The DOI matches its Crossref record; 79 of the 80 references it cites were found in a registry or an index.
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
Overview
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
The source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“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]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“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]
The cited source says what the claim attributes to it.
In the citing paper
“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]
The cited source says what the claim attributes to it.
In the citing paper
“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]
The cited source says what the claim attributes to it.
In the citing paper
“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]
In the citing paper
“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]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
Citations
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
Cited by
Sorted by citations
Jack, C. R., Knopman, D. S., Jagust, W. J., Petersen, R. C., Weiner, M. W., Aisen, P. S., Shaw, L. M., Vemuri, P., Wiste, H. J., Weigand, S. D., et al. (2013) · The Lancet Neurology · doi:10.1016/s1474-4422(12)70291-0 · Cited by 4,396
Apolipoprotein E and Alzheimer disease: risk, mechanisms and therapy
Liu, C.-C., Kanekiyo, T., Xu, H., & Bu, G. (2013) · Nature Reviews Neurology · doi:10.1038/nrneurol.2012.263 · Cited by 3,459
Alzheimer Disease: An Update on Pathobiology and Treatment Strategies
Long, J. M., & Holtzman, D. M. (2019) · Cell · doi:10.1016/j.cell.2019.09.001 · Cited by 3,204
Self-citationKarran, E., Mercken, M., & Strooper, B. D. (2011) · Nature Reviews Drug Discovery · doi:10.1038/nrd3505 · Cited by 2,188
The Amyloid-β Pathway in Alzheimer’s Disease
Hampel, H., Hardy, J., Blennow, K., Chen, C., Perry, G., Kim, S. H., Villemagne, V. L., Aisen, P., Vendruscolo, M., Iwatsubo, T., et al. (2021) · Molecular Psychiatry · doi:10.1038/s41380-021-01249-0 · Cited by 1,952
Preclinical Alzheimer’s Disease: Definition, Natural History, and Diagnostic Criteria
Dubois, B., Hampel, H., Feldman, H. H., Scheltens, P., Aisen, P., Andrieu, S., Bakardjian, H., Benali, H., Bertram, L., Blennow, K., et al. (2016) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2016.02.002 · Cited by 1,925
Self-citationPrevalence of Cerebral Amyloid Pathology in Persons Without Dementia: A Meta-analysis
Jansen, W. J., Ossenkoppele, R., Knol, D. L., Tijms, B. M., Scheltens, P., Verhey, F. R. J., Visser, P. J., Aalten, P., Aarsland, D., Alcolea, D., et al. (2015) · JAMA · doi:10.1001/jama.2015.4668 · Cited by 1,610
Self-citationApolipoprotein E and Alzheimer disease: pathobiology and targeting strategies
Yamazaki, Y., Zhao, N., Caulfield, T. R., Liu, C.-C., & Bu, G. (2019) · Nature Reviews Neurology · doi:10.1038/s41582-019-0228-7 · Cited by 1,425
Alzheimer’s Disease: The Challenge of the Second Century
Holtzman, D. M., Morris, J. C., & Goate, A. M. (2011) · Science Translational Medicine · doi:10.1126/scitranslmed.3002369 · Cited by 1,424
Self-citationThe Centiloid Project: standardizing quantitative amyloid plaque estimation by PET
Klunk, W. E., Koeppe, R. A., Price, J. C., Benzinger, T. L., Devous, M. D., Jagust, W. J., Johnson, K. A., Mathis, C. A., Minhas, D., Pontecorvo, M. J., et al. (2015) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2014.07.003 · Cited by 1,348
Self-citationAlzheimer’s Disease Risk Genes and Mechanisms of Disease Pathogenesis
Karch, C. M., & Goate, A. M. (2015) · Biological Psychiatry · doi:10.1016/j.biopsych.2014.05.006 · Cited by 1,357
Self-citationHuman ApoE isoforms differentially regulate brain amyloid-β peptide clearance
Castellano, J. M., Kim, J., Stewart, F. R., Jiang, H., DeMattos, R. B., Patterson, B. W., Fagan, A. M., Morris, J. C., Mawuenyega, K. G., Cruchaga, C., et al. (2011) · Science Translational Medicine · doi:10.1126/scitranslmed.3002156 · Cited by 1,242
“Interaction of nascent ApoE2, ApoE3, and ApoE4 isoforms expressed in mammalian cells with amyloid peptide beta (1-40).”
