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APOE predicts amyloid‐beta but not tau Alzheimer pathology in cognitively normal aging
Open accessAbstract
Objective: To examine interactions of apolipoprotein E ( APOE) genotype with age and with in vivo measures of preclinical Alzheimer disease (AD) in cognitively normal aging. Methods: Two hundred forty‐one cognitively normal individuals, aged 45–88 years, had cerebral amyloid imaging studies with Pittsburgh Compound‐B (PIB). Of the 241 individuals, 168 (70%) also had cerebrospinal fluid (CSF) assays of amyloid‐beta 42 (Aβ 42 ), tau, and phosphorylated tau (ptau 181 ). All individuals were genotyped for APOE . Results: The frequency of individuals with elevated mean cortical binding potential (MCBP) for PIB rose in an age‐dependent manner from 0% at ages 45–49 years to 30.3% at 80–88 years. Reduced levels of CSF Aβ 42 appeared to begin earlier (18.2% of those aged 45–49 years) and increase with age in higher frequencies (50% at age 80–88 years) than elevations of MCBP. There was a gene dose effect for the APOE4 genotype, with greater MCBP increases and greater reductions in CSF Aβ 42 with increased numbers of APOE4 alleles. Individuals with an APOE2 allele had no increase in MCBP with age and had higher CSF Aβ 42 levels than individuals without an APOE2 allele. There was no APOE4 or APOE2 effect on CSF tau or ptau 181 . Interpretation: Increasing cerebral Aβ deposition with age is the pathobiological phenotype of APOE4 . The biomarker sequence that detects Aβ deposition may first be lowered CSF Aβ 42 , followed by elevated MCBP for PIB. A substantial proportion of cognitively normal individuals have presumptive preclinical AD. ANN NEUROL 2010;67:122–131
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“The association of the APOE4 isoform with amyloid deposition has been well established in human studies, where APOE4 carriers exhibit higher A β plaque burden and earlier onset of amyloid positivity compared with non-carriers 35 -37 .”
From APOE2 attenuates APOE4-associated amyloid pathology and related toxicity in a mouse model of Alzheimer’s disease (2026) · cites this paper as [36]
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“APOE status has been found to modulate the onset of extracellular amyloid plaque deposition, one of the key pathognomonic features of the disease (6, 7).”
From Human ApoE isoforms differentially regulate brain amyloid-β peptide clearance (2011) · cites this paper as [7]
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“On the basis of previous studies (7, 27), individuals with mean cortical binding potential (MCBP) for PIB >0.18 were considered PIB-positive (PIB+).”
From Human ApoE isoforms differentially regulate brain amyloid-β peptide clearance (2011) · cites this paper as [7]
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“Given that a CSF Aβ42 concentration lower than 500 pg/mL has been utilized as a reliable threshold for the presence of cerebral Aβ deposition in humans (7, 19, 22, 26)”
From Human ApoE isoforms differentially regulate brain amyloid-β peptide clearance (2011) · cites this paper as [7]
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“Increasing age and ApoE genetic background are the strongest known risk factors for AD and plaque load (33, 48); thus it was critical that these parameters were controlled.”
From Serotonin signaling is associated with lower amyloid-β levels and plaques in transgenic mice and humans (2011) · cites this paper as [33]
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“Sex differences in Aβ burden alone have not been reported in older adults,11–13”
From Sex Differences in the Association of Global Amyloid and Regional Tau Deposition Measured by Positron Emission Tomography in Clinically Normal Older Adults (2019) · cites this paper as [13]
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“Previous cross-sectional studies indicate that Aβ42 levels decrease in the CSF as Aβ starts to accumulate, before fibrillar plaques can be detected with PET7–11.”
