Cortical atrophy and amyloid and tau deposition in Down syndrome : A longitudinal study
Padilla, Concepción (Institut d'Investigació Biomèdica Sant Pau)
Montal, Victor (Institut d'Investigació Biomèdica Sant Pau)
Walpert, Madeleine J. (University of Cambridge. Cambridge Intellectual and Developmental Disabilities Research Group. Department of Psychiatry)
Hong, Young T. (University of Cambridge. Wolfson Brain Imaging Centre. Department of Clinical Neurosciences)
Fryer, Tim D. (University of Cambridge. Wolfson Brain Imaging Centre. Department of Clinical Neurosciences)
Coles, Jonathan (University of Cambridge. Division of Anaesthesia. Department of Medicine)
Aigbirhio, Franklin I. (University of Cambridge. Wolfson Brain Imaging Centre. Department of Clinical Neurosciences)
Hartley, Sigan L. (University of Wisconsin-Madison. Waisman Center)
Cohen, Ann (University of Pittsburgh. Department of Psychiatry)
Tudorascu, Dana L. (University of Pittsburgh. Department of Psychiatry)
Christian, Bradley T. (University of Wisconsin-Madison. Waisman Center)
Handen, Benjamin L. (University of Pittsburgh. Department of Psychiatry)
Klunk, William E. (University of Pittsburgh. Department of Psychiatry)
Holland, Anthony John (Cambridgeshire and Peterborough NHS Foundation Trust. Fulbourn Hospital)
Zaman, Shahid (Cambridgeshire and Peterborough NHS Foundation Trust. Fulbourn Hospital)

Fecha:	2022
Resumen:	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.
Ayudas:	Instituto de Salud Carlos III CD20/00133
Nota:	Altres ajuts: Medical Research Council (grant ID number: 98480); the Alzheimer's Research UK (grant ID number: ARUK-PG2015-23); the National Institutes of Health (NIH) (grant ID number: U01AG051406-01).
Derechos:	Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original.
Lengua:	Anglès
Documento:	Article ; recerca ; Versió publicada
Materia:	Alzheimer's disease ; Amyloid deposition ; Cortical atrophy ; Down syndrome ; Longitudinal ; Tau deposition
Publicado en:	Alzheimer's & Dementia : Diagnosis, Assessment & Disease Monitoring, Vol. 14 Núm. 1 (2022) , p. e12288, ISSN 2352-8729

DOI: 10.1002/dad2.12288
PMID: 35386472

9 p, 634.4 KB

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