Zobrazeno 1 - 5
of 5
pro vyhledávání: '"Jon Ortiz-Abalia"'
Autor:
Xavier Altafaj, Eduardo D. Martín, Jon Ortiz-Abalia, Aitana Valderrama, Cristina Lao-Peregrín, Mara Dierssen, Cristina Fillat
Publikováno v:
Neurobiology of Disease, Vol 52, Iss , Pp 117-127 (2013)
The cognitive dysfunctions of Down Syndrome (DS) individuals are the most disabling alterations caused by the trisomy of human chromosome 21 (HSA21). In trisomic Ts65Dn mice, a genetic model for DS, the overexpression of HSA21 homologous genes has be
Externí odkaz:
https://doaj.org/article/708a6ae4ef8d4bb9b8c8cf2afa7fc8ac
Autor:
Aitana Valderrama, Xavier Altafaj, Eduardo D. Martín, Mara Dierssen, Cristina Lao-Peregrín, Jon Ortiz-Abalia, Cristina Fillat
Publikováno v:
Neurobiology of Disease, Vol 52, Iss, Pp 117-127 (2013)
The cognitive dysfunctions of Down Syndrome (DS) individuals are the most disabling alterations caused by the trisomy of human chromosome 21 (HSA21). In trisomic Ts65Dn mice, a genetic model for DS, the overexpression of HSA21 homologous genes has be
Autor:
Eulàlia Martí, Miriam Fernández, Cristina Fillat, Nuria Andreu, Julien Laffaire, Carmen González-García, Mara Dierssen, Valentín Ceña, M.-C. Potier, Xavier Altafaj, Jon Ortiz-Abalia
Publikováno v:
Neurobiology of Disease, Vol 32, Iss 3, Pp 377-384 (2008)
Transgenic mice overexpressing Dyrk1A (TgDyrk1A), a Down syndrome (DS) candidate gene, exhibit motor and cognitive alterations similar to those observed in DS individuals. To gain new insights into the molecular consequences of Dyrk1A overexpression
Publikováno v:
Behavior Genetics. 36:454-468
Trisomy 21 or Down syndrome (DS) is a complex syndrome, of genetic origin with multiple and variable neurobiological and neuropsychological manifestations. DS patients have consistent signs of brain damage along their lives, but understanding the bio
Autor:
Xavier Estivill, Jon Ortiz-Abalia, Cristina Fillat, Nuria Andreu, Ignasi Sahún, Mara Dierssen, Xavier Altafaj
Publikováno v:
The American Journal of Human Genetics. (4):479-488
Genetic-dissection studies carried out with Down syndrome (DS) murine models point to the critical contribution of Dyrk1A overexpression to the motor abnormalities and cognitive deficits displayed in DS individuals. In the present study we have used