From Earliest accumulation of β-amyloid occurs within the default-mode network and concurrently affects brain connectivity (2017) · cites this paper as [11]
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Cites
Folstein, M. F., Folstein, S. E., & McHugh, P. R. (1975) · Journal of Psychiatric Research · doi:10.1016/0022-3956(75)90026-6 · Cited by 88,282
Littell, R. C. (1996) · Medical Entomology and Zoology · Cited by 10,345
The Clinical Dementia Rating (CDR): Current version and scoring rules
Morris, J. C. (1993) · Neurology · doi:10.1212/wnl.43.11.2412-a · Cited by 9,882
Self-citationCorder, E. H., Saunders, A. M., Strittmatter, W. J., Schmechel, D. E., Gaskell, P. C., Small, G. W., Roses, A. D., Haines, J. L., & Pericak-Vance, M. A. (1993) · Science · doi:10.1126/science.8346443 · Cited by 9,429
Mild Cognitive Impairment: Clinical Characterization and Outcome
Petersen, R. C., Smith, G. E., Waring, S. C., Ivnik, R. J., Tangalos, E. G., & Kokmen, E. (1999) · Archives of Neurology · doi:10.1001/archneur.56.3.303 · Cited by 8,980
Talairach, J., Tournoux, P., & Rayport, M. (1988) · Thieme eBooks · Cited by 5,058
Imaging brain amyloid in Alzheimer's disease with Pittsburgh Compound‐B
Klunk, W. E., Engler, H., Nordberg, A., Wang, Y., Blomqvist, G., Holt, D. P., Bergström, M., Savitcheva, I., Huang, G., Estrada, S., et al. (2004) · Annals of Neurology · doi:10.1002/ana.20009 · Cited by 4,496
Strittmatter, W. J., Saunders, A. M., Schmechel, D., Pericak-Vance, M., Enghild, J., Salvesen, G. S., & Roses, A. D. (1993) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.90.5.1977 · Cited by 4,268
Shankar, G. M., Li, S., Mehta, T. H., Garcia-Munoz, A., Shepardson, N. E., Smith, I., Brett, F. M., Farrell, M. A., Rowan, M. J., Lemere, C. A., et al. (2008) · Nature Medicine · doi:10.1038/nm1782 · Cited by 3,685
Blennow, K., de Leon, M. J., & Zetterberg, H. (2006) · The Lancet · doi:10.1016/s0140-6736(06)69113-7 · Cited by 3,134
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APOE2 enhances neuroprotection against Alzheimer’s disease through multiple molecular mechanisms
Conejero-Goldberg, C., Gomar, J. J., Bobes-Bascaran, T., Hyde, T. M., Kleinman, J. E., Herman, M. M., Chen, S., Davies, P., & Goldberg, T. E. (2014) · Molecular Psychiatry · doi:10.1038/mp.2013.194 · Cited by 199
Recent Progress in Alzheimer’s Disease Research, Part 3: Diagnosis and Treatment
Hane, F. T., Robinson, M. J., Lee, B. Y., Bai, O., Leonenko, Z., & Albert, M. S. (2017) · Journal of Alzheimer s Disease · doi:10.3233/jad-160907 · Cited by 211
Multifaceted roles of APOE in Alzheimer disease
Jackson, R. J., Hyman, B. T., & Serrano-Pozo, A. (2024) · Nature Reviews Neurology · doi:10.1038/s41582-024-00988-2 · Cited by 193
Fagan, A. M., Shaw, L. M. J., Xiong, C., Vanderstichele, H., Mintun, M. A., Trojanowski, J. Q., Coart, E., Morris, J. C., & Holtzman, D. M. (2011) · Archives of Neurology · doi:10.1001/archneurol.2011.105 · Cited by 191
Self-citationBrain injury biomarkers are not dependent on β‐amyloid in normal elderly
Knopman, D. S., Jack, C. R., Wiste, H. J., Weigand, S. D., Vemuri, P., Lowe, V. J., Kantarci, K., Gunter, J. L., Senjem, M. L., Mielke, M. M., et al. (2013) · Annals of Neurology · doi:10.1002/ana.23816 · Cited by 183
β-arrestin 2 regulates Aβ generation and γ-secretase activity in Alzheimer's disease
Thathiah, A., Horré, K., Snellinx, A., Vandewyer, E., Huang, Y., Ciesielska, M., de Kloe, G. E., Munck, S., & Strooper, B. D. (2012) · Nature Medicine · doi:10.1038/nm.3023 · Cited by 189
APOE ε2 is associated with milder clinical and pathological Alzheimer disease
Serrano‐Pozo, A., Qian, J., Monsell, S. E., Betensky, R. A., & Hyman, B. T. (2015) · Annals of Neurology · doi:10.1002/ana.24369 · Cited by 176
Neural compensation in older people with brain amyloid-β deposition
Elman, J. A., Oh, H., Madison, C. M., Baker, S. L., Vogel, J. W., Marks, S. M., Crowley, S., O’Neil, J. P., & Jagust, W. J. (2014) · Nature Neuroscience · doi:10.1038/nn.3806 · Cited by 192
