine kinase receptor for Macrophage Stimulating Protein (MSP), originally isolated as a chemotactic factor for peritoneal macrophages. To elucidate the biological role of MSP we studied the expression of the Ron receptor in vivo, and the response to the factor in vitro. RON specific transcripts were detectable in mouse liver from early embryonal life (day 12.5 p.c.) through adult life. Adrenal gland, spinal ganglia, skin, lung and--unexpectedly--ossification centers of developing mandible, clavicle and ribs were also positive at later stages (day 13.5-16.5 p.c.). From day 17.5 RON was expressed in the gut epithelium and in a specific area of the central nervous system, corresponding to the nucleus of the hypoglossus. In adult mouse tissues RON transcripts were observed in brain, adrenal glands, gastro-intestinal tract, testis and kidney. Epithelial, osteoclast-like and neuroendocrine cells express the Ron receptor and respond to MSP in vitro. In the neuroendocrine PC12 cell line, while NGF induced growth arrest and morphological differentiation, MSP behaved as a strong mitogen. These findings show that the Ron receptor and its ligand are involved in the development of epithelial tissues, bones, and neuroendocrine derivatives driving cells towards the proliferation program.

Published
1995

31. Cloning and characterization of two members of the vertebrate Dlx gene family

Author

Simeone, A., Acampora, D., Pannese, M., D Esposito, M., Stornaiuolo, A., Massimo GULISANO, Mallamaci, A., Kastury, K., Druck, T., Huebner, K., and Boncinelli, E.

Subjects
Molecular Sequence Data, Restriction Mapping, Locus (genetics), Settore BIO/11 - Biologia Molecolare, Biology, Development, Mice, Gene mapping, Animals, Humans, Homeobox, Amino Acid Sequence, Cloning, Molecular, DLX gene family, In Situ Hybridization, Fluorescence, Genetics, Multidisciplinary, Sequence Homology, Amino Acid, Chromosome localization, Genes, Homeobox, Proteins, Brain, DLX6, DLX5, Cartilage, Multigene Family, embryonic structures, Gene expression, Homeotic gene, Research Article
Abstract

A number of vertebrate genes of the Dlx gene family have been cloned in mouse, frog, and zebrafish. These genes contain a homeobox related to that of Distalless, a gene expressed in the developing head and limbs of Drosophila embryos. We cloned and studied the expression of two members of this family, which we named Dlx5 and Dlx6, in human and mouse. The two human genes, DLX5 and DLX6, are closely linked in an inverted convergent configuration in a region of chromosome 7, at 7q22. Similarly, the two human genes DLX1 and DLX2 are closely linked in a convergent configuration at 2q32, near the HOXD (previously HOX4) locus. In situ hybridization experiments in mouse embryos revealed expression of Dlx5 and Dlx6 mRNA in restricted regions of ventral diencephalon and basal telencephalon, with a distribution very similar to that reported for Dlx1 and Dlx2 mRNA. A surprising feature of Dlx5 and Dlx6 is that they are also expressed in all skeletal structures of midgestation embryos after the first cartilage formation. The expression pattern of these genes, together with their chromosome localization, may provide useful cues for the study of congenital disorders in which there is a combination of craniofacial and limb defects.

Published
1994

33. Morphological organization of somatosensory cortex in Otx1(-/-) mice

Author

Cipelletti, B, Avanzini, G, Vitellaro Zuccarello, L, Franceschetti, S, Sancini, G, Lavazza, T, Acampora, D, Simeone, A, Spreafico, R, Frassoni, C, Frassoni, C., SANCINI, GIULIO ALFREDO, Cipelletti, B, Avanzini, G, Vitellaro Zuccarello, L, Franceschetti, S, Sancini, G, Lavazza, T, Acampora, D, Simeone, A, Spreafico, R, Frassoni, C, Frassoni, C., and SANCINI, GIULIO ALFREDO

