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Your search keyword '"Carton, Amelia"' showing total 3 results
Start Over Author "Carton, Amelia" Publisher oxford university press
3 results on '"Carton, Amelia"'

1. Longitudinal neuroanatomical and cognitive progression of posterior cortical atrophy

Author

Alzheimer's Research UK, Economic and Social Research Council (UK), Engineering and Physical Sciences Research Council (UK), Alzheimer Society of Canada, Brain Research Trust, Wolfson Foundation, National Institute for Health Research (UK), National Institutes of Health (US), European Commission, Firth, Nicholas C., Primativo, Silvia, Marinescu, Razvan-Valentin, Shakespeare, Timothy J., Suárez-González, Aida, Lehmann, Manja, Carton, Amelia, Ocal, Dilek, Pavisic, Ivanna, Paterson, Ross W., Slattery, Catherine F., Foulkes, Alexander J. M., Ridha, Basil H., Gil-Néciga, Eulogio, Oxtoby, Neil P., Young, Alexandra L., Modat, Marc, Cardoso, M. Jorge, Ourselin, Sebastien, Ryan, Natalie S., Miller, Bruce L., Rabinovici, Gil D., Warrington, Elizabeth K., Rossor, Martin N., Fox, Nick C., Warren, Jason D., Alexander, Daniel C., Schott, Jonathan M., Yong, Keir X. X., Crutch, Sebastian J., Alzheimer's Research UK, Economic and Social Research Council (UK), Engineering and Physical Sciences Research Council (UK), Alzheimer Society of Canada, Brain Research Trust, Wolfson Foundation, National Institute for Health Research (UK), National Institutes of Health (US), European Commission, Firth, Nicholas C., Primativo, Silvia, Marinescu, Razvan-Valentin, Shakespeare, Timothy J., Suárez-González, Aida, Lehmann, Manja, Carton, Amelia, Ocal, Dilek, Pavisic, Ivanna, Paterson, Ross W., Slattery, Catherine F., Foulkes, Alexander J. M., Ridha, Basil H., Gil-Néciga, Eulogio, Oxtoby, Neil P., Young, Alexandra L., Modat, Marc, Cardoso, M. Jorge, Ourselin, Sebastien, Ryan, Natalie S., Miller, Bruce L., Rabinovici, Gil D., Warrington, Elizabeth K., Rossor, Martin N., Fox, Nick C., Warren, Jason D., Alexander, Daniel C., Schott, Jonathan M., Yong, Keir X. X., and Crutch, Sebastian J.

Abstract

Posterior cortical atrophy is a clinico-radiological syndrome characterized by progressive decline in visual processing and atrophy of posterior brain regions. With the majority of cases attributable to Alzheimer’s disease and recent evidence for genetic risk factors specifically related to posterior cortical atrophy, the syndrome can provide important insights into selective vulnerability and phenotypic diversity. The present study describes the first major longitudinal investigation of posterior cortical atrophy disease progression. Three hundred and sixty-one individuals (117 posterior cortical atrophy, 106 typical Alzheimer’s disease, 138 controls) fulfilling consensus criteria for posterior cortical atrophy-pure and typical Alzheimer’s disease were recruited from three centres in the UK, Spain and USA. Participants underwent up to six annual assessments involving MRI scans and neuropsychological testing. We constructed longitudinal trajectories of regional brain volumes within posterior cortical atrophy and typical Alzheimer’s disease using differential equation models. We compared and contrasted the order in which regional brain volumes become abnormal within posterior cortical atrophy and typical Alzheimer’s disease using event-based models. We also examined trajectories of cognitive decline and the order in which different cognitive tests show abnormality using the same models. Temporally aligned trajectories for eight regions of interest revealed distinct (P < 0.002) patterns of progression in posterior cortical atrophy and typical Alzheimer’s disease. Patients with posterior cortical atrophy showed early occipital and parietal atrophy, with subsequent higher rates of temporal atrophy and ventricular expansion leading to tissue loss of comparable extent later. Hippocampal, entorhinal and frontal regions underwent a lower rate of change and never approached the extent of posterior cortical involvement. Patients with typical Alzheimer’s disease showed early h

Published
2019

2. Prominent effects and neural correlates of visual crowding in a neurodegenerative disease population

Author

Yong, Keir XX, Shakespeare, Timothy J, Cash, Dave, Henley, Susie MD, Nicholas, Jennifer M, Ridgway, Gerard R, Golden, Hannah L, Warrington, Elizabeth K, Carton, Amelia M, Kaski, Diego, Schott, Jonathan M, Warren, Jason D, and Crutch, Sebastian J

Subjects
Male, CORTEX, genetic structures, acquired dyslexia, Clinical Neurology, posterior cortical atrophy, behavioral disciplines and activities, 17 Psychology And Cognitive Sciences, OBJECT RECOGNITION, Task Performance and Analysis, Image Processing, Computer-Assisted, Humans, Attention, LETTER IDENTIFICATION, Aged, Aged, 80 and over, SPATIAL INTERACTION, Science & Technology, Neurology & Neurosurgery, Neurosciences, lateral masking, Neurodegenerative Diseases, 11 Medical And Health Sciences, Original Articles, Alzheimer's disease, Middle Aged, crowding, ALZHEIMERS-DISEASE, Space Perception, AREA V4, Visual Perception, Female, Neurosciences & Neurology, Atrophy, Life Sciences & Biomedicine, PERIPHERAL-VISION, Alzheimer’s disease, Photic Stimulation, psychological phenomena and processes
Abstract

