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Florbetaben for PET Imaging of Beta-Amyloid Plaques in the Brain.

ABSTRACT: Alzheimer's disease (AD) is a devastating neurodegenerative disorder affecting the elderly. Current clinical diagnostic tools are often ineffective in accurately diagnosing AD. However, new advances in diagnostic imaging, particularly positron emission tomography (PET) amyloid imaging, have shown increased sensitivity and specificity, as well as high inter-reader agreement. The most commonly studied tracer, PiB-C11, has shown high affinity binding to amyloid, but is limited in its use outside of research due to its short half-life. Instead, development of other PET ligands with increased half-life, such as fluorine-18-labeled ((18)F) tracers, allows for more widespread use of PET in clinical settings. In particular, recent phase II and III trials of (18)F-florbetaben have demonstrated the high accuracy of this PET tracer in identifying amyloid accumulation. This paper will examine the techniques of amyloid imaging, focusing particularly on the recently approved (18)F-florbetaben.

SUBMITTER: Richards D

PROVIDER: S-EPMC4386430 | biostudies-literature | 2014 Dec

REPOSITORIES: biostudies-literature

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Florbetaben for PET Imaging of Beta-Amyloid Plaques in the Brain.

Richards Danielle D Sabbagh Marwan N MN

Neurology and therapy 20141127 2

Alzheimer's disease (AD) is a devastating neurodegenerative disorder affecting the elderly. Current clinical diagnostic tools are often ineffective in accurately diagnosing AD. However, new advances in diagnostic imaging, particularly positron emission tomography (PET) amyloid imaging, have shown increased sensitivity and specificity, as well as high inter-reader agreement. The most commonly studied tracer, PiB-C11, has shown high affinity binding to amyloid, but is limited in its use outside of ...[more]

PMID: 26000224

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Project description:Individuals with familial Alzheimer's disease due to PSEN1 mutations develop high cortical fibrillar amyloid-β load but often have lower cortical 11C-Pittsburgh compound B (PiB) retention than Individuals with sporadic Alzheimer's disease. We hypothesized this is influenced by limited interactions of Pittsburgh compound B with cotton wool plaques, an amyloid-β plaque type common in familial Alzheimer's disease but rare in sporadic Alzheimer's disease. Histological sections of frontal and temporal cortex, caudate nucleus and cerebellum were obtained from 14 cases with sporadic Alzheimer's disease, 12 cases with familial Alzheimer's disease due to PSEN1 mutations, two relatives of a PSEN1 mutation carrier but without genotype information and three non-Alzheimer's disease cases. Sections were processed immunohistochemically using amyloid-β-targeting antibodies and the fluorescent amyloid stains cyano-PiB and X-34. Plaque load was quantified by percentage area analysis. Frozen homogenates from the same brain regions from five sporadic Alzheimer's disease and three familial Alzheimer's disease cases were analysed for 3H-PiB in vitro binding and concentrations of amyloid-β1-40 and amyloid-β1-42. Nine sporadic Alzheimer's disease, three familial Alzheimer's disease and three non-Alzheimer's disease participants had 11C-PiB PET with standardized uptake value ratios calculated using the cerebellum as the reference region. Cotton wool plaques were present in the neocortex of all familial Alzheimer's disease cases and one sporadic Alzheimer's disease case, in the caudate nucleus from four familial Alzheimer's disease cases, but not in the cerebellum. Cotton wool plaques immunolabelled robustly with 4G8 and amyloid-β42 antibodies but weakly with amyloid-β40 and amyloid-βN3pE antibodies and had only background cyano-PiB fluorescence despite labelling with X-34. Relative to amyloid-β plaque load, cyano-Pittsburgh compound B plaque load was similar in sporadic Alzheimer's disease while in familial Alzheimer's disease it was lower in the neocortex and the caudate nucleus. In both regions, insoluble amyloid-β1-42 and amyloid-β1-40 concentrations were similar in familial Alzheimer's disease and sporadic Alzheimer's disease groups, while 3H-PiB binding was lower in the familial Alzheimer's disease than the sporadic Alzheimer's disease group. Higher amyloid-β1-42 concentration associated with higher 3H-PiB binding in sporadic Alzheimer's disease but not familial Alzheimer's disease. 11C-PiB retention correlated with region-matched post-mortem amyloid-β plaque load; however, familial Alzheimer's disease cases with abundant cotton wool plaques had lower 11C-PiB retention than sporadic Alzheimer's disease cases with similar amyloid-β plaque loads. PiB has limited ability to detect amyloid-β aggregates in cotton wool plaques and may underestimate total amyloid-β plaque burden in brain regions with abundant cotton wool plaques.

Dataset Information

Florbetaben for PET Imaging of Beta-Amyloid Plaques in the Brain.

Publications

Florbetaben for PET Imaging of Beta-Amyloid Plaques in the Brain.

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