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A public resource of baseline data from the Alzheimer's Prevention Initiative Autosomal-Dominant Alzheimer's Disease Trial / Sergio Álvarez Vallejo    

Público ISBD Título : A public resource of baseline data from the Alzheimer's Prevention Initiative Autosomal-Dominant Alzheimer's Disease Trial Tipo de documento : documento electrónico Autores : Sergio Álvarez Vallejo, Fecha de publicación : 2022 Títulos uniformes : Alzheimer's & Dementia Idioma : Inglés (eng) Palabras clave : Alzheimer’s disease  amyloid  antibody  data sharing  magnetic resonance imaging  positron emission tomography  presenilin 1  primary prevention  secondary prevention Resumen : Introduction: The Alzheimer's Prevention Initiative Autosomal-Dominant Alzheimer's Disease (API ADAD) Trial evaluated the anti-oligomeric amyloid beta (Aβ) antibody therapy crenezumab in cognitively unimpaired members of the Colombian presenilin 1 (PSEN1) E280A kindred. We report availability, methods employed to protect confidentiality and anonymity of participants, and process for requesting and accessing baseline data. Methods: We developed mechanisms to share baseline data from the API ADAD Trial in consultation with experts and other groups sharing data from Alzheimer's disease (AD) prevention trials, balancing the need to protect anonymity and trial integrity with making data broadly available to accelerate progress in the field. We pressure-tested deliberate and inadvertent potential threats under specific assumptions, employed a system to suppress or mask both direct and indirect identifying variables, limited and firewalled data managers, and put forth specific principles requisite to receive data. Results: Baseline demographic, PSEN1 E280A and apolipoprotein E genotypes, florbetapir and fluorodeoxyglucose positron emission tomography, magnetic resonance imaging, clinical, and cognitive data can now be requested by interested researchers. Discussion: Baseline data are publicly available; treatment data and biological samples, including baseline and treatment-related blood-based biomarker data will become available in accordance with our original trial agreement and subsequently developed Collaboration for Alzheimer's Prevention principles. Sharing of these data will allow exploration of important questions including the differential effects of initiating an investigational AD prevention therapy both before as well as after measurable Aβ plaque deposition. Mención de responsabilidad : Eric M. Reiman, Jeremy J. Pruzin, Silvia Rios-Romenets, Chris Brown, Margarita Giraldo, Natalia Acosta-Baena, Carlos Tobon, Nan Hu, Yinghua Chen, Valentina Ghisays, Jessica Enos, Dhruman D. Goradia, Wendy Lee, Ji Luo, Michael Malek-Ahmadi, Hillary Protas, Ronald G. Thomas, Kewei Chen, Yi Su, Connie Boker, Diego Mastroeni, Sergio Alvarez, Yakeel T. Quiroz, Jessica B. Langbaum, Kaycee M. Sink, Francisco Lopera, Pierre N. Tariot, and the API ADAD Colombia Trial Group Referencia : Alzheimers Dement. 2022 Nov 14. DOI (Digital Object Identifier) : 10.1002/alz.12843 PMID : 36373344 Derechos de uso : CC BY-NC En línea : https://alz-journals.onlinelibrary.wiley.com/doi/10.1002/alz.12843 Enlace permanente : https://hospitalpablotobon.cloudbiteca.com/pmb/opac_css/index.php?lvl=notice_dis A public resource of baseline data from the Alzheimer's Prevention Initiative Autosomal-Dominant Alzheimer's Disease Trial [documento electrónico] / Sergio Álvarez Vallejo,  . - 2022. Obra : Alzheimer's & Dementia Idioma : Inglés (eng) Palabras clave : Alzheimer’s disease  amyloid  antibody  data sharing  magnetic resonance imaging  positron emission tomography  presenilin 1  primary prevention  secondary prevention Resumen : Introduction: The Alzheimer's Prevention Initiative Autosomal-Dominant Alzheimer's Disease (API ADAD) Trial evaluated the anti-oligomeric amyloid beta (Aβ) antibody therapy crenezumab in cognitively unimpaired members of the Colombian presenilin 1 (PSEN1) E280A kindred. We report availability, methods employed to protect confidentiality and anonymity of participants, and process for requesting and accessing baseline data. Methods: We developed mechanisms to share baseline data from the API ADAD Trial in consultation with experts and other groups sharing data from Alzheimer's disease (AD) prevention trials, balancing the need to protect anonymity and trial integrity with making data broadly available to accelerate progress in the field. We pressure-tested deliberate and inadvertent potential threats under specific assumptions, employed a system to suppress or mask both direct and indirect identifying variables, limited and firewalled data managers, and put forth specific principles requisite to receive data. Results: Baseline demographic, PSEN1 E280A and apolipoprotein E genotypes, florbetapir and fluorodeoxyglucose positron emission tomography, magnetic resonance imaging, clinical, and cognitive data can now be requested by interested researchers. Discussion: Baseline data are publicly available; treatment data and biological samples, including baseline and treatment-related blood-based biomarker data will become available in accordance with our original trial agreement and subsequently developed Collaboration for Alzheimer's Prevention principles. Sharing of these data will allow exploration of important questions including the differential effects of initiating an investigational AD prevention therapy both before as well as after measurable Aβ plaque deposition. Mención de responsabilidad : Eric M. Reiman, Jeremy J. Pruzin, Silvia Rios-Romenets, Chris Brown, Margarita Giraldo, Natalia Acosta-Baena, Carlos Tobon, Nan Hu, Yinghua Chen, Valentina Ghisays, Jessica Enos, Dhruman D. Goradia, Wendy Lee, Ji Luo, Michael Malek-Ahmadi, Hillary Protas, Ronald G. Thomas, Kewei Chen, Yi Su, Connie Boker, Diego Mastroeni, Sergio Alvarez, Yakeel T. Quiroz, Jessica B. Langbaum, Kaycee M. Sink, Francisco Lopera, Pierre N. Tariot, and the API ADAD Colombia Trial Group Referencia : Alzheimers Dement. 2022 Nov 14. DOI (Digital Object Identifier) : 10.1002/alz.12843 PMID : 36373344 Derechos de uso : CC BY-NC En línea : https://alz-journals.onlinelibrary.wiley.com/doi/10.1002/alz.12843 Enlace permanente : https://hospitalpablotobon.cloudbiteca.com/pmb/opac_css/index.php?lvl=notice_dis

