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30 results on '"Lezcano, Elena"'

9. Lrrk2 R1441G-related Parkinson’s disease: evidence of a common founding event in the seventh century in Northern Spain

Author

Mata, Ignacio F., Hutter, Carolyn M., González-Fernández, María C., de Pancorbo, Marian M., Lezcano, Elena, Huerta, Cecilia, Blazquez, Marta, Ribacoba, Renee, Guisasola, Luis M., Salvador, Carlos, Gómez-Esteban, Juan C., Zarranz, Juan J., Infante, Jon, Jankovic, Joseph, Deng, Hao, Edwards, Karen L., Alvarez, Victoria, and Zabetian, Cyrus P.

Published
2009
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23. Use of Ziprasidone in Parkinsonian Patients With Psychosis

Author

Gómez-Esteban, Juan Carlos, primary, Zarranz, Juan J, additional, Velasco, Fernando, additional, Lezcano, Elena, additional, Lachen, M C, additional, Rouco, Idoia, additional, Barcena, Joseba, additional, Boyero, Sabas, additional, Ciordia, Roberto, additional, and Allue, Isidro, additional

Published
2005
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25. The new mutation, E46K, of α‐synuclein causes parkinson and Lewy body dementia

Author

Zarranz, Juan J., primary, Alegre, Javier, additional, Gómez‐Esteban, Juan C., additional, Lezcano, Elena, additional, Ros, Raquel, additional, Ampuero, Israel, additional, Vidal, Lídice, additional, Hoenicka, Janet, additional, Rodriguez, Olga, additional, Atarés, Begoña, additional, Llorens, Verónica, additional, Tortosa, Estrella Gomez, additional, del Ser, Teodoro, additional, Muñoz, David G., additional, and de Yebenes, Justo G., additional

Published
2003
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26. Compatibilidad de mezclas de polímeros : estudio de la interacción del Poli(4-hidroxiestireno) con Poli(-caprolactona) y con polivinilacetato

Author

González Lezcano, Elena and González Lezcano, Elena

Abstract

Se ha llevado a cabo un estudio termodinamico de la miscibilidad del poli (4-hidroxiestireno), (p4hs) con la poli- -caprolactona, (pcl) y con el polivinilacetato, (pva) por las técnicas de calorimetria diferencial de barrido, dsc, cromatografía de gases inversa, igc, y de la microestructura por la técnica de fluorescencia. En ambos sistemas se produce la formación de enlaces de hidrogeno entre los constituyentes de los mismos. El sistema pcl+p4hs esta constituido por un polímero semicristalino y un polímero amorfo y el sistema pva+p4hs esta constituido por dos polimeros amorfos. Puesto que el sistema pva+p4hs ya había sido previamente estudiado en nuestro laboratorio por dsc, se ha realizado en primer lugar la caracterización térmica del sistema pcl+p4hs, determinando su temperatura de transición vítrea, con el fin de determinar la miscibilidad del mismo, además se ha podido obtener el parámetro de interacción x23 a través del descenso de la temperatura de fusión de la pcl y se ha analizado el comportamiento térmico (fusión y cristalización) de este sistema. Una vez confirmada de esta forma la miscibilidad de ambos sistemas, se ha realizado la determinación de los parámetros de interacción por igc, a través de medidas realizadas con distintos disolventes de diferente interacción con los polimeros, aplicando posteriormente algunos de los métodos teóricos propuestos en la bibliografía, intentando dilucidar la obtención de parámetros x23 independientes del disolvente y característicos de las mezclas. Los resultados obtenidos se han correlacionado con los resultados del estudio por dsc para el sistema pcl+p4hs y con medidas del parámetro x del sistema pva+p4hs por la técnica de presión de vapor que se estaba estudiando simultáneamente a la realización de este trabajo. Finalmente, puesto que el p4hs es un polimero que contiene grupos aromáticos, se ha podido realizar un estudio del comportamiento fluorescente de ambos sistemas, con el fin de analizar a nivel molecular su

Published
1993

28. The new mutation, E46K, of α-synuclein causes parkinson and Lewy body dementia

Author

Zarranz, Juan J., Alegre, Javier, Gómez-Esteban, Juan C., Lezcano, Elena, Ros, Raquel, Ampuero, Israel, Vidal, Lídice, Hoenicka, Janet, Rodriguez, Olga, Atarés, Begoña, Llorens, Verónica, Tortosa, Estrella Gomez, Ser, Teodoro del, and Muñoz, David G.

