Aβ-amyloid and Tau Imaging in Dementia

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• 作者：Victor L. Villemagne ; MD^* ; ^&dagger ; ; ^&Dagger ; ; ^{victorlv@unimelb.edu.au} ; Vincent Doré ; PhD^* ; ^§ ; ; Pierrick Bourgeat ; PhD^§ ; ; Samantha C. Burnham ; PhD^║ ; Simon Laws ; PhD^¶ ; ; Olivier Salvado ; PhD^§ ; ; Colin L. Masters ; MD^&Dagger ; ; Christopher C. Rowe ; MD^⁎ ; ^&dagger ;
• 刊名：Seminars in Nuclear Medicine
• 出版年：2017
• 出版时间：January 2017
• 年：2017
• 卷：47
• 期：1
• 页码：75-88
• 全文大小：1279 K
• 卷排序：47

文摘

The introduction of in vivo imaging of Aβ-amyloid (Αβ) pathology more than a decade ago, transformed the assessment of Alzheimer disease (AD) allowing the evaluation of Aβ deposition over time by providing highly accurate, reliable, and reproducible quantitative statements of regional or global Aβ burden in the brain to the extent that Aβ imaging has already been approved for clinical use and is being used for both patient recruitment and outcome measure in current anti-Αβ therapeutic trials. Aβ imaging studies have deepened our insight into Aβ deposition, showing that Aβ accumulation is a slow and protracted process extending for more than two decades before the onset of the clinical phenotype. Although cross-sectional evaluation of Αβ burden does not strongly correlate with cognitive impairment in AD, Αβ burden does correlate with memory impairment and a higher risk for cognitive decline in the aging population and mild cognitive impairment subjects. These associations suggest that Αβ deposition is not a benign process. The recent addition of selective tau imaging will allow to elucidate if these effects are directly associated with Αβ deposition or if they are mediated, in toto or in parte, by tau as it spreads out of the mesial temporal lobe into neocortical association areas. The combination of Aβ and tau imaging studies would likely help elucidate the relationship or interplay between the two pathologic hallmarks of the disease. Longitudinal observations to assess their potential independent or synergistic, sequential or parallel effects on cognition, disease progression, and other disease-specific biomarkers of neurodegeneration would be required to further clarify the respective role of Αβ and tau deposition play in the course of AD.