Please use this identifier to cite or link to this item: http://ahro.austin.org.au/austinjspui/handle/1/11300
Title: Amyloid imaging.
Authors: Villemagne, Victor L;Rowe, Christopher C
Affiliation: Department of Nuclear Medicine and Centre for PET, Austin Health, Victoria, Australia. villemagne@petnm.unimelb.edu.au
Issue Date: 1-Sep-2011
Citation: International Psychogeriatrics / Ipa; 23 Suppl 2(): S41-9
Abstract: Molecular neuroimaging techniques such as PET are proving valuable in the early and differential diagnosis of Alzheimer's disease (AD).With the advent of new therapeutic strategies aimed at reducing β-amyloid (Aβ) burden in the brain to potentially prevent or delay functional and irreversible cognitive loss, there is increased interest in developing agents that allow assessment of Aβ burden in vivo. Amyloid imaging with PET has proven useful in the discrimination of dementias, showing significantly higher Aβ burden in the gray matter of AD patients when compared with healthy controls or patients with frontotemporal dementia. ApoE ε4 carriers, independent of diagnosis or disease severity, present with higher Aβ burden than non-ε4 carriers. Amyloid imaging matches histopathological reports in aging and dementia, reflecting the true regional density of Aβ plaques in cortical areas. It also appears to be more sensitive than FDG-PET for the diagnosis of AD. In healthy older people there is an increasing prevalence of amyloid positive scans with age, rising from 20% in the seventh decade to 60% in the ninth decade. Of people with mild cognitive impairment (MCI), 40-60% present with detectable cortical Aβ deposition. In both groups, Aβ deposition is associated with a higher risk for cognitive decline and dementia due to AD. These observations suggest that Aβ deposition is not part of normal aging, supporting the hypothesis that it occurs well before the onset of symptoms and is likely to represent preclinical AD in asymptomatic persons and prodromal AD in MCI. Further longitudinal observations, coupled with different disease-specific tracers and biomarkers, are required to confirm this hypothesis and further elucidate the precise role of Aβ deposition in the course of AD.
Internal ID Number: 21729418
URI: http://ahro.austin.org.au/austinjspui/handle/1/11300
DOI: 10.1017/S1041610211000895
URL: http://www.ncbi.nlm.nih.gov/pubmed/21729418
Type: Journal Article
Subjects: Alzheimer Disease.metabolism.radionuclide imaging
Cerebral Cortex.metabolism.radionuclide imaging
Early Diagnosis
Fluorodeoxyglucose F18.diagnostic use
Humans
Mild Cognitive Impairment.metabolism.radionuclide imaging
Molecular Imaging.methods
Neuroimaging.methods
Positron-Emission Tomography
Tomography, Emission-Computed, Single-Photon
Appears in Collections:Journal articles

Files in This Item:
There are no files associated with this item.


Items in AHRO are protected by copyright, with all rights reserved, unless otherwise indicated.