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. 2017 Dec 12;89(24):2438-2446.
doi: 10.1212/WNL.0000000000004733. Epub 2017 Nov 17.

Increased florbetapir binding in the temporal neocortex from age 20 to 60 years

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Increased florbetapir binding in the temporal neocortex from age 20 to 60 years

Julie Gonneaud et al. Neurology. .

Abstract

Objective: To improve our understanding of early β-amyloid (Aβ) accumulation processes using florbetapir-PET scan in 20- to 60-year-old individuals.

Methods: Seventy-six cognitively normal individuals aged 20 to 60 years, 57 cognitively normal older individuals (61-84 years old), and 70 patients with mild cognitive impairment or probable Alzheimer disease (AD) underwent a florbetapir-PET scan. Images were spatially normalized and scaled using the whole cerebellum. The relationship with age was assessed on the mean neocortical standardized uptake value ratio (SUVR) and voxelwise in the younger group to assess early Aβ accumulation processes. To compare the topography of early-age-related vs AD-related changes, Aβ increase in patients vs cognitively normal older adults was also assessed.

Results: A linear increase of Aβ deposition from 20 to 60 years old was found on the mean neocortical SUVR, and more specifically on the temporal neocortex. By contrast, increase in patients predominated in frontal and medial parietal areas. The temporal increase in healthy participants was still significant when including only the 20- to 50-year-old individuals and controlling for several possible methodologic confounds.

Conclusions: Florbetapir binding increases linearly from 20 to 60 years old in the temporal lobe. Pending replication, including with other PET tracers, this study suggests that the well-described medial frontal and parietal accumulation in late adulthood and AD might superimpose to a physiologic accumulation of Aβ, starting from young adulthood, in temporal lobes.

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