Abstract

Familial parkinsonism and dementia with cortical and subcortical Lewy bodies is uncommon, and no genetic defect has been reported in the previously described sibships. We present a Spanish family with autosomal dominant parkinsonism, dementia, and visual hallucinations of variable severity. The postmortem examination showed atrophy of the substantia nigra, lack of Alzheimer pathology, and numerous Lewy bodies which were immunoreactive to α-synuclein and ubiquitin in cortical and subcortical areas. Sequencing of the α-synuclein gene showed a novel, nonconservative E46K mutation in heterozygosis. The E46K mutation was present in all affected family members and in three young asymptomatic subjects, but it was absent in healthy and pathological controls. The novel mutation, that substitutes a dicarboxylic amino acid, glutamic acid, with a basic amino acid such as lysine in a much conserved area of the protein, is likely to produce severe disturbance of protein function. Our data show that, in addition to the previously described hereditary α-synucleinopathies, dementia with Lewy bodies is related to mutation of α-synuclein.

Published
2004
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29. Familial prion diseases in the Basque Country (Spain).

Author

Zarranz JJ, Digon A, Atarés B, Arteagoitia JM, Carrera N, Fernández-Manchola I, Fernández-Martínez M, Fernández-Maiztegui C, Forcadas I, Galdos L, Ibáñez A, Lezcano E, Martí-Massó JF, Mendibe MM, Urtasun M, Uterga JM, Saracibar N, Velasco F, and González de Galdeano L

Subjects
Adult, Aged, Cluster Analysis, Family, Female, Humans, Male, Middle Aged, Mutation genetics, Pedigree, Population Surveillance, Registries, Spain epidemiology, Prion Diseases epidemiology, Prion Diseases genetics
Abstract

In 1995, a surveillance system for prion diseases was set up in the Basque Country, an autonomous region in northern Spain (2.1 million inhabitants). In the period from January 1993 to December 2003, we diagnosed 21 patients with familial prion diseases prospectively and another 4 patients retrospectively. They represent 35% of all the cases referred to the epidemiological registry. Two main possible explanations for this unusual high incidence of familial prion diseases are proposed: first, comprehensive case ascertainment by public health neurologists; second, a probable cluster of the D178N mutation within families of Basque origin related to a still unconfirmed common ancestor. Further genetic and genealogical studies should resolve this issue.

Published
2005
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30. The new mutation, E46K, of alpha-synuclein causes Parkinson and Lewy body dementia.

Author

Zarranz JJ, Alegre J, Gómez-Esteban JC, Lezcano E, Ros R, Ampuero I, Vidal L, Hoenicka J, Rodriguez O, Atarés B, Llorens V, Gomez Tortosa E, del Ser T, Muñoz DG, and de Yebenes JG

Subjects
Aged, Amino Acid Sequence, Base Sequence, DNA Mutational Analysis, DNA Primers, Female, Humans, Immunohistochemistry, Lewy Bodies pathology, Male, Middle Aged, Molecular Sequence Data, Mutation, Nerve Degeneration pathology, Parkinson Disease pathology, Pedigree, Polymerase Chain Reaction, Sequence Homology, Synucleins, Tomography, Emission-Computed, Single-Photon, alpha-Synuclein, Brain pathology, Lewy Body Disease genetics, Nerve Tissue Proteins genetics, Parkinson Disease genetics
Abstract

Familial parkinsonism and dementia with cortical and subcortical Lewy bodies is uncommon, and no genetic defect has been reported in the previously described sibships. We present a Spanish family with autosomal dominant parkinsonism, dementia, and visual hallucinations of variable severity. The postmortem examination showed atrophy of the substantia nigra, lack of Alzheimer pathology, and numerous Lewy bodies which were immunoreactive to alpha-synuclein and ubiquitin in cortical and subcortical areas. Sequencing of the alpha-synuclein gene showed a novel, nonconservative E46K mutation in heterozygosis. The E46K mutation was present in all affected family members and in three young asymptomatic subjects, but it was absent in healthy and pathological controls. The novel mutation, that substitutes a dicarboxylic amino acid, glutamic acid, with a basic amino acid such as lysine in a much conserved area of the protein, is likely to produce severe disturbance of protein function. Our data show that, in addition to the previously described hereditary alpha-synucleinopathies, dementia with Lewy bodies is related to mutation of alpha-synuclein.

Published
2004
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