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Longitudinal amyloid and tau accumulation in autosomal dominant Alzheimer's disease: findings from the Colombia-Boston (COLBOS) biomarker study / Martín Ochoa Escudero ; Sergio Álvarez Vallejo    

Público ISBD Título : Longitudinal amyloid and tau accumulation in autosomal dominant Alzheimer's disease: findings from the Colombia-Boston (COLBOS) biomarker study Tipo de documento : documento electrónico Autores : Martín Ochoa Escudero, ; Sergio Álvarez Vallejo, Fecha de publicación : 2021 Títulos uniformes : Alzheimer's Research & Therapy Idioma : Inglés (eng) Palabras clave : Alzheimer’s  Amyloid  Autosomal-Dominant  Imaging  Longitudinal  Tau Resumen : Background: Neuroimaging studies of autosomal dominant Alzheimer's disease (ADAD) enable characterization of the trajectories of cerebral amyloid-β (Aβ) and tau accumulation in the decades prior to clinical symptom onset. Longitudinal rates of regional tau accumulation measured with positron emission tomography (PET) and their relationship with other biomarker and cognitive changes remain to be fully characterized in ADAD. Methods: Fourteen ADAD mutation carriers (Presenilin-1 E280A) and 15 age-matched non-carriers from the Colombian kindred underwent 2-3 sessions of Aβ (11C-Pittsburgh compound B) and tau (18F-flortaucipir) PET, structural magnetic resonance imaging, and neuropsychological evaluation over a 2-4-year follow-up period. Annualized rates of change for imaging and cognitive variables were compared between carriers and non-carriers, and relationships among baseline measurements and rates of change were assessed within carriers. Results: Longitudinal measurements were consistent with a sequence of ADAD-related changes beginning with Aβ accumulation (16 years prior to expected symptom onset, EYO), followed by entorhinal cortex (EC) tau (9 EYO), neocortical tau (6 EYO), hippocampal atrophy (6 EYO), and cognitive decline (4 EYO). Rates of tau accumulation among carriers were most rapid in parietal neocortex (~ 9%/year). EC tau PET signal at baseline was a significant predictor of subsequent neocortical tau accumulation and cognitive decline within carriers. Conclusions: Our results are consistent with the sequence of biological changes in ADAD implied by cross-sectional studies and highlight the importance of EC tau as an early biomarker and a potential link between Aβ burden and neocortical tau accumulation in ADAD. Mención de responsabilidad : Justin S. Sanchez, Bernard J. Hanseeuw, Francisco Lopera, Reisa A. Sperling, Ana Baena, Yamile Bocanegra, David Aguillon, Edmarie Guzmán-Vélez, Enmanuelle Pardilla-Delgado, Liliana Ramirez-Gomez, Clara Vila-Castelar, Jairo E. Martinez, Joshua T. Fox-Fuller, Claudia Ramos, Martin Ochoa-Escudero, Sergio Alvarez, Heidi I. L. Jacobs, Aaron P. Schultz, Jennifer R. Gatchel, J. Alex Becker, Samantha R. Katz, Danielle V. Mayblyum, Julie C. Price, Eric M. Reiman, Keith A. Johnson and Yakeel T. Quiroz Referencia : Alzheimers Res Ther. 2021 Jan 15;13(1):27. DOI (Digital Object Identifier) : 10.1186/s13195-020-00765-5 PMID : 33451357 Derechos de uso : CC BY En línea : https://alzres.biomedcentral.com/articles/10.1186/s13195-020-00765-5 Enlace permanente : https://hospitalpablotobon.cloudbiteca.com/pmb/opac_css/index.php?lvl=notice_dis Longitudinal amyloid and tau accumulation in autosomal dominant Alzheimer's