Yeungnam Univ J Med.  2018 Jun;35(1):1-6. 10.12701/yujm.2018.35.1.1.

Beta-amyloid imaging in dementia

• Chun KA

• KMID: 2415727
• DOI: http://doi.org/10.12701/yujm.2018.35.1.1

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder associated with extracellular plaques, composed of amyloid-beta (Aβ), in the brain. Although the precise mechanism underlying the neurotoxicity of Aβ has not been established, Aβ accumulation is the primary event in a cascade of events that lead to neurofibrillary degeneration and dementia. In particular, the Aβ burden, as assessed by neuroimaging, has proved to be an excellent predictive biomarker. Positron emission tomography, using ligands such as ¹¹C-labeled Pittsburgh Compound B or ¹â¸F-labeled tracers, such as ¹â¸F-florbetaben, ¹â¸F-florbetapir, and ¹â¸F-flutemetamol, which bind to Aβ deposits in the brain, has been a valuable technique for visualizing and quantifying the deposition of Aβ throughout the brain in living subjects. Aβ imaging has very high sensitivity for detecting AD pathology. In addition, it can predict the progression from mild cognitive impairment to AD, and contribute to the development of disease-specific therapies.

Keyword

Alzheimer's disease; Amyloid-beta; Positron emission tomography

MeSH Terms

Alzheimer Disease
Brain
Dementia*
Ligands
Mild Cognitive Impairment
Neurodegenerative Diseases
Neuroimaging
Pathology
Positron-Emission Tomography
Ligands

Figure

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  Fig. 1. Chronological relationships among pathology, clinical symptoms and biomarkers. Based on biomarker studies, β-amyloid protein accumulation appears to start-20 years before the onset of dementia (adapted from Yoshiyama et al. J Neurol Neurosurg Psychiatry 2013;84:784-95, with permission of British Medical Association). MCI, mild cognitive impairment; sMRI, structural MRI; FDG, 2-[18F]-fluoro-2-deoxy-D-glucose; PET, positron emission tomography; CSF, cerebrospinal fluid; Aβ, β-amyloid protein; fMRI, functional magnetic resonance imaging.

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  Fig. 2. Molecular and cellular processes presumed to participate in AD pathogenesis. Aβ peptides produced by neurons and other brain cells and build-up of pathogenic Aβ assemblies could result from increased production or aggregation or from deficient clearance mechanisms (adapted from Roberson et al. Science 2006;314:781-4, with permission of American Association for the Advancement of Science). AD, Alzheimer’s disease; Aβ, β-amyloid protein.

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  Fig. 3. Axial view of 18F-flutemetamol positron emission tomography scans. Negative image (A) shows a white matter sulcal pattern at the frontal and lateral temporal regions with a color intensity that tapers to the periphery, as well as less radioactivity in the striatal region(s). Positive image (B) shows absence of the white matter sulcal pattern with intensity radiating to a sharply defined convex edge, as well as more radioactivity in the striatum.

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