Chandra, A., Valkimadi, P., Pagano, G., Cousins, O., Dervenoulas, G., Politis, M., & Initiative, A. D. N. (2019) · Human Brain Mapping · doi:10.1002/hbm.24782 · Cited by 197
Amyloid is linked to cognitive decline in patients with Parkinson disease without dementia
Gomperts, S. N., Locascio, J. J., Rentz, D. M., Santarlasci, A., Marquié, M., Johnson, K. A., & Growdon, J. H. (2012) · Neurology · doi:10.1212/wnl.0b013e31827b1a07 · Cited by 189
Colocalization of cerebral iron with Amyloid beta in Mild Cognitive Impairment
Bergen, J. M. G. V., Li, X., Hua, J., Schreiner, S. J., Steininger, S. C., Quevenco, F. C., Wyss, M. T., Gietl, A. F., Treyer, V., Leh, S. E., et al. (2016) · Scientific Reports · doi:10.1038/srep35514 · Cited by 186
Cholesterol Level and Statin Use in Alzheimer Disease
Shepardson, N. E. (2011) · Archives of Neurology · doi:10.1001/archneurol.2011.242 · Cited by 190
Alzheimer disease: new concepts on its neurobiology and the clinical role imaging will play
Jack, C. R. (2012) · Radiology · doi:10.1148/radiol.12110433 · Cited by 211
Brookmeyer, R., & Abdalla, N. (2018) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2018.03.005 · Cited by 176
AV-1451 PET imaging of tau pathology in preclinical Alzheimer disease: Defining a summary measure
Mishra, S., Gordon, B. A., Su, Y., Christensen, J. J., Friedrichsen, K. A., Jackson, K., Hornbeck, R. C., Balota, D. A., Cairns, N. J., Morris, J. C., et al. (2017) · NeuroImage · doi:10.1016/j.neuroimage.2017.07.050 · Cited by 178
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Vlassenko, A. G., Benzinger, T. L. S., & Morris, J. C. (2011) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2011.11.005 · Cited by 188
Self-citationBrain amyloid and cognition in Lewy body diseases
Gomperts, S. N., Locascio, J. J., Marquié, M., Santarlasci, A., Rentz, D. M., Maye, J. E., Johnson, K. A., & Growdon, J. H. (2012) · Movement Disorders · doi:10.1002/mds.25048 · Cited by 171
Apolipoprotein E, not fibrillar β-amyloid, reduces cerebral glucose metabolism in normal aging
Jagust, W. J., Landau, S. M., & Initiative, F. T. A. D. N. (2012) · The Journal of Neuroscience · doi:10.1523/jneurosci.3266-12.2012 · Cited by 162
Recent Progress in Alzheimer’s Disease Research, Part 2: Genetics and Epidemiology
Robinson, M. J., Lee, B. Y., & Hane, F. T. (2017) · Journal of Alzheimer s Disease · doi:10.3233/jad-161149 · Cited by 179
Association Between Midlife Risk Factors and Late-Onset Epilepsy
Johnson, E. L., Krauss, G. L., Lee, A. K., Schneider, A. L. C., Dearborn, J. L., Kucharska‐Newton, A., Huang, J., Alonso, Á., & Gottesman, R. F. (2018) · JAMA Neurology · doi:10.1001/jamaneurol.2018.1935 · Cited by 166
Sato, N., & Morishita, R. (2015) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2015.00199 · Cited by 167
Two rare AKAP9 variants are associated with Alzheimer's disease in African Americans
Logue, M. W., Schu, M., Vardarajan, B. N., Farrell, J., Bennett, D. A., Buxbaum, J. D., Byrd, G. S., Ertekin‐Taner, N., Evans, D., Foroud, T., et al. (2014) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2014.06.010 · Cited by 136
Self-citationGenetic Susceptibility for Alzheimer Disease Neuritic Plaque Pathology
Shulman, J. M., Chen, K., Keenan, B. T., Chibnik, L. B., Fleisher, A., Thiyyagura, P., Roontiva, A., Aubin, C., Patsopoulos, N. A., Corneveaux, J. J., et al. (2013) · JAMA Neurology · doi:10.1001/jamaneurol.2013.2815 · Cited by 162
APOE modifies the association between Aβ load and cognition in cognitively normal older adults
Kantarci, K., Lowe, V. J., Przybelski, S. A., Weigand, S. D., Senjem, M. L., Ivnik, R. J., Preboske, G. M., Roberts, R. O., Geda, Y. E., Boeve, B. F., et al. (2011) · Neurology · doi:10.1212/wnl.0b013e31824365ab · Cited by 168
Albert, M., Soldan, A., Gottesman, R. F., McKhann, G. M., Sacktor, N. C., Farrington, L., Grega, M. A., Turner, R. S., Lu, Y., Li, S., et al. (2014) · Current Alzheimer Research · doi:10.2174/156720501108140910121920 · Cited by 158
Depression and the hippocampus: cause or effect?
