The ART of Loss: Aβ Imaging in the Evaluation of Alzheimer’s Disease and other Dementias

被引:0
作者
Victor L. Villemagne
Michelle T. Fodero-Tavoletti
Kerryn E. Pike
Roberto Cappai
Colin L. Masters
Christopher C. Rowe
机构
[1] Centre for PET,Department of Nuclear Medicine
[2] Austin Health,Department of Pathology
[3] The University of Melbourne,Centre for Neuroscience
[4] The Mental Research Institute of Victoria,Bio21 Institute
[5] The University of Melbourne,Department of Medicine
[6] The University of Melbourne,undefined
[7] The University of Melbourne,undefined
来源
Molecular Neurobiology | 2008年 / 38卷
关键词
Alzheimer’s disease; Aβ; Emission tomography; Neurodegenerative disorders; Brain imaging;
D O I
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中图分类号
学科分类号
摘要
Molecular neuroimaging based on annihilation radiation tomographic (ART) techniques such as positron emission tomography (PET), in conjunction with related biomarkers in plasma and cerebrospinal fluid (CSF), 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. Aβ burden as assessed by molecular imaging matches histopathological reports of Aβ plaque distribution in aging and dementia and appears more accurate than FDG for the diagnosis of AD. Aβ imaging is also a very powerful tool in the differential diagnosis of AD from fronto-temporal dementia (FTD). Although Aβ burden as assessed by PET does not correlate with measures of cognitive decline in AD, it does correlate with memory impairment and rate of memory decline in mild cognitive impairment (MCI) and healthy older subjects. Approximately 30% of asymptomatic controls present cortical 11C-PiB retention. These observations suggest that Aβ deposition is not part of normal ageing, supporting the hypothesis that Aβ deposition occurs well before the onset of symptoms and is likely to represent preclinical AD. Further longitudinal observations are required to confirm this hypothesis and to better elucidate the role of Aβ deposition in the course of Alzheimer’s disease.
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页码:1 / 15
页数:14
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  • [21] Weinman NA(1999)The levels of soluble versus insoluble brain Ab distinguish Alzheimer’s disease from normal and pathologic aging Exp Neurol 158 328-337
  • [22] Multhaup G(2002)Naturally secreted oligomers of amyloid beta protein potently inhibit hippocampal long-term potentiation in vivo Nature 416 535-539
  • [23] McDonald BL(2005)The role of cell-derived oligomers of abeta in Alzheimer’s disease and avenues for therapeutic intervention Biochem Soc Trans 33 1087-1090
  • [24] Beyreuther K(1984)Clinical diagnosis of Alzheimer’s disease: report of the NINCDS-ADRDA work group under the auspices of Department of Health and Human Services Task Force on Alzheimer’s disease Neurology 34 939-944
  • [25] Cappai R(2001)Practice parameter: early detection of dementia: mild cognitive impairment (an evidence-based review)—report of the Quality Standards Subcommittee of the American Academy of Neurology Neurology 56 1133-1142
  • [26] White AR(2000)Mild cognitive impairment: transition between aging and Alzheimer’s disease Neurologia 15 93-101
  • [27] Selkoe DJ(1999)Mild cognitive impairment: clinical characterization and outcome Arch Neurol 56 303-308
  • [28] Hardy JA(2006)Alzheimer’s centennial legacy: prospects for rational therapeutic intervention targeting the abeta amyloid pathway Brain 129 2823-2839
  • [29] Higgins GA(2006)La Lunga Attesa: towards a molecular approach to neuroimaging and therapeutics in Alzheimer’s disease The Neuroradiology Journal 19 51-75
  • [30] Checler F(1992)Detection in life of confirmed Alzheimer’s idsease using a simple measurement of medial temporal lobe atrophy by computed tomography Lancet 340 1179-1183