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Molecular neuroimaging in dominantly inherited versus sporadic early-onset Alzheimer's disease.

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dc.contributor.author Iaccarino, Leonardo
dc.contributor.author Llibre Guerra, Jorge J.
dc.contributor.author McDade, Eric
dc.contributor.author Edwards, Lauren
dc.contributor.author Gordon, Brian A.
dc.contributor.author Benzinger, Tammie L.S.
dc.contributor.author Hassenstab, Jason
dc.contributor.author Kramer, Joel H.
dc.contributor.author Li, Yan
dc.contributor.author Miller, Bruce L.
dc.contributor.author Miller, Zachary
dc.contributor.author Morris, John C.
dc.contributor.author Mundada, Nidhi
dc.contributor.author Perrin, Richard J.
dc.contributor.author Rosen, Howard J.
dc.contributor.author Soleimani Meigooni, David
dc.contributor.author Strom, Amelia
dc.contributor.author Tsoy, Elena
dc.contributor.author Wang, Guoqiao
dc.contributor.author Xiong, Chengjie
dc.contributor.author Allegri, Ricardo Francisco
dc.contributor.author Chrem Méndez, Patricio Alexis
dc.contributor.author Vázquez, Silvia
dc.date.accessioned 2024-07-15T12:42:21Z
dc.date.available 2024-07-15T12:42:21Z
dc.date.issued 2024-05-03
dc.identifier.citation Iaccarino L, Llibre-Guerra JJ, McDade E, Edwards L, Gordon B, Benzinger T, Hassenstab J, Kramer JH, Li Y, Miller BL, Miller Z, Morris JC, Mundada N, Perrin RJ, Rosen HJ, Soleimani-Meigooni D, Strom A, Tsoy E, Wang G, Xiong C, Allegri R, Chrem P, Vazquez S, Berman SB, Chhatwal J, Masters CL, Farlow MR, Jucker M, Levin J, Salloway S, Fox NC, Day GS, Gorno-Tempini ML, Boxer AL, La Joie R, Bateman R, Rabinovici GD. Molecular neuroimaging in dominantly inherited versus sporadic early-onset Alzheimer's disease. Brain Commun. 2024 May 3;6(3):fcae159. doi: 10.1093/braincomms/fcae159. es_ES
dc.identifier.uri https://doi.org/10.1093/braincomms/fcae159
dc.identifier.uri https://repositorio.fleni.org.ar/xmlui/handle/123456789/1147
dc.description.abstract Approximately 5% of Alzheimer's disease patients develop symptoms before age 65 (early-onset Alzheimer's disease), with either sporadic (sporadic early-onset Alzheimer's disease) or dominantly inherited (dominantly inherited Alzheimer's disease) presentations. Both sporadic early-onset Alzheimer's disease and dominantly inherited Alzheimer's disease are characterized by brain amyloid-β accumulation, tau tangles, hypometabolism and neurodegeneration, but differences in topography and magnitude of these pathological changes are not fully elucidated. In this study, we directly compared patterns of amyloid-β plaque deposition and glucose hypometabolism in sporadic early-onset Alzheimer's disease and dominantly inherited Alzheimer's disease individuals. Our analysis included 134 symptomatic sporadic early-onset Alzheimer's disease amyloid-Positron Emission Tomography (PET)-positive cases from the University of California, San Francisco, Alzheimer's Disease Research Center (mean ± SD age 59.7 ± 5.6 years), 89 symptomatic dominantly inherited Alzheimer's disease cases (age 45.8 ± 9.3 years) and 102 cognitively unimpaired non-mutation carriers from the Dominantly Inherited Alzheimer Network study (age 44.9 ± 9.2). Each group underwent clinical and cognitive examinations, 11C-labelled Pittsburgh Compound B-PET and structural MRI. 18F-Fluorodeoxyglucose-PET was also available for most participants. Positron Emission Tomography scans from both studies were uniformly processed to obtain a standardized uptake value ratio (PIB50-70 cerebellar grey reference and FDG30-60 pons reference) images. Statistical analyses included pairwise global and voxelwise group comparisons and group-independent component analyses. Analyses were performed also adjusting for covariates including age, sex, Mini-Mental State Examination, apolipoprotein ε4 status and average composite cortical of standardized uptake value ratio. Compared with dominantly inherited Alzheimer's disease, sporadic early-onset Alzheimer's disease participants were older at age of onset (mean ± SD, 54.8 ± 8.2 versus 41.9 ± 8.2, Cohen's d = 1.91), with more years of education (16.4 ± 2.8 versus 13.5 ± 3.2, d = 1) and more likely to be apolipoprotein ε4 carriers (54.6% ε4 versus 28.1%, Cramer's V = 0.26), but similar Mini-Mental State Examination (20.6 ± 6.1 versus 21.2 ± 7.4, d = 0.08). Sporadic early-onset Alzheimer's disease had higher global cortical Pittsburgh Compound B-PET binding (mean ± SD standardized uptake value ratio, 1.92 ± 0.29 versus 1.58 ± 0.44, d = 0.96) and greater global cortical 18F-fluorodeoxyglucose-PET hypometabolism (mean ± SD standardized uptake value ratio, 1.32 ± 0.1 versus 1.39 ± 0.19, d = 0.48) compared with dominantly inherited Alzheimer's disease. Fully adjusted comparisons demonstrated relatively higher Pittsburgh Compound B-PET standardized uptake value ratio in the medial occipital, thalami, basal ganglia and medial/dorsal frontal regions in dominantly inherited Alzheimer's disease versus sporadic early-onset Alzheimer's disease. Sporadic early-onset Alzheimer's disease showed relatively greater 18F-fluorodeoxyglucose-PET hypometabolism in Alzheimer's disease signature temporoparietal regions and caudate nuclei, whereas dominantly inherited Alzheimer's disease showed relatively greater hypometabolism in frontal white matter and pericentral regions. Independent component analyses largely replicated these findings by highlighting common and unique Pittsburgh Compound B-PET and 18F-fluorodeoxyglucose-PET binding patterns. In summary, our findings suggest both common and distinct patterns of amyloid and glucose hypometabolism in sporadic and dominantly inherited early-onset Alzheimer's disease. es_ES
dc.language.iso eng es_ES
dc.publisher Oxford University Press es_ES
dc.rights info:eu-repo/semantics/openAccess
dc.subject Alzheimer Disease es_ES
dc.subject Enfermedad de Alzheimer es_ES
dc.subject Glucosa es_ES
dc.subject Glucose es_ES
dc.subject Metabolismo es_ES
dc.subject Metabolism es_ES
dc.title Molecular neuroimaging in dominantly inherited versus sporadic early-onset Alzheimer's disease. es_ES
dc.type info:eu-repo/semantics/article es_ES
dc.type info:eu-repo/semantics/publishedVersion
dc.description.fil Fil: Allegri, Ricardo Francisco. Fleni. Departamento de Neurología. Servicio de Neurología Cognitiva, Neuropsicología y Neuropsiquiatría; Argentina.
dc.relation.ispartofVOLUME 6
dc.relation.ispartofNUMBER 3
dc.relation.ispartofPAGINATION fcae159
dc.relation.ispartofCOUNTRY Inglaterra
dc.relation.ispartofCITY Oxford
dc.relation.ispartofTITLE Brain communications
dc.relation.ispartofISSN 2632-1297
dc.type.snrd info:ar-repo/semantics/artículo es_ES


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