Amyloid-beta plaque growth in cognitively normal adults: Longitudinal [11C]Pittsburgh compound B data

Vlassenko AG, Mintun MA, Xiong C, Sheline YI, Goate AM, Benzinger TLS, Morris JC. ; Annals of Neurology 2011; 70:857-861. Read More

Abstract

Amyloid-beta (Aβ) accumulation was evaluated with 2 [11C]Pittsburgh compound B (PiB) positron emission tomography scans about 2.5 years apart in 146 cognitively normal adults. Seventeen of 21 participants with initially elevated Aβ deposition demonstrated subsequent Aβ plaque growth (approximately 8.0% per year), and none reverted to a state of no Aβ deposits. Ten individuals converted from negative to positive PiB status, based on a threshold of the mean cortical binding potential, representing a conversion rate of 3.1% per year. Individuals with an ε4 allele of apolipoprotein E demonstrated increased incidence of conversion (7.0% per year). Our findings suggest that the major growth in Aβ burden occurs during a preclinical stage of Alzheimer disease (AD), prior to the onset of AD-related symptoms. Ann Neurol 2011

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Posted on February 11, 2014
Posted in: HPAN, Neurodegeneration, Neurogenetics, Publications Authors: , ,