Sheline, Y. I. (2011) · Biological Psychiatry · doi:10.1016/j.biopsych.2011.06.006 · Cited by 159
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Hong, Y. T., Veenith, T., Dewar, D., Outtrim, J. G., Mani, V., Williams, C., Pimlott, S., Hutchinson, P. J. A., Tavares, A., Canales, R., et al. (2014) · JAMA Neurology · doi:10.1001/jamaneurol.2013.4847 · Cited by 158
Huang, C.-L., Hsiao, I., Lin, H.-C., Wang, C., Huang, Y.-J., & Chuang, C. (2014) · Environmental Research · doi:10.1016/j.envres.2014.11.006 · Cited by 165
Longitudinal brain imaging in preclinical Alzheimer disease: impact of APOE ε4 genotype
Mishra, S., Blazey, T. M., Holtzman, D. M., Cruchaga, C., Su, Y., Morris, J. C., Benzinger, T. L. S., & Gordon, B. A. (2018) · Brain · doi:10.1093/brain/awy103 · Cited by 151
Self-citationYassine, H. N., Braskie, M. N., Mack, W. J., Castor, K., Fonteh, A. N., Schneider, L. S. S., Harrington, M. G., & Chui, H. C. (2017) · JAMA Neurology · doi:10.1001/jamaneurol.2016.4899 · Cited by 165
Alzheimer's disease first symptoms are age dependent: Evidence from the NACC dataset
Barnes, J., Dickerson, B. C., Frost, C. D., Jiskoot, L. C., Wolk, D. A., & van der Flier, W. M. (2015) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2014.12.007 · Cited by 164
Castellano, J. M., Deane, R., Gottesdiener, A. J., Verghese, P. B., Stewart, F. R., West, T., Paoletti, A. C., Kasper, T. R., DeMattos, R. B., Zlokovic, B. V., et al. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1206446109 · Cited by 154
Self-citationMormino, E. C., Brandel, M. G., Madison, C. M., Marks, S. M., Baker, S. L., & Jagust, W. J. (2011) · Cerebral Cortex · doi:10.1093/cercor/bhr255 · Cited by 151
Genetic influences on cognitive decline in Parkinson's disease
Morley, J. F., Xie, S. X., Hurtig, H. I., Stern, M. B., Colcher, A., Horn, S. S., Dahodwala, N. A., Duda, J. E., Weintraub, D. A., Chen‐Plotkin, A. S., et al. (2012) · Movement Disorders · doi:10.1002/mds.24946 · Cited by 152
Besson, F. L., La Joie, R., Doeuvre, L., Gaubert, M., Mezenge, F., Egret, S., Landeau, B., Barre, L., Abbas, A., Ibazizene, M., et al. (2015) · Journal of Neuroscience · doi:10.1523/jneurosci.0150-15.2015 · Cited by 141
Increased brain atrophy rates in cognitively normal older adults with low cerebrospinal fluid Aβ1‐42
Schott, J. M., Bartlett, J. W., Fox, N. C., Barnes, J., & Initiative, A. D. N. (2010) · Annals of Neurology · doi:10.1002/ana.22315 · Cited by 146
Koelewijn, L., Lancaster, T. M., Linden, D. E. J., Dima, D. C., Routley, B. C., Magazzini, L., Barawi, K., Brindley, L. M., Adams, R., Tansey, K. E., et al. (2019) · eLife · doi:10.7554/elife.36011 · Cited by 151
Ushering in the study and treatment of preclinical Alzheimer disease
Langbaum, J. B. S., Fleisher, A., Chen, K., Ayutyanont, N., Lopera, F. J., Quiroz, Y. T., Caselli, R. J., Tariot, P. N., & Reiman, E. M. (2013) · Nature Reviews Neurology · doi:10.1038/nrneurol.2013.107 · Cited by 149
The role of apolipoprotein E (APOE) genotype in early mild cognitive impairment (E-MCI)
Risacher, S. L. (2013) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2013.00011 · Cited by 151
Integrative genomics identifies APOE ε4 effectors in Alzheimer's disease
Rhinn, H., Fujita, R., Qiang, L., Cheng, R., Lee, J. H., & Abeliovich, A. (2013) · Nature · doi:10.1038/nature12415 · Cited by 151
RetractedVlassenko, A. G., Mintun, M. A., Xiong, C., Sheline, Y. I., Goate, A., Benzinger, T. L. S., & Morris, J. C. (2011) · Annals of Neurology · doi:10.1002/ana.22608 · Cited by 148
Self-citationGarai, K., Verghese, P. B., Baban, B., Holtzman, D. M., & Frieden, C. (2014) · Biochemistry · doi:10.1021/bi5008172 · Cited by 145