disease: findings from the Colombia-Boston (COLBOS) biomarker study [documento electrónico] / Martín Ochoa Escudero, ; Sergio Álvarez Vallejo,  . - 2021. Obra : Alzheimer's Research & Therapy Idioma : Inglés (eng) Palabras clave : Alzheimer’s  Amyloid  Autosomal-Dominant  Imaging  Longitudinal  Tau Resumen : Background: Neuroimaging studies of autosomal dominant Alzheimer's disease (ADAD) enable characterization of the trajectories of cerebral amyloid-β (Aβ) and tau accumulation in the decades prior to clinical symptom onset. Longitudinal rates of regional tau accumulation measured with positron emission tomography (PET) and their relationship with other biomarker and cognitive changes remain to be fully characterized in ADAD. Methods: Fourteen ADAD mutation carriers (Presenilin-1 E280A) and 15 age-matched non-carriers from the Colombian kindred underwent 2-3 sessions of Aβ (11C-Pittsburgh compound B) and tau (18F-flortaucipir) PET, structural magnetic resonance imaging, and neuropsychological evaluation over a 2-4-year follow-up period. Annualized rates of change for imaging and cognitive variables were compared between carriers and non-carriers, and relationships among baseline measurements and rates of change were assessed within carriers. Results: Longitudinal measurements were consistent with a sequence of ADAD-related changes beginning with Aβ accumulation (16 years prior to expected symptom onset, EYO), followed by entorhinal cortex (EC) tau (9 EYO), neocortical tau (6 EYO), hippocampal atrophy (6 EYO), and cognitive decline (4 EYO). Rates of tau accumulation among carriers were most rapid in parietal neocortex (~ 9%/year). EC tau PET signal at baseline was a significant predictor of subsequent neocortical tau accumulation and cognitive decline within carriers. Conclusions: Our results are consistent with the sequence of biological changes in ADAD implied by cross-sectional studies and highlight the importance of EC tau as an early biomarker and a potential link between Aβ burden and neocortical tau accumulation in ADAD. Mención de responsabilidad : Justin S. Sanchez, Bernard J. Hanseeuw, Francisco Lopera, Reisa A. Sperling, Ana Baena, Yamile Bocanegra, David Aguillon, Edmarie Guzmán-Vélez, Enmanuelle Pardilla-Delgado, Liliana Ramirez-Gomez, Clara Vila-Castelar, Jairo E. Martinez, Joshua T. Fox-Fuller, Claudia Ramos, Martin Ochoa-Escudero, Sergio Alvarez, Heidi I. L. Jacobs, Aaron P. Schultz, Jennifer R. Gatchel, J. Alex Becker, Samantha R. Katz, Danielle V. Mayblyum, Julie C. Price, Eric M. Reiman, Keith A. Johnson and Yakeel T. Quiroz Referencia : Alzheimers Res Ther. 2021 Jan 15;13(1):27. DOI (Digital Object Identifier) : 10.1186/s13195-020-00765-5 PMID : 33451357 Derechos de uso : CC BY En línea : https://alzres.biomedcentral.com/articles/10.1186/s13195-020-00765-5 Enlace permanente : https://hospitalpablotobon.cloudbiteca.com/pmb/opac_css/index.php?lvl=notice_dis

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PET evidence of preclinical cerebellar amyloid plaque deposition in autosomal dominant Alzheimer's disease-causing Presenilin-1 E280A mutation carriers / Sergio Álvarez Vallejo    

Público ISBD 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_dis 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. 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_dis

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