dc.creatorLopera Restrepo, Francisco Javier
dc.creatorHanseeuw, Bernard J.
dc.creatorSperling, Reisa A.
dc.creatorNorton, Daniel J.
dc.creatorGuzman Velez, Edmarie
dc.creatorBaena, Ana
dc.creatorPardilla Delgado, Enmanuelle
dc.creatorSchultz, Aaron P.
dc.creatorGatchel, Jennifer
dc.creatorJin, David
dc.creatorChein, Kewei
dc.creatorReiman, Eric M.
dc.creatorJohnson, Keith A.
dc.creatorQuiroz, Yakeel T.
dc.date2023-04-11T21:26:42Z
dc.date2023-04-11T21:26:42Z
dc.date2019
dc.date.accessioned2024-04-23T18:11:13Z
dc.date.available2024-04-23T18:11:13Z
dc.identifier1758-9193
dc.identifierhttps://hdl.handle.net/10495/34633
dc.identifier10.1186/s13195-019-0468-1
dc.identifier1758-9193
dc.identifier.urihttps://repositorioslatinoamericanos.uchile.cl/handle/2250/9230504
dc.descriptionABSTRACT: Background: Autosomal dominant Alzheimer’s disease (ADAD) is distinguished from late-onset AD by early striatal amyloid-β deposition. To determine whether striatal Pittsburgh compound B (PiB)-PET measurements of amyloid-β can help predict disease severity in ADAD, we compared relationships of striatal and neocortical PiB-PET to age, tau-PET, and memory performance in the Colombian Presenilin 1 E280A kindred. Methods: Fourteen carriers (age = 28–42, Mini-Mental State Examination = 26–30) and 20 age-matched noncarriers were evaluated using PiB, flortaucipir (FTP; tau), and memory testing (CERAD Word List Learning). PiB-PET signal was measured in neocortical and striatal aggregates. FTP-PET signal was measured in entorhinal cortex.Results: Compared to non-carriers, mutation carriers had age-related elevations in both neocortical and striatal PiB binding. The PiB elevation in carriers was significantly greater in the striatum than in the neocortex. In mutation carriers, PiB binding in both the neocortex and the striatum is related to entorhinal FTP; however, the association was stronger with the striatum. Only striatal PiB was associated with worse memory. Remarkably, PiB binding in the striatum, but not in the neocortex, predicted entorhinal FTP and lower memory scores after adjusting for age, indicating that striatal PiB identified the carriers with the most severe disease. Conclusions: Based on these preliminary cross-sectional findings, striatal PiB-PET measurements may offer particular value in the detection and tracking of preclinical ADAD, informing a mutation carrier’s prognosis and evaluating amyloid-β-modifying ADAD treatments.
dc.descriptionCOL0010744
dc.format6
dc.formatapplication/pdf
dc.formatapplication/pdf
dc.languageeng
dc.publisherBioMed Central Ltd
dc.publisherGrupo de Neurociencias de Antioquia
dc.publisherInglaterra
dc.relationAlzheimer's Res. Ther.
dc.rightsinfo:eu-repo/semantics/openAccess
dc.rightshttp://creativecommons.org/licenses/by/2.5/co/
dc.rightshttp://purl.org/coar/access_right/c_abf2
dc.rightshttps://creativecommons.org/licenses/by/4.0/
dc.subjectMemory
dc.subjectMemoria
dc.subjectAlzheimer Disease
dc.subjectEnfermedad de Alzheimer
dc.subjectCorpus Striatum
dc.subjectCuerpo Estriado
dc.titleStriatal Amyloid is Associated with Tauopathy and Memory Decline in Familial Alzheimer's Disease
dc.typeinfo:eu-repo/semantics/article
dc.typeinfo:eu-repo/semantics/publishedVersion
dc.typehttp://purl.org/coar/resource_type/c_2df8fbb1
dc.typehttps://purl.org/redcol/resource_type/ART
dc.typeArtículo de investigación


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