Self-citationCerebrospinal fluid soluble TREM2 in aging and Alzheimer’s disease
Henjum, K., Almdahl, I. S., Årskog, V., Minthon, L., Hansson, O., Fladby, T., & Nilsson, L. N. G. (2016) · Alzheimer s Research & Therapy · doi:10.1186/s13195-016-0182-1 · Cited by 145
Alzheimer disease biomarkers are associated with body mass index
Vidoni, E. D., Townley, R. A., Honea, R. A., Burns, J. M., & Initiative, A. D. N. (2011) · Neurology · doi:10.1212/wnl.0b013e318238eec1 · Cited by 140
Vemuri, P., Knopman, D. S., Lesnick, T. G., Przybelski, S. A., Mielke, M. M., Graff‐Radford, J., Murray, M. E., Roberts, R. O., Vassilaki, M. E., Lowe, V. J., et al. (2017) · JAMA Neurology · doi:10.1001/jamaneurol.2017.0244 · Cited by 144
Huynh, T.-P. V., Wang, C., Tran, A. C., Tabor, G. T., Mahan, T. E., Francis, C. M., Finn, M. B., Spellman, R., Manis, M., Tanzi, R. E., et al. (2019) · Molecular Neurodegeneration · doi:10.1186/s13024-019-0337-1 · Cited by 139
Self-citationMulti-method investigation of factors influencing amyloid onset and impairment in three cohorts
Betthauser, T. J., Bilgel, M., Koscik, R. L., Jedynak, B., An, Y., Kellett, K. A., Moghekar, A., Jonaitis, E. M., Stone, C. K., Engelman, C. D., et al. (2022) · Brain · doi:10.1093/brain/awac213 · Cited by 133
3D PIB and CSF biomarker associations with hippocampal atrophy in ADNI subjects
Apostolova, L. G., Hwang, K., Andrawis, J. P., Green, A. E., Babakchanian, S., Morra, J. H., Cummings, J. L., Toga, A. W., Trojanowski, J. Q., Shaw, L. M. J., et al. (2010) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2010.05.003 · Cited by 144
Amyloid tracers detect multiple binding sites in Alzheimer's disease brain tissue
Ni, R., Gillberg, P., Bergfors, A., Marutle, A., & Nordberg, A. K. (2013) · Brain · doi:10.1093/brain/awt142 · Cited by 135
Progranulin Mutations as Risk Factors for Alzheimer Disease
Perry, D. C., Lehmann, M., Yokoyama, J. S., Karydas, A., Lee, J. J., Coppola, G., Grinberg, L. T., Geschwind, D. H., Seeley, W. W., Miller, B. L., et al. (2013) · JAMA Neurology · doi:10.1001/2013.jamaneurol.393 · Cited by 133
Sabuncu, M. R., Buckner, R. L., Smoller, J. W., Lee, P. H., Fischl, B. R., & Sperling, R. A. (2011) · Cerebral Cortex · doi:10.1093/cercor/bhr348 · Cited by 134
Brain imaging in the study of Alzheimer's disease
Reiman, E. M., & Jagust, W. J. (2011) · NeuroImage · doi:10.1016/j.neuroimage.2011.11.075 · Cited by 139
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Ewers, M., Insel, P. S., Stern, Y., Weiner, M. W., & Initiative, A. D. N. (2013) · Neurology · doi:10.1212/wnl.0b013e31828970c2 · Cited by 138
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Baek, M. S., Cho, H., Lee, H. S., Lee, J., Ryu, Y. H., & Lyoo, C. H. (2020) · Alzheimer s Research & Therapy · doi:10.1186/s13195-020-00710-6 · Cited by 137
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Jack, C. R., Barrio, J. R., & Kepe, V. (2013) · Acta Neuropathologica · doi:10.1007/s00401-013-1185-7 · Cited by 137
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Abraham, C. R., & Li, A. (2022) · Ageing Research Reviews · doi:10.1016/j.arr.2022.101766 · Cited by 133
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Klunk, W. E. (2011) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2011.09.006 · Cited by 131
Predicting progression from normal cognition to mild cognitive impairment for individuals at 5 years
Albert, M., Zhu, Y., Moghekar, A., Mori, S., Miller, M. I., Soldan, A., Pettigrew, C., Selnes, O., Li, S., & Wang, M.-C. (2018) · Brain · doi:10.1093/brain/awx365 · Cited by 118
