[1]
Braak H, Braak E, Bohl J. Staging of Alzheimer-related cortical destruction. Eur Neurol 33(6): 403-8.(1993);
[2]
Chetelat G, Desgranges B, de la Sayette V, Viader F, Eustache F, Baron JC. Mild cognitive impairment: Can FDG-PET predict who is to rapidly convert to Alzheimer’s disease? Neurology 60(8): 1374-7.(2003);
[3]
Chetelat G, Eustache F, Viader F, De La Sayette V, Pelerin A, Mezenge F, et al. FDG-PET measurement is more accurate than neuropsychological assessments to predict global cognitive deterioration in patients with mild cognitive impairment. Neurocase 11(1): 14-25.(2005);
[4]
Landau SM, Harvey D, Madison CM, Koeppe RA, Reiman EM, Foster NL, et al. Associations between cognitive, functional, and FDG-PET measures of decline in AD and MCI. Neurobiol Aging 32(7): 1207-18.(2011);
[5]
Kawachi T, Ishii K, Sakamoto S, Sasaki M, Mori T, Yamashita F, et al. Comparison of the diagnostic performance of FDG-PET and VBM-MRI in very mild Alzheimer’s disease. Eur J Nucl Med Mol Imaging 33(7): 801-9.(2006);
[6]
Mosconi L, Tsui WH, Herholz K, Pupi A, Drzezga A, Lucignani G, et al. Multicenter standardized 18F-FDG PET diagnosis of mild cognitive impairment, Alzheimer’s disease, and other dementias. J Nucl Med 49(3): 390-8.(2008);
[7]
Mosconi L, De Santi S, Li J, Tsui WH, Li Y, Boppana M, et al. Hippocampal hypometabolism predicts cognitive decline from normal aging. Neurobiol Aging 29(5): 676-92.(2008);
[8]
de Leon MJ, Convit A, Wolf OT, Tarshish CY, DeSanti S, Rusinek H, et al. Prediction of cognitive decline in normal elderly subjects with 2-[18F]fluoro-2-deoxy-D-glucose/poitron-emission tomogra-phy (FDG/PET). Proc Natl Acad Sci USA 98(19): 10966-71.(2001);
[9]
Landau SM, Mintun MA, Joshi AD, Koeppe RA, Petersen RC, Aisen PS, et al. Amyloid deposition, hypometabolism, and longitudinal cognitive decline. Ann Neurol 72(4): 578-86.(2012);
[10]
Edison P, Archer HA, Hinz R, Hammers A, Pavese N, Tai YF, et al. Amyloid, hypometabolism, and cognition in Alzheimer disease: an [11C]PIB and [18F]FDG PET study. Neurology 68(7): 501-8.(2007);
[11]
Li Y, Rinne JO, Mosconi L, Pirraglia E, Rusinek H, DeSanti S, et al. Regional analysis of FDG and PIB-PET images in normal aging, mild cognitive impairment, and Alzheimer’s disease. Eur J Nucl Med Mol Imaging 35(12): 2169-81.(2008);
[12]
Minoshima S, Frey KA, Koeppe RA, Foster NL, Kuhl DE. A diagnostic approach in Alzheimer’s disease using three-dimensional stereotactic surface projections of fluorine-18-FDG PET. J Nucl Med 36(7): 1238-48.(1995);
[13]
Verhoeff NP, Wilson AA, Takeshita S, Trop L, Hussey D, Singh K, et al. In-vivo imaging of Alzheimer disease beta-amyloid with [11C]SB-13 PET. Am J Geriatr Psychiatry 12(6): 584-95.(2004);
[14]
Kemppainen NM, Aalto S, Wilson IA, Nagren K, Helin S, Bruck A, et al. Voxel-based analysis of PET amyloid ligand [11C]PIB uptake in Alzheimer disease. Neurology 67(9): 1575-80.(2006);
[15]
Farrer LA, Cupples LA, Haines JL, Hyman B, Kukull WA, Mayeux R, et al. Effects of age, sex, and ethnicity on the association between apolipoprotein E genotype and Alzheimer disease. A meta-analysis. APOE and Alzheimer Disease Meta Analysis Consortium. JAMA 278(16): 1349-56.(1997);
[16]
Scheinin NM, Wikman K, Jula A, Perola M, Vahlberg T, Rokka J, et al. Cortical (1)(1)C-PIB uptake is associated with age, APOE genotype, and gender in “healthy aging”. J Alzheimers Dis 41(1): 193-202.(2014);
[17]
Yi D, Lee DY, Sohn BK, Choe YM, Seo EH, Byun MS, et al. Beta-Amyloid Associated Differential Effects of APOE epsilon4 on Brain Metabolism in Cognitively Normal Elderly. Am J Geriatr Psychiatry 22(10): 961-70.(2014);
[18]
Hsiao IT, Huang CC, Hsieh CJ, Hsu WC, Wey SP, Yen TC, et al. Correlation of early-phase 18F-florbetapir (AV-45/Amyvid) PET images to FDG images: preliminary studies. Eur J Nucl Med Mol Imaging 39(4): 613-20.(2012);
[19]
Forsberg A, Engler H, Blomquist G, Langstrom B, Nordberg A. The use of PIB-PET as a dual pathological and functional biomarker in AD. Biochim Biophys Acta 1822(3): 380-5.(2012);
[20]
Meltzer CC, Zubieta JK, Brandt J, Tune LE, Mayberg HS, Frost JJ. Regional hypometabolism in Alzheimer’s disease as measured by positron emission tomography after correction for effects of partial volume averaging. Neurology 47(2): 454-61.(1996);
[21]
Brendel M, Delker A, Rotzer C, Boning G, Carlsen J, Cyran C, et al. Impact of partial volume effect correction on cerebral beta-amyloid imaging in APP-Swe mice using [18F]-florbetaben PET. Neuroimage 84: 843-53.(2014);
[22]
Samuraki M, Matsunari I, Chen WP, Yajima K, Yanase D, Fujikawa A, et al. Partial volume effect-corrected FDG PET and grey matter volume loss in patients with mild Alzheimer’s disease. Eur J Nucl Med Mol Imaging 34(10): 1658-69.(2007);
[23]
Ibanez V, Pietrini P, Alexander GE, Furey ML, Teichberg D, Rajapakse JC, et al. Regional glucose metabolic abnormalities are not the result of atrophy in Alzheimer’s disease. Neurology 50(6): 1585-93.(1998);
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