Zobrazeno 1 - 3
of 3
pro vyhledávání: '"Alejandro Anton Fernandez"'
Autor:
Eleanor K. Pickett, Abigail G. Herrmann, Jamie McQueen, Kimberly Abt, Owen Dando, Jane Tulloch, Pooja Jain, Sophie Dunnett, Sadaf Sohrabi, Maria P. Fjeldstad, Will Calkin, Leo Murison, Rosemary J. Jackson, Makis Tzioras, Anna Stevenson, Marie d’Orange, Monique Hooley, Caitlin Davies, Marti Colom-Cadena, Alejandro Anton-Fernandez, Declan King, Iris Oren, Jamie Rose, Chris-Anne McKenzie, Elizabeth Allison, Colin Smith, Oliver Hardt, Christopher M. Henstridge, Giles E. Hardingham, Tara L. Spires-Jones
Publikováno v:
Cell Reports, Vol 29, Iss 11, Pp 3592-3604.e5 (2019)
Summary: A key knowledge gap blocking development of effective therapeutics for Alzheimer’s disease (AD) is the lack of understanding of how amyloid beta (Aβ) peptide and pathological forms of the tau protein cooperate in causing disease phenotype
Externí odkaz:
https://doaj.org/article/5c607706c23f4f7d92a682e925ca0372
Autor:
Javier DeFelipe, Félix Hernández, Alejandro Anton Fernandez, Guillermo Aparicio Torres, Alberto Muñoz, Jesús Avila, Silvia Tapia Gonzalez, Jesús Merchan Rubira
Publikováno v:
Alzheimer's & Dementia. 13
Autor:
Colin Smith, Caitlin Davies, Rosemary J. Jackson, Makis Tzioras, Sadaf Sohrabi, Abigail G. Herrmann, Monique Hooley, Declan King, Pooja Jain, Jamie McQueen, Iris Oren, Oliver Hardt, Tara L. Spires-Jones, Christopher M. Henstridge, Eleanor K. Pickett, Anna J. Stevenson, Sophie Dunnett, Maria P. Fjeldstad, Jamie Rose, Marie d'Orange, Giles E. Hardingham, Owen Dando, Alejandro Anton-Fernandez, Martí Colom-Cadena, C. McKenzie, Jane Tulloch, Leo Murison, Will Calkin, Elizabeth Allison, Kimberly Abt
Publikováno v:
Cell Reports
Cell Reports, Vol 29, Iss 11, Pp 3592-3604.e5 (2019)
Pickett, E K, Herrmann, A G, McQueen, J, Abt, K, Dando, O, Tulloch, J, Jain, P, Dunnett, S, Sohrabi, S, Fjeldstad, M P, Calkin, W, Murison, L, Jackson, R J, Tzioras, M, Stevenson, A, d'Orange, M, Hooley, M, Davies, C, Colom Cadena, M, Anton Fernandez, A, King, D, Oren, I, Rose, J, McKenzie, C-A, Allison, E, Smith, C, Hardt, O, Henstridge, C M, Hardingham, G E & Spires-Jones, T L 2019, ' Amyloid Beta and Tau Cooperate to Cause Reversible Behavioral and Transcriptional Deficits in a Model of Alzheimer’s Disease ', Cell Reports, vol. 29, no. 11, pp. 3592-3604.E5 . https://doi.org/10.1016/j.celrep.2019.11.044
Cell Reports, Vol 29, Iss 11, Pp 3592-3604.e5 (2019)
Pickett, E K, Herrmann, A G, McQueen, J, Abt, K, Dando, O, Tulloch, J, Jain, P, Dunnett, S, Sohrabi, S, Fjeldstad, M P, Calkin, W, Murison, L, Jackson, R J, Tzioras, M, Stevenson, A, d'Orange, M, Hooley, M, Davies, C, Colom Cadena, M, Anton Fernandez, A, King, D, Oren, I, Rose, J, McKenzie, C-A, Allison, E, Smith, C, Hardt, O, Henstridge, C M, Hardingham, G E & Spires-Jones, T L 2019, ' Amyloid Beta and Tau Cooperate to Cause Reversible Behavioral and Transcriptional Deficits in a Model of Alzheimer’s Disease ', Cell Reports, vol. 29, no. 11, pp. 3592-3604.E5 . https://doi.org/10.1016/j.celrep.2019.11.044
Summary A key knowledge gap blocking development of effective therapeutics for Alzheimer’s disease (AD) is the lack of understanding of how amyloid beta (Aβ) peptide and pathological forms of the tau protein cooperate in causing disease phenotypes