Cruchaga, C., Kauwe, J. S. K., Mayo, K., Spiegel, N., Bertelsen, S., Nowotny, P., Shah, A. R., Abraham, R., Hollingworth, P., Harold, D., et al. (2010) · PLoS Genetics · doi:10.1371/journal.pgen.1001101 · Cited by 128
Self-citationMolecular and cellular pathophysiology of preclinical Alzheimer’s disease
Mufson, E. J., Ikonomović, M. D., Counts, S., Perez, S. E., Malek‐Ahmadi, M. H., Scheff, S. W., & Ginsberg, S. D. (2016) · Behavioural Brain Research · doi:10.1016/j.bbr.2016.05.030 · Cited by 134
Mattsson, N., Lönneborg, A., Boccardi, M., Blennow, K., & Hansson, O. (2017) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2016.02.034 · Cited by 136
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Wisniewski, T., & Drummond, E. (2020) · Neurobiology of Disease · doi:10.1016/j.nbd.2020.104784 · Cited by 131
Förster, S., Grimmer, T., Miederer, I., Henriksen, G., Yousefi, B. H., Graner, P., Wester, H.-J., Förstl, H., Kurz, A., Dickerson, B. C., et al. (2012) · Biological Psychiatry · doi:10.1016/j.biopsych.2011.04.023 · Cited by 119
Knopman, D. S., Jack, C. R., Wiste, H. J., Lundt, E. S., Weigand, S. D., Vemuri, P., Lowe, V. J., Kantarci, K., Gunter, J. L., Senjem, M. L., et al. (2014) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2014.03.006 · Cited by 128
Hansson, O., Mikulskis, A., Fagan, A. M., Teunissen, C. E., Zetterberg, H., Vanderstichele, H., Molinuevo, J. L., Shaw, L. M. J., Vandijck, M. L. J., Verbeek, M. M., et al. (2018) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2018.05.008 · Cited by 123
Self-citationBos, I., Vos, S. J. B., Verhey, F. R. J., Scheltens, P., Teunissen, C. E., Engelborghs, S., Sleegers, K., Frisoni, G. B., Blin, O., Richardson, J. C., et al. (2019) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2019.01.004 · Cited by 122
Grundman, M., Pontecorvo, M. J., Salloway, S., Doraiswamy, P. M., Fleisher, A., Sadowsky, C., Nair, A. K., Siderowf, A. D., Lu, M., Arora, A., et al. (2012) · Alzheimer Disease & Associated Disorders · doi:10.1097/wad.0b013e318279d02a · Cited by 123
Self-citationAssociations of the Top 20 Alzheimer Disease Risk Variants With Brain Amyloidosis
Apostolova, L. G., Risacher, S. L., Duran, T., Stage, E., Goukasian, N., West, J. D., Do, T. M., Grotts, J. F., Wilhalme, H. M., Nho, K. T., et al. (2018) · JAMA Neurology · doi:10.1001/jamaneurol.2017.4198 · Cited by 130
Benedet, A. L., Leuzy, A., Pascoal, T. A., Ashton, N. J., Mathotaarachchi, S. S., Savard, M., Therriault, J., Kang, M. S., Chamoun, M., Schöll, M., et al. (2020) · Brain · doi:10.1093/brain/awaa342 · Cited by 126
Interaction of Age and APOE Genotype on Cerebral Blood Flow at Rest
Wierenga, C. E., Clark, L. R., Dev, S. I., Shin, D. D., Jurick, S. M., Rissman, R. A., Liu, T. T., & Bondi, M. W. (2013) · Journal of Alzheimer s Disease · doi:10.3233/jad-121897 · Cited by 126
Elman, J. A., Madison, C. M., Baker, S. L., Vogel, J. W., Marks, S. M., Crowley, S., O’Neil, J. P., & Jagust, W. J. (2014) · Cerebral Cortex · doi:10.1093/cercor/bhu259 · Cited by 122
Hypothetical Preclinical Alzheimer Disease Groups and Longitudinal Cognitive Change
Soldan, A., Pettigrew, C. A., Cai, Q., Wang, M., Moghekar, A., O’Brien, R., Selnes, O. A., & Albert, M. (2016) · JAMA Neurology · doi:10.1001/jamaneurol.2016.0194 · Cited by 120
Mormino, E. C., & Papp, K. V. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-179928 · Cited by 124
Deters, K., Napolioni, V., Sperling, R. A., Greicius, M. D., Mayeux, R. P., Hohman, T. J., & Mormino, E. C. (2021) · Neurology · doi:10.1212/wnl.0000000000011599 · Cited by 118
