Título : |
Cortical thickness across the lifespan in a Colombian cohort with autosomal-dominant Alzheimer's disease: A cross-sectional study |
Tipo de documento : |
documento electrónico |
Autores : |
Sergio Álvarez Vallejo, ; Martín Ochoa Escudero, |
Fecha de publicación : |
2021 |
Títulos uniformes : |
Alzheimer’s & Dementia. Diagnosis, Assessment & Disease Monitoring
|
Idioma : |
Inglés (eng) |
Palabras clave : |
age-related cortical thickness familial Alzheimer's disease lifespan presenilin1 trajectory |
Resumen : |
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. |
Mención de responsabilidad : |
Joshua T. Fox-Fuller, Heirangi Torrico-Teave, Federico d'Oleire Uquillas, Kewei Chen, Yi Su, Yinghua Chen, Michael Brickhouse, Justin S. Sanchez, Cinthya Aguero, Heidi I.L. Jacobs, Olivia Hampton, Edmarie Guzmán-Vélez, Clara Vila-Castelar, Daniel C. Aguirre-Acevedo, Ana Baena, Arabiye Artola, Jairo Martinez, Celina F. Pluim, Sergio Alvarez, Martin Ochoa-Escudero, Eric M. Reiman, Reisa A. Sperling, Francisco Lopera, Keith A. Johnson, Bradford C. Dickerson, Yakeel T. Quiroz |
Referencia : |
Alzheimers Dement (Amst). 2021 Sep 14;13(1):e12233. |
DOI (Digital Object Identifier) : |
10.1002/dad2.12233 |
PMID : |
34541287 |
Derechos de uso : |
CC BY-NC-ND |
En línea : |
https://alz-journals.onlinelibrary.wiley.com/doi/10.1002/dad2.12233 |
Enlace permanente : |
https://hospitalpablotobon.cloudbiteca.com/pmb/opac_css/index.php?lvl=notice_display&id=5885 |
Cortical thickness across the lifespan in a Colombian cohort with autosomal-dominant Alzheimer's disease: A cross-sectional study [documento electrónico] / Sergio Álvarez Vallejo, ; Martín Ochoa Escudero, . - 2021. Obra : Alzheimer’s & Dementia. Diagnosis, Assessment & Disease MonitoringIdioma : Inglés ( eng) Palabras clave : |
age-related cortical thickness familial Alzheimer's disease lifespan presenilin1 trajectory |
Resumen : |
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. |
Mención de responsabilidad : |
Joshua T. Fox-Fuller, Heirangi Torrico-Teave, Federico d'Oleire Uquillas, Kewei Chen, Yi Su, Yinghua Chen, Michael Brickhouse, Justin S. Sanchez, Cinthya Aguero, Heidi I.L. Jacobs, Olivia Hampton, Edmarie Guzmán-Vélez, Clara Vila-Castelar, Daniel C. Aguirre-Acevedo, Ana Baena, Arabiye Artola, Jairo Martinez, Celina F. Pluim, Sergio Alvarez, Martin Ochoa-Escudero, Eric M. Reiman, Reisa A. Sperling, Francisco Lopera, Keith A. Johnson, Bradford C. Dickerson, Yakeel T. Quiroz |
Referencia : |
Alzheimers Dement (Amst). 2021 Sep 14;13(1):e12233. |
DOI (Digital Object Identifier) : |
10.1002/dad2.12233 |
PMID : |
34541287 |
Derechos de uso : |
CC BY-NC-ND |
En línea : |
https://alz-journals.onlinelibrary.wiley.com/doi/10.1002/dad2.12233 |
Enlace permanente : |
https://hospitalpablotobon.cloudbiteca.com/pmb/opac_css/index.php?lvl=notice_display&id=5885 |
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