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Review
. 2012 Mar;1822(3):370-9.
doi: 10.1016/j.bbadis.2011.11.005. Epub 2011 Nov 12.

PET amyloid-beta imaging in preclinical Alzheimer's disease

Andrei G Vlassenko  1 , Tammie L S Benzinger, John C Morris
Affiliations
Review

PET amyloid-beta imaging in preclinical Alzheimer's disease

Andrei G Vlassenko et al. Biochim Biophys Acta. 2012 Mar.

Abstract

Alzheimer's disease (AD) is the leading cause of dementia, accounting for 60-70% of all cases [Hebert et al., 2003, 1]. The need for effective therapies for AD is great. Current approaches, including cholinesterase inhibitors and N-methyl-d-aspartate (NMDA) receptor antagonists, are symptomatic treatments for AD but do not prevent disease progression. Many diagnostic and therapeutic approaches to AD are currently changing due to the knowledge that underlying pathology starts 10 to 20 years before clinical signs of dementia appear [Holtzman et al., 2011, 2]. New therapies which focus on prevention or delay of the onset or cognitive symptoms are needed. Recent advances in the identification of AD biomarkers now make it possible to detect AD pathology in the preclinical stage of the disease, in cognitively normal (CN) individuals; this biomarker data should be used in the selection of high-risk populations for clinical trials. In vivo visualization of AD neuropathology and biological, biochemical or physiological confirmation of the effects of treatment likely will substantially improve development of novel pharmaceuticals. Positron emission tomography (PET) is the leading neuroimaging tool to detect and provide quantitative measures of AD amyloid pathology in vivo at the early stages and follow its course longitudinally. This article is part of a Special Issue entitled: Imaging Brain Aging and Neurodegenerative disease.

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Figures

Figure 1
Figure 1
Mean MRI and PET [11C]PIB distribution in a standard atlas coordinate system from 10 subjects with dementia of the Alzheimer type. PET data represent [11C]PIB activity in the late (30 to 60 minutes after injection) distribution and has been normalized to standardize display and increase contrast. Brain areas used to detect raised [11C] PIB uptake in nondemented subjects are indicated with arrows. PFC = prefrontal cortex; Temp = temporal cortex; Precun = precuneus region. Reproduced with permission from [84].
Figure 2
Figure 2
Schematic maps showing [11C] PIB BP distribution on lateral and medial cortical surfaces of the left (L) and right (R) hemispheres of the human brain. A, Healthy young (< 50 y. o) adults; B–D, Cognitively normal older (> 50 y. o.) adults with low (B), moderate (C) and high (D) Aβ deposition; E, Individuals with dementia of Alzheimer’s type (modified from Vlassenko et al. 2010 with permission).
See this image and copyright information in PMC

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