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Your search keyword '"Masters, C. L."' showing total 8 results
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8 results on '"Masters, C. L."'

2. Dominantly Inherited Alzheimer Network Trials Unit (DIAN-TU): Trial Satisfaction and Attitudes towards Future Clinical Trials

Author

Liu, Haiyan, Li, J., Ziegemeier, E., Adams, S., McDade, E., Clifford, D. B., Cao, Y., Wang, G., Li, Y., Mills, S. L., Santacruz, A. M., Belyew, S., Grill, J. D., Snider, B. J., Mummery, C. J., Surti, G., Hannequin, D., Wallon, D., Berman, S. B., Jimenez-Velazquez, I. Z., Roberson, E. D., van Dyck, C. H., Honig, L. S., Sanchez-Valle, R., Brooks, W. S., Gauthier, S., Galasko, D., Masters, C. L., Brosch, J., Hsiung, G.-Y. R., Jayadev, S., Formaglio, M., Masellis, M., Clarnette, R., Pariente, J., Dubois, B., Pasquier, F., Bateman, R. J., and Llibre-Guerra, Jorge J.

Published
2024
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4. Can We Use Blood Biomarkers as Entry Criteria and for Monitoring Drug Treatment Effects in Clinical Trials? A Report from the EU/US CTAD Task Force

Author

Angioni, D., Hansson, O., Bateman, R. J., Rabe, C., Toloue, M., Braunstein, J. B., Agus, S., Sims, J. R., Bittner, T., Carrillo, M. C., Fillit, H., Masters, C. L., Salloway, S., Aisen, P., Weiner, M., Vellas, B., Gauthier, S., Abushakra, Susan, Afshar, Mohammad, Alam, John, Algeciras-Schimnich, Alicia, Andrieu, Sandrine, Ballard, Clive, Baruch, Amos, Batrla, Richard, Baudler, Monika, Bell, Joanne, Bozeat, Sasha, Brooks, Dawn, Brooks, Tricia, Bullain, Szofia, Burmeister, Jan, Cho, Min, Collins, Emily, Cook, Gavin, Cummings, Jeffrey, Dague, Chris, De Santi, Susan, Doody, Rachelle, Dunn, Billy, Egan, Michael, Eriksson, Sven, Esquivel, Rianne, Fagan, Tom, Ferrell, Phyllis, Gallagher, Michela, Grönblad, Anna-Kaija, Hains, Avis, Hampel, Harald, Hefting, Nanco, Hendrix, Suzanne, Ho, Carole, Hu, Helen, Ismail, Zahinoor, Jones, Daryl, Kinney, Gene, Kinnon, Paul, Kurzman, Ricky, Lannfelt, Lars, Lawson, John, LeBastard, Nathalie, Legrand, Valérie, Lewandowski, Nicole, Lim, Carine, Lyketsos, Costantine, Masterman, Donna, Lu, Ming, Mintun, Mark, Molinuevo, José Luis, Monteiro, Cecilia, Navia, Bradford, Odergren, Tomas, Osswald, Gunilla, Penny, Lewis, Pontecorvo, Michael, Porsteinsson, Anton, Raman, Rema, Respondek, Gesine, Reyderman, Larisa, Rogers, Sharon, Rosenberg, Paul, Rosenzweig-Lipson, Sharon, Roskey, Mark, Carrie, Rubel, Saad, Ziad, Schindler, Rachel, Selkoe, Dennis, Shulman, Melanie, Sink, Kaycee, Sipe, Lisa, Skovronsky, Daniel, Somers, Elizabeth, Soto, Maria, Streffer, Johannes, Such, Pedro, Suhy, Joyce, Touchon, Jacques, Vandijck, Manu, White, Anne, Wilson, David, Zago, Wagner, and Zhou, Jin

Published
2023
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7. Axonal damage and astrocytosis are biological correlates of grey matter network integrity loss: a cohort study in autosomal dominant Alzheimer disease.