Visual crowding is a perceptual phenomenon whereby recognition of a stimulus is disrupted by the presence of flanker stimuli. Yong et al. observe excessive crowding in individuals with a neurodegenerative condition (posterior cortical atrophy) and identify associations between prominent crowding and lower grey matter volume in the right collateral sulcus., Crowding is a breakdown in the ability to identify objects in clutter, and is a major constraint on object recognition. Crowding particularly impairs object perception in peripheral, amblyopic and possibly developing vision. Here we argue that crowding is also a critical factor limiting object perception in central vision of individuals with neurodegeneration of the occipital cortices. In the current study, individuals with posterior cortical atrophy (n = 26), typical Alzheimer’s disease (n = 17) and healthy control subjects (n = 14) completed centrally-presented tests of letter identification under six different flanking conditions (unflanked, and with letter, shape, number, same polarity and reverse polarity flankers) with two different target-flanker spacings (condensed, spaced). Patients with posterior cortical atrophy were significantly less accurate and slower to identify targets in the condensed than spaced condition even when the target letters were surrounded by flankers of a different category. Importantly, this spacing effect was observed for same, but not reverse, polarity flankers. The difference in accuracy between spaced and condensed stimuli was significantly associated with lower grey matter volume in the right collateral sulcus, in a region lying between the fusiform and lingual gyri. Detailed error analysis also revealed that similarity between the error response and the averaged target and flanker stimuli (but not individual target or flanker stimuli) was a significant predictor of error rate, more consistent with averaging than substitution accounts of crowding. Our findings suggest that crowding in posterior cortical atrophy can be regarded as a pre-attentive process that uses averaging to regularize the pathologically noisy representation of letter feature position in central vision. These results also help to clarify the cortical localization of feature integration components of crowding. More broadly, we suggest that posterior cortical atrophy provides a neurodegenerative disease model for exploring the basis of crowding. These data have significant implications for patients with, or who will go on to develop, dementia-related visual impairment, in whom acquired excessive crowding likely contributes to deficits in word, object, face and scene perception.

Published
2014

3. Longitudinal neuroanatomical and cognitive progression of posterior cortical atrophy.

Author

Firth NC, Primativo S, Marinescu RV, Shakespeare TJ, Suarez-Gonzalez A, Lehmann M, Carton A, Ocal D, Pavisic I, Paterson RW, Slattery CF, Foulkes AJM, Ridha BH, Gil-Néciga E, Oxtoby NP, Young AL, Modat M, Cardoso MJ, Ourselin S, Ryan NS, Miller BL, Rabinovici GD, Warrington EK, Rossor MN, Fox NC, Warren JD, Alexander DC, Schott JM, Yong KXX, and Crutch SJ

Subjects
Alzheimer Disease complications, Case-Control Studies, Cognitive Dysfunction complications, Disease Progression, Female, Humans, Longitudinal Studies, Magnetic Resonance Imaging, Male, Middle Aged, Models, Neurological, Neuropsychological Tests, Alzheimer Disease pathology, Cerebral Cortex pathology, Cognitive Dysfunction pathology
Abstract

Posterior cortical atrophy is a clinico-radiological syndrome characterized by progressive decline in visual processing and atrophy of posterior brain regions. With the majority of cases attributable to Alzheimer's disease and recent evidence for genetic risk factors specifically related to posterior cortical atrophy, the syndrome can provide important insights into selective vulnerability and phenotypic diversity. The present study describes the first major longitudinal investigation of posterior cortical atrophy disease progression. Three hundred and sixty-one individuals (117 posterior cortical atrophy, 106 typical Alzheimer's disease, 138 controls) fulfilling consensus criteria for posterior cortical atrophy-pure and typical Alzheimer's disease were recruited from three centres in the UK, Spain and USA. Participants underwent up to six annual assessments involving MRI scans and neuropsychological testing. We constructed longitudinal trajectories of regional brain volumes within posterior cortical atrophy and typical Alzheimer's disease using differential equation models. We compared and contrasted the order in which regional brain volumes become abnormal within posterior cortical atrophy and typical Alzheimer's disease using event-based models. We also examined trajectories of cognitive decline and the order in which different cognitive tests show abnormality using the same models. Temporally aligned trajectories for eight regions of interest revealed distinct (P < 0.002) patterns of progression in posterior cortical atrophy and typical Alzheimer's disease. Patients with posterior cortical atrophy showed early occipital and parietal atrophy, with subsequent higher rates of temporal atrophy and ventricular expansion leading to tissue loss of comparable extent later. Hippocampal, entorhinal and frontal regions underwent a lower rate of change and never approached the extent of posterior cortical involvement. Patients with typical Alzheimer's disease showed early hippocampal atrophy, with subsequent higher rates of temporal atrophy and ventricular expansion. Cognitive models showed tests sensitive to visuospatial dysfunction declined earlier in posterior cortical atrophy than typical Alzheimer's disease whilst tests sensitive to working memory impairment declined earlier in typical Alzheimer's disease than posterior cortical atrophy. These findings indicate that posterior cortical atrophy and typical Alzheimer's disease have distinct sites of onset and different profiles of spatial and temporal progression. The ordering of disease events both motivates investigation of biological factors underpinning phenotypic heterogeneity, and informs the selection of measures for clinical trials in posterior cortical atrophy., (© The Author(s) (2019). Published by Oxford University Press on behalf of the Guarantors of Brain.)

Published
2019
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