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The Scientific World Journal
Volume 2012 (2012), Article ID 712048, 6 pages
Cerebrospinal Fluid BACE1 Activity and Brain Amyloid Load in Alzheimer's Disease
1Department of Psychiatry and Psychotherapy, Klinikum rechts der Isar, Technische Universität München, Ismaninger Street 22, 81675 München, Germany
2Department of Nuclear Medicine, Klinikum rechts der Isar, Technische Universität München, Ismaninger Street 22, 81675 München, Germany
Received 17 October 2011; Accepted 2 November 2011
Academic Editors: E. Ghebremedhin and D. R. Thal
Copyright © 2012 Timo Grimmer et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
- K. Blennow, H. Hampel, M. Weiner, and H. Zetterberg, “Cerebrospinal fluid and plasma biomarkers in Alzheimer disease,” Nature Reviews Neurology, vol. 6, no. 3, pp. 131–144, 2010.
- J. Hardy and D. J. Selkoe, “The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics,” Science, vol. 297, no. 5580, pp. 353–356, 2002.
- H. Cai, Y. Wang, D. McCarthy et al., “BACE1 is the major β-secretase for generation of Aβ peptides by neurons,” Nature Neuroscience, vol. 4, no. 3, pp. 233–234, 2001.
- R. Vassar, B. D. Bennett, S. Babu-Khan et al., “β-secretase cleavage of Alzheimer's amyloid precursor protein by the transmembrane aspartic protease BACE,” Science, vol. 286, no. 5440, pp. 735–741, 1999.
- L. B. Yang, K. Lindholm, R. Yan et al., “Elevated β-secretase expression and enzymatic activity detected in sporadic Alzheimer disease,” Nature Medicine, vol. 9, no. 1, pp. 3–4, 2003.
- R. M. D. Holsinger, J. S. Lee, A. Boyd, C. L. Masters, and S. J. Collins, “CSF BACE1 activity is increased in CJD and Alzheimer disease versus [corrected] other dementias,” Neurology, vol. 67, no. 4, pp. 710–712, 2006.
- Z. Zhong, M. Ewers, S. Teipel et al., “Levels of β-secretase (BACE1) in cerebrospinal fluid as a predictor of risk in mild cognitive impairment,” Archives of General Psychiatry, vol. 64, no. 6, pp. 718–726, 2007.
- M. Ewers, Z. Zhong, K. Bürger et al., “Increased CSF-BACE 1 activity is associated with ApoE-ε4 genotype in subjects with mild cognitive impairment and Alzheimer's disease,” Brain, vol. 131, no. 5, pp. 1252–1258, 2008.
- H. Zetterberg, U. Andreasson, O. Hansson et al., “Elevated cerebrospinal fluid BACE1 activity in incipient Alzheimer disease,” Archives of Neurology, vol. 65, no. 8, pp. 1102–1107, 2008.
- M. T. Fodero-Tavoletti, D. P. Smith, C. A. McLean et al., “In vitro characterization of Pittsburgh compound-B binding to Lewy bodies,” Journal of Neuroscience, vol. 27, no. 39, pp. 10365–10371, 2007.
- A. Lockhart, J. R. Lamb, T. Osredkar et al., “PIB is a non-specific imaging marker of amyloid-beta (Aβ) peptide-related cerebral amyloidosis,” Brain, vol. 130, no. 10, pp. 2607–2615, 2007.
- M. D. Ikonomovic, W. E. Klunk, E. E. Abrahamson et al., “Post-mortem correlates of in vivo PiB-PET amyloid imaging in a typical case of Alzheimer's disease,” Brain, vol. 131, no. 6, pp. 1630–1645, 2008.
- L. Ye, A. Velasco, G. Fraser et al., “In vitro high affinity α-synuclein binding sites for the amyloid imaging agent PIB are not matched by binding to Lewy bodies in postmortem human brain,” Journal of Neurochemistry, vol. 105, no. 4, pp. 1428–1437, 2008.
- T. Grimmer, S. Tholen, B. H. Yousefi et al., “Progression of cerebral amyloid load is associated with the apolipoprotein e ε4 genotype in Alzheimer's disease,” Biological Psychiatry, vol. 68, no. 10, pp. 879–884, 2010.
- A. Kadir, O. Almkvist, A. Forsberg et al., “Dynamic changes in PET amyloid and FDG imaging at different stages of Alzheimer's disease,” Neurobiology of Aging. In press.
- H. Engler, A. Forsberg, O. Almkvist et al., “Two-year follow-up of amyloid deposition in patients with Alzheimer's disease,” Brain, vol. 129, no. 11, pp. 2856–2866, 2006.
- A. Forsberg, H. Engler, O. Almkvist et al., “PET imaging of amyloid deposition in patients with mild cognitive impairment,” Neurobiology of Aging, vol. 29, no. 10, pp. 1456–1465, 2008.
- A. M. Fagan, M. A. Mintun, R. H. Mach et al., “Inverse relation between in vivo amyloid imaging load and cerebrospinal fluid Abeta42 in humans,” Annals of Neurology, vol. 59, no. 3, pp. 512–519, 2006.
- A. Forsberg, O. Almkvist, H. Engler, A. Wall, B. Långström, and A. Nordberg, “High PIB retention in Alzheimer's disease is an early event with complex relationship with CSF biomarkers and functional parameters,” Current Alzheimer Research, vol. 7, no. 1, pp. 56–66, 2010.
