Cortical thickness across the lifespan in a Colombian cohort with autosomal‐dominant Alzheimer's disease: A cross‐sectional study

Introduction Cortical thinning is a marker of neurodegeneration in Alzheimer's disease (AD). We investigated the age‐related trajectory of cortical thickness across the lifespan (9‐59 years) in a Colombian kindred with autosomal dominant AD (ADAD). Methods Two hundred eleven participants (105 p...

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Published in:Alzheimer's & dementia : diagnosis, assessment & disease monitoring assessment & disease monitoring, 2021, Vol.13 (1), p.e12233-n/a
Main Authors: Fox‐Fuller, Joshua T., Torrico‐Teave, Heirangi, d'Oleire Uquillas, Federico, Chen, Kewei, Su, Yi, Chen, Yinghua, Brickhouse, Michael, Sanchez, Justin S., Aguero, Cinthya, Jacobs, Heidi I.L., Hampton, Olivia, Guzmán‐Vélez, Edmarie, Vila‐Castelar, Clara, Aguirre‐Acevedo, Daniel C., Baena, Ana, Artola, Arabiye, Martinez, Jairo, Pluim, Celina F., Alvarez, Sergio, Ochoa‐Escudero, Martin, Reiman, Eric M., Sperling, Reisa A., Lopera, Francisco, Johnson, Keith A., Dickerson, Bradford C., Quiroz, Yakeel T.
Format: Article
Language:English
Subjects:
Adults
Age
age‐related
Alzheimer's disease
Biomarkers
Brain
Cognitive ability
Consent
Consortia
cortical thickness
Cross-sectional studies
Dementia
familial Alzheimer's disease
Families & family life
lifespan
Magnetic resonance imaging
Mutation
Neurodegeneration
Neuroimaging
presenilin1
trajectory
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Summary:Introduction Cortical thinning is a marker of neurodegeneration in Alzheimer's disease (AD). We investigated the age‐related trajectory of cortical thickness across the lifespan (9‐59 years) in a Colombian kindred with autosomal dominant AD (ADAD). Methods Two hundred eleven participants (105 presenilin‐1 [PSEN1] E280A mutation carriers, 16 with cognitive impairment; 106 non‐carriers) underwent magnetic resonance imaging. A piecewise linear regression identified change‐points in the age‐related trajectory of cortical thickness in carriers and non‐carriers. Results Unimpaired carriers exhibited elevated cortical thickness compared to non‐carriers, and thickness more negatively correlated with age and cognition in carriers relative to non‐carriers. We found increased cortical thickness in child carriers, after which thickness steadied compared to non‐carriers prior to a rapid reduction in the decade leading up to the expected age at cognitive impairment in carriers. Discussion Findings suggest that cortical thickness may fluctuate across the ADAD lifespan, from early‐life increased thickness to atrophy proximal to clinical onset.
ISSN:2352-8729
2352-8729
DOI:10.1002/dad2.12233