Author

Vermunt L, Sutphen C, Dicks E, de Leeuw DM, Allegri R, Berman SB, Cash DM, Chhatwal JP, Cruchaga C, Day G, Ewers M, Farlow M, Fox NC, Ghetti B, Graff-Radford N, Hassenstab J, Jucker M, Karch CM, Kuhle J, Laske C, Levin J, Masters CL, McDade E, Mori H, Morris JC, Perrin RJ, Preische O, Schofield PR, Suárez-Calvet M, Xiong C, Scheltens P, Teunissen CE, Visser PJ, Bateman RJ, Benzinger TLS, Fagan AM, Gordon BA, and Tijms BM

Abstract

Brain development and maturation leads to grey matter networks that can be measured using magnetic resonance imaging. Network integrity is an indicator of information processing capacity which declines in neurodegenerative disorders such as Alzheimer disease (AD). The biological mechanisms causing this loss of network integrity remain unknown. Cerebrospinal fluid (CSF) protein biomarkers are available for studying diverse pathological mechanisms in humans and can provide insight into decline. We investigated the relationships between 10 CSF proteins and network integrity in mutation carriers (N=219) and noncarriers (N=136) of the Dominantly Inherited Alzheimer Network Observational study. Abnormalities in Aβ, Tau, synaptic (SNAP-25, neurogranin) and neuronal calcium-sensor protein (VILIP-1) preceded grey matter network disruptions by several years, while inflammation related (YKL-40) and axonal injury (NfL) abnormalities co-occurred and correlated with network integrity. This suggests that axonal loss and inflammation play a role in structural grey matter network changes., Key Points: Abnormal levels of fluid markers for neuronal damage and inflammatory processes in CSF are associated with grey matter network disruptions.The strongest association was with NfL, suggesting that axonal loss may contribute to disrupted network organization as observed in AD.Tracking biomarker trajectories over the disease course, changes in CSF biomarkers generally precede changes in brain networks by several years.

Published
2023
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8. Cerebrospinal fluid neurofilament light predicts the rate of executive function decline in younger-onset dementia.

Author

Walia N, Eratne D, Loi SM, Li QX, Varghese S, Malpas CB, Walterfang M, Evans AH, Parker S, Collins SJ, Masters CL, and Velakoulis D

Subjects
Amyloid beta-Peptides, Biomarkers, Executive Function, Humans, Intermediate Filaments, Middle Aged, Neurofilament Proteins, Peptide Fragments, tau Proteins, Alzheimer Disease, Cognitive Dysfunction
Abstract

Introduction: Determining disease severity and predicting prognosis in younger onset-dementia (YOD) remains challenging. Whether CSF biomarkers neurofilament light (NfL), tau and amyloidβ 42 (Aβ42) can help provide such information has been underexplored., Methods: Patients with YOD and CSF analysis were identified. We compared baseline NfL, tau and Aβ42 concentrations with contemporaneous Neuropsychiatry Unit Cognitive Assessment Tool (NUCOG) scores to assess their association with severity of cognitive impairment. Cognitive decline, as measured by longitudinal NUCOG assessment, was correlated against baseline biomarker levels to assess their utility in predicting the rate of cognitive decline., Results: 78 patients with YOD (mean age = 56 years, SD = 8) and CSF analysis were identified. Dementia types included Alzheimer's disease, behavioural variant frontotemporal dementia, dementia not-otherwise-specified and other. Tau was associated with contemporaneous memory dysfunction (r = -0.556, 95% CI:[-0.702,-0.393], p < .001). 21 patients had longitudinal cognitive assessment up to 82 months from CSF sampling. NfL was associated with the rate of executive function decline (r = 0.755, 95% CI:[0.259,0.937], p < .001). Aβ42 was associated with the rate of memory decline (r = -0.582, 95% CI:[-0.855,-0.274], p = .007) and rate of total NUCOG decline (r = -0.515, 95% CI: [-0.809, -0.227], p = .017)., Conclusion: CSF tau is related to contemporaneous memory impairment in YOD. NfL and Aβ42 levels are associated with the rate of executive function and memory decline, respectively, and may have a role in prognostication in YOD., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Published
2022
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