- T. Grimmer, M. Riemenschneider, H. Förstl et al., “Beta amyloid in Alzheimer's disease: increased deposition in brain is reflected in reduced concentration in cerebrospinal fluid,” Biological Psychiatry, vol. 65, no. 11, pp. 927–934, 2009.
- N. Tolboom, W. M. van der Flier, M. Yaqub et al., “Relationship of cerebrospinal fluid markers to 11C-PiB and 18F-FDDNP binding,” Journal of Nuclear Medicine, vol. 50, no. 9, pp. 1464–1470, 2009.
- M. Degerman Gunnarsson, M. Lindau, A. Wall et al., “Pittsburgh compound-B and Alzheimer's disease biomarkers in CSF, plasma and urine: an exploratory study,” Dementia and Geriatric Cognitive Disorders, vol. 29, no. 3, pp. 204–212, 2010.
- L. Mosconi, W. H. Tsui, K. Herholz et al., “Multicenter standardized 18F-FDG PET diagnosis of mild cognitive impairment, Alzheimer's disease, and other dementias,” Journal of Nuclear Medicine, vol. 49, no. 3, pp. 390–398, 2008.
- P. R. Wenham, W. H. Price, and G. Blandell, “Apolipoprotein E genotyping by one-stage PCR,” The Lancet, vol. 337, no. 8750, pp. 1158–1159, 1991.
- F. Hulstaert, K. Blennow, A. Ivanoiu et al., “Improved discrimination of AD patients using β-amyloid(1-42) and tau levels in CSF,” Neurology, vol. 52, no. 8, pp. 1555–1562, 1999.
- A. Drzezga, T. Grimmer, G. Henriksen et al., “Effect of APOE genotype on amyloid plaque load and gray matter volume in Alzheimer disease,” Neurology, vol. 72, no. 17, pp. 1487–1494, 2009.
- C. C. Rowe, K. A. Ellis, M. Rimajova et al., “Amyloid imaging results from the Australian Imaging, Biomarkers and Lifestyle (AIBL) study of aging,” Neurobiology of Aging, vol. 31, no. 8, pp. 1275–1283, 2010.
- E. H. Corder, E. Ghebremedhin, M. G. Taylor, D. R. Thal, T. G. Ohm, and H. Braak, “The biphasic relationship between regional brain senile plaque and neurofibrillary tangle distributions: modification by age, sex, and APOE polymorphism,” Annals of the New York Academy of Sciences, vol. 1019, pp. 24–28, 2004.
- R. Vassar, “BACE1: the β-secreiase enzyme in Alzheimer's disease,” Journal of Molecular Neuroscience, vol. 23, no. 1-2, pp. 105–113, 2004.
- A. Sun, G. Koelsch, J. Tang, and G. Bing, “Localization of β-secretase memapsin 2 in the brain of Alzheimer's patients and normal aged controls,” Experimental Neurology, vol. 175, no. 1, pp. 10–22, 2002.
- G. Leuba, G. Wernli, A. Vernay, R. Kraftsik, M. H. Mohajeri, and K. D. Saini, “Neuronal and nonneuronal quantitative BACE immunocytochemical expression in the entorhinohippocampal and frontal regions in Alzheimer's disease,” Dementia and Geriatric Cognitive Disorders, vol. 19, no. 4, pp. 171–183, 2005.
- H. Fukumoto, B. S. Cheung, B. T. Hyman, and M. C. Irizarry, “β-secretase protein and activity are increased in the neocortex in Alzheimer disease,” Archives of Neurology, vol. 59, no. 9, pp. 1381–1389, 2002.
- A. Schmechel, M. Strauss, A. Schlicksupp et al., “Human BACE forms dimers and colocalizes with APP,” Journal of Biological Chemistry, vol. 279, no. 38, pp. 39710–39717, 2004.
- M. C. Herzig, P. Paganetti, M. Staufenbiel, and M. Jucker, “BACE1 and mutated presenilin-1 differently modulate Aβ40 and Aβ42 levels and cerebral amyloidosis in APPDutch transgenic mice,” Neurodegenerative Diseases, vol. 4, no. 2-3, pp. 127–135, 2007.
- M. C. Irizarry, J. J. Locascio, and B. T. Hyman, “β-site APP cleaving enzyme mRNA expression in APP transgenic mice: anatomical overlap with transgene expression and static levels with aging,” The American Journal of Pathology, vol. 158, no. 1, pp. 173–177, 2001.
- M. J. Chiocco, L. S. Kulnane, L. Younkin, S. Younkin, G. Evin, and B. T. Lamb, “Altered amyloid-β metabolism and deposition in genomic-based β-secretaee transgenic mice,” Journal of Biological Chemistry, vol. 279, no. 50, pp. 52535–52542, 2004.
- M. J. Chiocco and B. T. Lamb, “Spatial and temporal control of age-related APP processing in genomic-based β-secretase transgenic mice,” Neurobiology of Aging, vol. 28, no. 1, pp. 75–84, 2007.
- A. Brodbelt and M. Stoodley, “CSF pathways: a review,” British Journal of Neurosurgery, vol. 21, no. 5, pp. 510–520, 2007.
- E. T. Zhang, H. K. Richards, S. Kida, and R. O. Weller, “Directional and compartmentalised drainage of interstitial fluid and cerebrospinal fluid from the rat brain,” Acta Neuropathologica, vol. 83, no. 3, pp. 233–239, 1992.
- J. C. Morris, D. W. McKeel, K. Fulling, R. M. Torack, and L. Berg, “Validation of clinical diagnostic criteria for Alzheimer's disease,” Annals of Neurology, vol. 24, no. 1, pp. 17–22, 1988.