Abstract

Knock-out Otx1 mice show brain hypoplasia, spontaneous epileptic seizures and abnormalities of the dorsal region of the neocortex. We investigated structural alterations in excitatory and inhibitory circuits in somatosensory cortex of Otx1(-/-) mice by immunocytochemistry using light, confocal and electron microscopy. Immunostaining for non-phosphorylated neurofilament SMI311 and subunit 1 of the NMDA receptor - used as markers of pyramidal neurons - showed reduced layer V pyramidal cells and ectopic pyramidal cells in layers II and III of the mutant cortex. Immunostaining for calcium-binding proteins calbindin, calretinin and parvalbumin - markers of non-overlapping types of GABAergic interneurons - showed no differences between wild-type and knock-out cortex for calbindin and calretinin neurons, while parvalbumin neurons were only patchily distributed in Otx1(-/-) cortex. The pattern of positivity of the GABAergic marker glutamic acid decarboxylase in Otx1(-/-) cortex was also altered and similar to that of parvalbumin. GABA transporter 1 immunoreactivity was greater in Otx1(-/-) than wild-type; quantitation of structures immunoreactive for this transporter in layer V showed that they were increased overall in Otx1(-/-) but the density of inhibitory terminals on pyramidal neurons in the same layer labeled with this transporter was similar to that in wild-type mice. No differences in the distribution or intensity of the glial markers GABA transporter 3 or glial fibrillary acidic protein were found. The defects found in the cortical GABAergic system of the Otx1(-/-) mouse can plausibly explain the cortical hyperexcitability that produces seizures in these animals.

Published
2002

35. Potentially epileptogenic dysfunction of cortical NMDA- and GABA-mediated neurotransmission in Otx1-/- mice

Author

Sancini, G, Franceschetti, S, Lavazza, T, Panzica, F, Cipelletti, B, Frassoni, C, Spreafico, R, Acampora, D, Avanzini, G, SANCINI, GIULIO ALFREDO, Avanzini, G., Sancini, G, Franceschetti, S, Lavazza, T, Panzica, F, Cipelletti, B, Frassoni, C, Spreafico, R, Acampora, D, Avanzini, G, SANCINI, GIULIO ALFREDO, and Avanzini, G.

Abstract

Knockout Otx1 mice present a microcephalic phenotype mainly due to reduced deep neocortical layers and spontaneous recurrent seizures. We investigated the excitable properties of layer V pyramidal neurons in neocortical slices prepared from Otx1-/- mice and age-matched controls. The qualitative firing properties of the neurons of Otx1-/- mice were identical to those found in wild-type controls, but the proportion of intrinsically bursting (IB) neurons was significantly smaller. This is in line with the lack of the Otx1 gene contribution to the generation and differentiation of neurons destined for the deep neocortical layers, in which IB neurons are located selectively in wild-type rodents. The pyramidal neurons recorded in Otx1-/- mice responded to near-threshold electrical stimulation of the underlying white matter, with aberrant polysynaptic excitatory potentials often leading to late action potential generation. When the strength of the stimulus was increased, the great majority of the Otx1-/- neurons (78%) responded with a prominent biphasic inhibitory postsynaptic potential that was significantly larger than that observed in the wild-type mice, and was often followed by complex postinhibitory depolarizing events. Both late excitatory postsynaptic potentials and postinhibitory excitation were selectively suppressed by NMDA receptor antagonists, but not by AMPA antagonists. We conclude that the cortical abnormalities of Otx1-/- neocortex due to a selective loss of large projecting neurons lead to a complex rearrangement of local circuitry, which is characterized by an excess of N-methyl-D-aspartate-mediated polysynaptic excitation that is counteracted by GABA-mediated inhibition in only a limited range of stimulus intensity. Prominent postsynaptic inhibitory potentials may also act as a further pro-epileptogenic event by synchronizing abnormal excitatory potentials.