Teipel, S. J., Grothe, M. J., Zhou, J. H., Sepulcre, J., Dyrba, M., Sorg, C., & Babiloni, C. (2016) · Journal of the International Neuropsychological Society · doi:10.1017/s1355617715000995 · Cited by 117
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Villemagne, V. L., Doré, V., Bourgeat, P., Burnham, S. C., Laws, S., Salvado, O., Masters, C. L., & Rowe, C. C. (2017) · Seminars in Nuclear Medicine · doi:10.1053/j.semnuclmed.2016.09.006 · Cited by 110
Belloy, M. E., Napolioni, V., Han, S. S., Le Guen, Y., Greicius, M. D., & Initiative, F. T. A. D. N. (2020) · JAMA Neurology · doi:10.1001/jamaneurol.2020.0414 · Cited by 110
Fortea, J., Sala‐Llonch, R., Bartrés‐Faz, D., Lladó, A., Solé‐Padullés, C., Bosch, B., Antonell, A., Olives, J., Sánchez‐Valle, R., Molinuevo, J. L., et al. (2011) · Biological Psychiatry · doi:10.1016/j.biopsych.2011.02.017 · Cited by 112
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Jagust, W. (2016) · Brain · doi:10.1093/brain/awv326 · Cited by 110
Caselli, R. J., & Reiman, E. M. (2012) · Journal of Alzheimer s Disease · doi:10.3233/jad-2012-129026 · Cited by 111
Meyer, P. T., Hellwig, S., Amtage, F., Rottenburger, C., Sahm, U., Reuland, P., Weber, W., & Hüll, M. (2011) · Journal of Nuclear Medicine · doi:10.2967/jnumed.110.083683 · Cited by 112
Fišar, Z. (2022) · Biomolecules · doi:10.3390/biom12111676 · Cited by 113
Zhao, L., Gottesdiener, A. J., Parmar, M., Li, M., Kaminsky, S. M., Chiuchiolo, M. J., Sondhi, D., Sullivan, P. M., Holtzman, D. M., Crystal, R. G., et al. (2016) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2016.04.020 · Cited by 107
Self-citationFluid and PET biomarkers for amyloid pathology in Alzheimer's disease
Cohen, A. D., Landau, S. M., Snitz, B. E., Klunk, W. E., Blennow, K., & Zetterberg, H. (2018) · Molecular and Cellular Neuroscience · doi:10.1016/j.mcn.2018.12.004 · Cited by 112
APOE-related biomarker profiles in non-pathological aging and early phases of Alzheimer's disease
Reinvang, I., Espeseth, T., & Westlye, L. T. (2013) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2013.05.006 · Cited by 109
Tse, K., & Herrup, K. (2017) · Journal of Neurochemistry · doi:10.1111/jnc.14079 · Cited by 107
CSF biomarker changes precede symptom onset of mild cognitive impairment
Moghekar, A., Li, S., Lu, Y., Li, M., Wang, M.-C., Albert, M., O’Brien, R., & For the BIOCARD Research Team (2013) · Neurology · doi:10.1212/01.wnl.0000435558.98447.17 · Cited by 103
Keene, C. D., Cudaback, E., Li, X., Montine, K. S., & Montine, T. J. (2011) · Current Opinion in Neurobiology · doi:10.1016/j.conb.2011.08.002 · Cited by 103
Selnes, P., Aarsland, D., Bjørnerud, A., Gjerstad, L., Wallin, A., Hessen, E., Reinvang, I., Grambaitė, R., Auning, E., Kjærvik, V. K., et al. (2013) · Journal of Alzheimer s Disease · doi:10.3233/jad-2012-121603 · Cited by 103
Cerebral β-amyloid deposition predicts HIV-associated neurocognitive disorders in APOE ε4 carriers
Soontornniyomkij, V., Moore, D. J., Gouaux, B. D., Soontornniyomkij, B., Tatro, E. T., Umlauf, A., Masliah, E., Levine, A. J., Singer, E. J., Vinters, H. V., et al. (2012) · AIDS · doi:10.1097/qad.0b013e32835a117c · Cited by 102
Menopause Status Moderates Sex Differences in Tau Burden: A Framingham PET Study
Buckley, R. F., O’Donnell, A., McGrath, E. R., Jacobs, H. I. L., Lois, C., Satizábal, C. L., Ghosh, S., Rubinstein, Z. B., Murabito, J. M., Sperling, R. A., et al. (2022) · Annals of Neurology · doi:10.1002/ana.26382 · Cited by 101
Rates of Decline in Alzheimer Disease Decrease with Age
Holland, D., Desikan, R. S., Dale, A. M., McEvoy, L. K., & Initiative, A. D. N. (2012) · PLoS ONE · doi:10.1371/journal.pone.0042325 · Cited by 104
