Cortical atrophy and amyloid and tau deposition in Down syndrome
Introduction: The Down syndrome population has a high prevalence for dementia, often showing their first clinical symptoms in their 40s. Methods: In a longitudinal cohort, we investigate whether amyloid deposition at time point 1 (TP1) could predict cortical thickness change at time point 2 (TP2). T...
| Autores: | , , , , , , , , , , , , , , |
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| Tipo de recurso: | artículo |
| Fecha de publicación: | 2022 |
| País: | España |
| Institución: | Universitat Autònoma de Barcelona |
| Repositorio: | Dipòsit Digital de Documents de la UAB |
| Idioma: | inglés |
| OAI Identifier: | oai:ddd.uab.cat:284462 |
| Acceso en línea: | https://ddd.uab.cat/record/284462 https://dx.doi.org/urn:doi:10.1002/dad2.12288 |
| Access Level: | acceso abierto |
| Palabra clave: | Alzheimer's disease Amyloid deposition Cortical atrophy Down syndrome Longitudinal Tau deposition |
| Sumario: | Introduction: The Down syndrome population has a high prevalence for dementia, often showing their first clinical symptoms in their 40s. Methods: In a longitudinal cohort, we investigate whether amyloid deposition at time point 1 (TP1) could predict cortical thickness change at time point 2 (TP2). The association between tau burden and cortical thickness was also examined at time point 3 (TP3). Results: Between TP1 and TP2 there was pronounced cortical thinning in temporo-parietal cortices and cortical thickening in the frontal cortex. Baseline amyloid burden was strongly associated to cortical thinning progression, especially in the temporo-parietal regions. At TP3, tau deposition negatively correlated with cortical atrophy in regions where tau usually accumulates at later Braak stages. Discussion: A higher amount of amyloid accumulation triggers a cascade of changes of disease-causing processes that eventually lead to dementia. As expected, we found that regions where tau usually accumulates were those also displaying high levels of cortical atrophy. |
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