Zobrazeno 1 - 6
of 6
pro vyhledávání: '"Elisabeth Mangiameli"'
Publikováno v:
Methods in cell biology. 171
Human neural stem cells (hNSCs) hold great promises for the development of cell-based therapies for neurodegenerative diseases, given their capability to provide immunomodulatory and trophic support and to replace, to a limited extent, damaged, or lo
Publikováno v:
Methods in cell biology. 171
For a long time, the understanding of neurological diseases has been limited by the lack of representative experimental models able to recapitulate essential features of the human pathologies. Human induced pluripotent stem cells (hiPSCs) have emerge
Publikováno v:
Methods in Cell Biology ISBN: 9780323900188
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::fc3576b13167cafa5186ad709e81a7b3
https://doi.org/10.1016/bs.mcb.2022.04.012
https://doi.org/10.1016/bs.mcb.2022.04.012
Publikováno v:
Methods in Cell Biology ISBN: 9780323900188
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::93f674f5e510b7616d8c02975e97c673
https://doi.org/10.1016/bs.mcb.2022.04.007
https://doi.org/10.1016/bs.mcb.2022.04.007
Autor:
Angela Bachi, Elisabeth Mangiameli, Vittoria Matafora, Angela Pesenti Gritti, Lucrezia della Volpe, Lucia Susani, Daniela Gnani, Marianna Paulis, Francesca Sanvito, Sabata Martino, Anna Cecchele, Raffaella Di Micco, Francesco Morena, Angela Cattaneo
Publikováno v:
Stem Cell Reports
Summary Globoid cell leukodystrophy (GLD) is a rare neurodegenerative lysosomal storage disease caused by an inherited deficiency of β-galactocerebrosidase (GALC). GLD pathogenesis and therapeutic correction have been poorly studied in patient neura
Autor:
Elisabeth Mangiameli, Ilaria Pelizzoni, Franca Codazzi, Myriam Rai, Floramarida Salerno Scarzella, Amélie Hu, Massimo Pandolfo, Fabio Grohovaz, Simona Donatello
Publikováno v:
Human molecular genetics. 25(22)
We employed induced pluripotent stem cell (iPSC)-derived neurons obtained from Friedreich ataxia (FRDA) patients and healthy subjects, FRDA neurons and CT neurons, respectively, to unveil phenotypic alterations related to frataxin (FXN) deficiency an