Zobrazeno 1 - 7
of 7
pro vyhledávání: '"Sophie Dunnett"'
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:
Yuen Shan Ho, Yan Liu, Sophie Dunnett, John M.T. Chu, Tim Yan, Ying Chen, Gordon Tin Chun Wong, Raymond Chuen-Chung Chang
Publikováno v:
Laboratory Investigation. 99:943-957
Growing evidence has shown the beneficial influence of exercise on humans. Apart from classic cardioprotection, numerous studies have demonstrated that different exercise regimes provide a substantial improvement in various brain functions. Although
Autor:
Tara L. Spires-Jones, Monique Hooley, Colin Smith, Anton-Fernandez A, Jamie Rose, Susan M. Catalano, Makis Tzioras, Rosemary J. Jackson, J. H. Catterson, Nicholas J. Izzo, Claire L. Davies, Tempelaar R, Martí Colom-Cadena, Jane Tulloch, Sophie Dunnett
Synapse loss correlates with cognitive decline in Alzheimer’s disease (AD), and soluble amyloid beta (Aβ) is implicated in synaptic dysfunction and loss. An important knowledge gap is the lack of understanding of how synaptic accumulation of Aβ l
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::ed92cd0edcf16138aa25188d4a80a123
https://doi.org/10.1101/2021.02.01.428238
https://doi.org/10.1101/2021.02.01.428238
Publikováno v:
Alzheimer's & Dementia. 16
Autor:
C. McKenzie, Jane Tulloch, Monique Hooley, Rosemary J. Jackson, Sadaf Sohrabi, Marie d'Orange, Elizabeth Allison, Kimberly Abt, Makis Tzioras, Anna J. Stevenson, Maria P. Fjeldstad, Sophie Dunnett, Will Calkin, Colin Smith, Giles E. Hardingham, Owen Dando, Caitlin Davies, Leo Murison, Eleanor K. Pickett, Tara L. Spires-Jones, Iris Oren, Christopher M. Henstridge, Jamie McQueen, Abigail G. Herrmann, Oliver Hardt, Jamie Rose, Pooja Jain
Publikováno v:
SSRN Electronic Journal.
SummaryOne of the key knowledge gaps blocking development of effective therapeutics for Alzheimer’s disease (AD) is the lack of understanding of how amyloid beta (Aβ) and tau cooperate in causing disease phenotypes. Within a mouse tau deficient ba
The role of sleep deprivation and circadian rhythm disruption as risk factors of Alzheimer’s disease
Publikováno v:
Frontiers in Neuroendocrinology. 54:100764
Emerging evidence suggests that sleep deprivation (SD) and circadian rhythm disruption (CRD) may interact and increase the risk for the development of Alzheimer's disease (AD). This review inspects different pathophysiological aspects of SD and CRD,
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