Longitudinal modeling of frontal cognition in APOE ε4 homozygotes, heterozygotes, and noncarriers
Caselli, R. J., Dueck, A. C., Locke, D. E. C., Hoffman‐Snyder, C. R., Woodruff, B. K., Rapcsak, S. Z., & Reiman, E. M. (2011) · Neurology · doi:10.1212/wnl.0b013e3182167147 · Cited by 105
Using Pittsburgh Compound B for In Vivo PET Imaging of Fibrillar Amyloid-Beta
Cohen, A. D., Rabinovici, G. D., Mathis, C. A., Jagust, W. J., Klunk, W. E., & Ikonomović, M. D. (2012) · Advances in pharmacology · doi:10.1016/b978-0-12-394816-8.00002-7 · Cited by 103
In vivo assessment of amyloid‐β deposition in nondemented very elderly subjects
Mathis, C. A., Kuller, L. H., Klunk, W. E., Snitz, B. E., Price, J. C., Weissfeld, L. A., Rosario, B. L., Lopresti, B. J., Saxton, J. A., Aizenstein, H. J., et al. (2013) · Annals of Neurology · doi:10.1002/ana.23797 · Cited by 98
High-Density Lipoproteins and Cerebrovascular Integrity in Alzheimer’s Disease
Stukas, S. K., Robert, J., & Wellington, C. L. (2014) · Cell Metabolism · doi:10.1016/j.cmet.2014.01.003 · Cited by 101
Barthel, H., Luthardt, J., Becker, G., Patt, M., Hammerstein, E., Hartwig, K., Eggers, B., Sattler, B., Schildan, A., Hesse, S., et al. (2011) · European Journal of Nuclear Medicine and Molecular Imaging · doi:10.1007/s00259-011-1821-1 · Cited by 101
Cohen, A. D., Mowrey, W. B., Weissfeld, L. A., Aizenstein, H. J., McDade, E., Mountz, J. M., Nebes, R. D., Saxton, J. A., Snitz, B. E., DeKosky, S. T., et al. (2013) · NeuroImage · doi:10.1016/j.neuroimage.2013.01.015 · Cited by 99
Simon, R., Girod, M., Fonbonne, C., Salvador, A., Clément, Y., Lantéri, P., Amouyel, P., Lambert, J. C., & Lemoine, J. (2012) · Molecular & Cellular Proteomics · doi:10.1074/mcp.m112.018861 · Cited by 92
Fate of microglia during HIV‐1 infection: From activation to senescence?
Chen, N. C., Partridge, A. T., Sell, C., Torres, C. A., & Martín‐García, J. (2016) · Glia · doi:10.1002/glia.23081 · Cited by 94
Metadata
- Authors
- Morris, J. C., Roe, C. M., Xiong, C., Fagan, A. M., Goate, A. M., Holtzman, D. M., & Mintun, M. A.
- Affiliations
- Washington University in St. Louis (US)
- Corresponding author
- Morris, John C.
- ORCID
- Venue
- Annals of Neurology
- Publisher
- Wiley
- Published
- 2010-01
- Volume
- 67
- Issue
- 1
- Pages
- 122-131
- ISSN
- 0364-5134 (ISSN-L)
- 1531-8249
- PMC
- PMC2830375
- OpenAlex
- W2014897304
- Cited by
- 830
- References
- 80
- Citations by year
- 2026: 21 · 2025: 23 · 2024: 38 · 2023: 39 · 2022: 54 · 2021: 40 · 2020: 53 · 2019: 53 · 2018: 49 · 2017: 58 · 2016: 54 · 2015: 48 · 2014: 65 · 2013: 76 · 2012: 63
- FWCI
- 32.20
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Annals of Neurology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (UL1TR000448)
- National Institute on Aging (P50AG005681, P01AG003991, P01AG026276)
- National Center for Research Resources (UL1RR024992)
- National Center for Advancing Translational Sciences
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Oncology › Cancer-related cognitive impairment studies
- Keywords
- apolipoprotein E, APOE ε4, APOE2, amyloid-beta, tau protein, preclinical Alzheimer's disease, Pittsburgh compound B, cerebrospinal fluid biomarkers, gene dosage effect, phosphorylated tau
- MeSH terms
- Aged, Aged, 80 and over, Aging, Alzheimer Disease, Aniline Compounds, Apolipoproteins E, Brain, Female, Follow-Up Studies, Genotype, Humans, Longitudinal Studies, Male, Middle Aged, Peptide Fragments, Phosphorylation, Thiazoles, Amyloid beta-Peptides, tau Proteins, Apolipoprotein E4, Apolipoprotein E2, Plaque, Amyloid
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