Topography of 11C-Pittsburgh compound B uptake in Alzheimer’s disease: a voxel-based investigation of cortical and white matter regions

• Autor(a) principal: Faria,Daniele de P.
• Data de Publicação: 2019
• Outros Autores: Duran,Fabio L., Squarzoni,Paula, Coutinho,Artur M., Garcez,Alexandre T., Santos,Pedro P., Brucki,Sonia M., de Oliveira,Maira O., Trés,Eduardo S., Forlenza,Orestes V., Nitrini,Ricardo, Buchpiguel,Carlos A., Busatto Filho,Geraldo
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Brazilian Journal of Psychiatry (São Paulo. 1999. Online)
• Texto Completo: http://old.scielo.br/scielo.php?script=sci_arttext&pid=S1516-44462019000200003
• topic: Amyloid PET imaging; Alzheimer’s disease; statistical parametric mapping

Objective: To compare results of positron emission tomography (PET) with carbon-11-labeled Pittsburgh compound B (11C-PIB) obtained with cerebellar or global brain uptake for voxel intensity normalization, describe the cortical sites with highest tracer uptake in subjects with mild Alzheimer’s disease (AD), and explore possible group differences in 11C-PIB binding to white matter. Methods: 11C-PIB PET scans were acquired from subjects with AD (n=17) and healthy elderly controls (n=19). Voxel-based analysis was performed with statistical parametric mapping (SPM). Results: Cerebellar normalization showed higher 11C-PIB uptake in the AD group relative to controls throughout the cerebral cortex, involving the lateral temporal, orbitofrontal, and superior parietal cortices. With global uptake normalization, greatest cortical binding was detected in the orbitofrontal cortex; decreased 11C-PIB uptake in white matter was found in the posterior hippocampal region, corpus callosum, pons, and internal capsule. Conclusion: The present case-control voxelwise 11C-PIB PET comparison highlighted the regional distribution of amyloid deposition in the cerebral cortex of mildly demented AD patients. Tracer uptake was highest in the orbitofrontal cortex. Decreased 11C-PIB uptake in white-matter regions in this patient population may be a marker of white-matter damage in AD.