| Título : |
PET evidence of preclinical cerebellar amyloid plaque deposition in autosomal dominant Alzheimer's disease-causing Presenilin-1 E280A mutation carriers |
| Tipo de documento : |
documento electrónico |
| Autores : |
Sergio Álvarez Vallejo, |
| Fecha de publicación : |
2021 |
| Títulos uniformes : |
NeuroImage. Clinical
|
| Idioma : |
Inglés (eng) |
| Palabras clave : |
Brain imaging PET Amyloid Cerebellum Pons Autosomal dominant Alzheimer’s disease |
| Resumen : |
Background: In contrast to sporadic Alzheimer’s disease, autosomal dominant Alzheimer’s disease (ADAD) is associated with greater neuropathological evidence of cerebellar amyloid plaque (Aβ) deposition. In this study, we used positron emission tomography (PET) measurements of fibrillar Aβ burden to characterize the presence and age at onset of cerebellar Aβ deposition in cognitively unimpaired (CU) Presenilin-1 (PSEN1) E280A mutation carriers from the world’s largest extended family with ADAD. Methods: 18F florbetapir and 11C Pittsburgh compound B (PiB) PET data from two independent studies – API ADAD Colombia Trial (NCT01998841) and Colombia-Boston (COLBOS) longitudinal biomarker study were included. The tracers were selected independently by the respective sponsors prior to the start of each study and used exclusively throughout. Template-based cerebellar Aβ-SUVR (standard-uptake value ratios) using a known-to-be-spared pons reference region (cerebellar SUVR_pons), to a) compare 28–56-year-old CU carriers and non-carriers; b) estimate the age at which cerebellar SUVR_pons began to differ significantly in carrier and non-carrier groups; and c) characterize in carriers associations with age, cortical SUVR_pons, delayed recall memory, and API ADAD composite score. Results: Florbetapir and PiB cerebellar SUVR_pons were significantly higher in carriers than non-carriers (p |
| Mención de responsabilidad : |
Valentina Ghisays, Francisco Lopera, Dhruman D. Goradia, Hillary D. Protas, Michael H. Malek-Ahmadi, Yinghua Chen, Vivek Devadas, Ji Luo, Wendy Lee, Ana Baena, Yamile Bocanegra, Edmarie Guzman-Vélez, Enmanuelle Pardilla-Delgado, Clara Vila-Castelar, Joshua T. Fox-Fuller, Nan Hu, David Clayton, Ronald G. Thomas, Sergio Alvarez, Alejandro Espinosa, Natalia Acosta-Baena, Margarita M. Giraldo, Silvia Rios-Romenets, Jessica B. Langbaum, Kewei Chen, Yi Su, Pierre N. Tariot, Yakeel T. Quiroz, Eric M. Reiman, API ADAD Colombia Trial Group |
| Referencia : |
Neuroimage Clin. 2021;31:102749. |
| DOI (Digital Object Identifier) : |
10.1016/j.nicl.2021.102749 |
| PMID : |
34252876 |
| Derechos de uso : |
CC BY-NC-ND |
| En línea : |
https://linkinghub.elsevier.com/retrieve/pii/S2213158221001935 |
| Enlace permanente : |
https://hospitalpablotobon.cloudbiteca.com/pmb/opac_css/index.php?lvl=notice_display&id=5875 |
PET evidence of preclinical cerebellar amyloid plaque deposition in autosomal dominant Alzheimer's disease-causing Presenilin-1 E280A mutation carriers [documento electrónico] / Sergio Álvarez Vallejo, . - 2021. Obra : NeuroImage. ClinicalIdioma : Inglés ( eng) | Palabras clave : |
Brain imaging PET Amyloid Cerebellum Pons Autosomal dominant Alzheimer’s disease |
| Resumen : |
Background: In contrast to sporadic Alzheimer’s disease, autosomal dominant Alzheimer’s disease (ADAD) is associated with greater neuropathological evidence of cerebellar amyloid plaque (Aβ) deposition. In this study, we used positron emission tomography (PET) measurements of fibrillar Aβ burden to characterize the presence and age at onset of cerebellar Aβ deposition in cognitively unimpaired (CU) Presenilin-1 (PSEN1) E280A mutation carriers from the world’s largest extended family with ADAD. Methods: 18F florbetapir and 11C Pittsburgh compound B (PiB) PET data from two independent studies – API ADAD Colombia Trial (NCT01998841) and Colombia-Boston (COLBOS) longitudinal biomarker study were included. The tracers were selected independently by the respective sponsors prior to the start of each study and used exclusively throughout. Template-based cerebellar Aβ-SUVR (standard-uptake value ratios) using a known-to-be-spared pons reference region (cerebellar SUVR_pons), to a) compare 28–56-year-old CU carriers and non-carriers; b) estimate the age at which cerebellar SUVR_pons began to differ significantly in carrier and non-carrier groups; and c) characterize in carriers associations with age, cortical SUVR_pons, delayed recall memory, and API ADAD composite score. Results: Florbetapir and PiB cerebellar SUVR_pons were significantly higher in carriers than non-carriers (p |
| Mención de responsabilidad : |
Valentina Ghisays, Francisco Lopera, Dhruman D. Goradia, Hillary D. Protas, Michael H. Malek-Ahmadi, Yinghua Chen, Vivek Devadas, Ji Luo, Wendy Lee, Ana Baena, Yamile Bocanegra, Edmarie Guzman-Vélez, Enmanuelle Pardilla-Delgado, Clara Vila-Castelar, Joshua T. Fox-Fuller, Nan Hu, David Clayton, Ronald G. Thomas, Sergio Alvarez, Alejandro Espinosa, Natalia Acosta-Baena, Margarita M. Giraldo, Silvia Rios-Romenets, Jessica B. Langbaum, Kewei Chen, Yi Su, Pierre N. Tariot, Yakeel T. Quiroz, Eric M. Reiman, API ADAD Colombia Trial Group |
| Referencia : |
Neuroimage Clin. 2021;31:102749. |
| DOI (Digital Object Identifier) : |
10.1016/j.nicl.2021.102749 |
| PMID : |
34252876 |
| Derechos de uso : |
CC BY-NC-ND |
| En línea : |
https://linkinghub.elsevier.com/retrieve/pii/S2213158221001935 |
| Enlace permanente : |
https://hospitalpablotobon.cloudbiteca.com/pmb/opac_css/index.php?lvl=notice_display&id=5875 |
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PET evidence of preclinical cerebellar amyloid plaque deposition in autosomal dominant Alzheimer's disease-causing Presenilin-1 E280A mutation carriers