Published
2001

37. Synaptic properties of neocortical neurons in epileptic mice lacking the Otx1 gene

Author

Avanzini, G, Spreafico, R, Cipelletti, B, Sancini, G, Frassoni, C, Franceschetti, S, Lavazza, T, Panzica, F, Acampora, D, Simeone, A, Simeone, A., SANCINI, GIULIO ALFREDO, Avanzini, G, Spreafico, R, Cipelletti, B, Sancini, G, Frassoni, C, Franceschetti, S, Lavazza, T, Panzica, F, Acampora, D, Simeone, A, Simeone, A., and SANCINI, GIULIO ALFREDO

Abstract

The murine homeobox-containing Otx gene is required for correct nervous system and sense organ development. Otx1-/1 mice obtained by replacing Otx with the lac Z gene show developmental abnormalities of the cerebellum, mesencephalon, and cerebral cortex associated with spontaneous epileptic seizures (1). The epileptogenic mechanisms accounting for these seizures were investigated by means of electrophysiological recordings made from neocortical slices.

Published
2000

45. Evolutionary conservation of otd/Otx2 transcription factor action: a genome-wide microarray analysis in Drosophila

Author

Montalta-He, H., Leemans, R., Loop, T., Strahm, M., Certa, U., Michael Primig, Acampora, D., Simeone, A., and Reichert, H.

Subjects
Homeodomain Proteins, Embryo, Nonmammalian, Genome, Otx Transcription Factors, Reverse Transcriptase Polymerase Chain Reaction, Research, Gene Expression Profiling, Gene Expression Regulation, Developmental, Reproducibility of Results, Genes, Insect, Nerve Tissue Proteins, Embryo, Mammalian, Animals, Genetically Modified, Evolution, Molecular, Trans-Activators, Animals, Drosophila Proteins, Humans, Drosophila, RNA, Messenger, Oligonucleotide Array Sequence Analysis, Signal Transduction
Abstract

Background Homeobox genes of the orthodenticle (otd)/Otx family have conserved roles in the embryogenesis of head and brain. Gene replacement experiments show that the Drosophila otd gene and orthologous mammalian Otx genes are functionally equivalent, in that overexpression of either gene in null mutants of Drosophila or mouse can restore defects in cephalic and brain development. This suggests that otd and Otx genes control a comparable subset of downstream target genes in either organism. Here we use quantitative transcript imaging to analyze this equivalence of otd and Otx gene action at a genomic level. Results Oligonucleotide arrays representing 13,400 annotated Drosophila genes were used to study differential gene expression in flies in which either the Drosophila otd gene or the human Otx2 gene was overexpressed. Two hundred and eighty-seven identified transcripts showed highly significant changes in expression levels in response to otd overexpression, and 682 identified transcripts showed highly significant changes in expression levels in response to Otx2 overexpression. Among these, 93 showed differential expression changes following overexpression of either otd or Otx2, and for 90 of these, comparable changes were observed under both experimental conditions. We postulate that these transcripts are common downstream targets of the fly otd gene and the human Otx2 gene in Drosophila. Conclusion Our experiments indicate that approximately one third of the otd-regulated transcripts also respond to overexpression of the human Otx2 gene in Drosophila. These common otd/Otx2 downstream genes are likely to represent the molecular basis of the functional equivalence of otd and Otx2 gene action in Drosophila.

Published
2002

46. Transient dwarfism and hypogonadism in mice lacking Otx1 reveal prepubescent stage-specific control of pituitary levels of GH, FSH and LH

Author

Acampora, D., primary, Mazan, S., additional, Tuorto, F., additional, Avantaggiato, V., additional, Tremblay, J.J., additional, Lazzaro, D., additional, di Carlo, A., additional, Mariano, A., additional, Macchia, P.E., additional, Corte, G., additional, Macchia, V., additional, Drouin, J., additional, Brulet, P., additional, and Simeone, A., additional

Published
1998
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