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EJNMMI Res. 2013 Jun 03;3(1):43. doi: 10.1186/2191-219X-3-43.

Cortical florbetapir-PET amyloid load in prodromal Alzheimer's disease patients.

EJNMMI research

Laure Saint-Aubert, Emmanuel J Barbeau, Patrice Péran, Federico Nemmi, Celine Vervueren, Helene Mirabel, Pierre Payoux, Anne Hitzel, Fabrice Bonneville, Raluca Gramada, Mathieu Tafani, Christian Vincent, Michele Puel, Sophie Dechaumont, Francois Chollet, Jeremie Pariente

Affiliations

  1. INSERM, Imagerie Cérébrale et Handicaps Neurologiques UMR 825, Centre Hospitalier Universitaire de Toulouse, Place Dr Baylac, Pavillon Baudot, Toulouse CEDEX 9 31059, France. [email protected].

PMID: 23731789 PMCID: PMC3733998 DOI: 10.1186/2191-219X-3-43

Abstract

BACKGROUND: Florbetapir (AV-45) has been shown to be a reliable tool to assess amyloid load in patients with Alzheimer's disease (AD) at demential stages. Longitudinal studies also suggest that AV-45 has the ability to bind amyloid in the early stages of AD. In this study, we investigated AV-45 binding and its relation with cognitive performance in a group of patients at the prodromal stage of Alzheimer's disease, recruited according to strict inclusion criteria.

METHODS: We recruited patients at the prodromal stage of AD and matched control subjects. AV-45 binding was assessed using an innovative extraction method allowing quantifying uptake in the cortex only. AV-45 uptake was compared between groups in the precuneus, posterior cingulate, anterior cingulate, and orbito-frontal regions. Correlations between AV-45 uptake and cognitive performance were assessed.

RESULTS: Twenty-two patients and 17 matched control subjects were included in the study. We report a significant increase of cortical AV-45 uptake in the patients compared to the control subjects in all regions of interest. Specific correlations were found within the patient group between mean global amyloid cortical load and cognitive performance in three different memory tests.

CONCLUSIONS: These findings suggest that at the prodromal stage of AD, memory decline is linked to an increase of cortical β-amyloid load.

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