Amyloid-beta plaque growth in cognitively normal adults: longitudinal [11C]Pittsburgh compound B data
- PMID: 22162065
- PMCID: PMC3243969
- DOI: 10.1002/ana.22608
Amyloid-beta plaque growth in cognitively normal adults: longitudinal [11C]Pittsburgh compound B data
Abstract
Amyloid-beta (Aβ) accumulation was evaluated with 2 [(11)C]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.
Copyright © 2011 American Neurological Association.
References
-
- Hardy J, Selkoe DJ. The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics. Science. 2002;297:353–6. - PubMed
-
- Holmes C, Boche D, Wilkinson D, et al. Long-term effects of Abeta42 immunisation in Alzheimer's disease: follow-up of a randomised, placebo-controlled phase I trial. Lancet. 2008;372:216–23. - PubMed
-
- Price JL, Ko AI, Wade MJ, Tsou SK, McKeel DW, Morris JC. Neuron number in the entorhinal cortex and CA1 in preclinical Alzheimer disease. Arch Neurol. 2001;58:1395–402. - PubMed
-
- Price JL, Morris JC. Tangles and plaques in nondemented aging and “preclinical” Alzheimer's disease. AnnNeurol. 1999;45:358–68. - PubMed
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