InfluentialSelf-citationBiomarker Modeling of Alzheimer’s Disease
Jack, C. R., & Holtzman, D. M. (2013) · Neuron · doi:10.1016/j.neuron.2013.12.003 · Cited by 1,002
Self-citationPalmqvist, S., Schöll, M., Strandberg, O., Mattsson, N., Stomrud, E., Zetterberg, H., Blennow, K., Landau, S., Jagust, W., & Hansson, O. (2017) · Nature Communications · doi:10.1038/s41467-017-01150-x · Cited by 911
Brain Imaging in Alzheimer Disease
Johnson, K. A., Fox, N. C., Sperling, R. A., & Klunk, W. E. (2012) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a006213 · Cited by 875
Apolipoprotein E in Alzheimer’s disease and other neurological disorders
Verghese, P. B., Castellano, J. M., & Holtzman, D. M. (2011) · The Lancet Neurology · doi:10.1016/s1474-4422(10)70325-2 · Cited by 857
Self-citationLongitudinal assessment of Aβ and cognition in aging and Alzheimer disease
Villemagne, V. L., Pike, K. E., Chételat, G., Ellis, K. A., Mulligan, R. S., Bourgeat, P., Ackermann, U., Jones, G., Szoeke, C., Salvado, O., et al. (2011) · Annals of Neurology · doi:10.1002/ana.22248 · Cited by 833
Fjell, A. M., McEvoy, L., Holland, D., Dale, A. M., & Walhovd, K. B. (2014) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2014.02.004 · Cited by 799
López, J. A., González, H. M., & Léger, G. C. (2019) · Handbook of clinical neurology · doi:10.1016/b978-0-12-804766-8.00013-3 · Cited by 887
Apolipoprotein E and Apolipoprotein E Receptors: Normal Biology and Roles in Alzheimer Disease
Holtzman, D. M., Herz, J., & Bu, G. (2012) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a006312 · Cited by 782
Self-citationThree dimensions of the amyloid hypothesis: time, space and 'wingmen'
Musiek, E. S., & Holtzman, D. M. (2015) · Nature Neuroscience · doi:10.1038/nn.4018 · Cited by 662
Self-citationVandenberghe, R. R., Laere, K. V., Ivanoiu, A., Salmon, É., Bastin, C., Triau, E., Hasselbalch, S. G., Law, I. G., Andersen, A., Kørner, A., et al. (2010) · Annals of Neurology · doi:10.1002/ana.22068 · Cited by 664
Imaging the evolution and pathophysiology of Alzheimer disease
Jagust, W. (2018) · Nature Reviews Neuroscience · doi:10.1038/s41583-018-0067-3 · Cited by 604
Johnson, K. A., Minoshima, S., Bohnen, N. I., Donohoe, K. J., Foster, N. L., Herscovitch, P., Karlawish, J. H., Rowe, C. C., Carrillo, M. C., Hartley, D. M., et al. (2013) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2013.01.002 · Cited by 603
Barthel, H., Gertz, H., Dresel, S. H. J., Peters, O., Bartenstein, P., Büerger, K., Hiemeyer, F. J., Wittemer‐Rump, S., Seibyl, J. P., Reininger, C. B., et al. (2011) · The Lancet Neurology · doi:10.1016/s1474-4422(11)70077-1 · Cited by 600
Wang, C., & Holtzman, D. M. (2020) · Neuropsychopharmacology · doi:10.1038/s41386-019-0478-5 · Cited by 615
Self-citationA Quarter Century of APOE and Alzheimer’s Disease: Progress to Date and the Path Forward
Belloy, M. E., Napolioni, V., & Greicius, M. D. (2019) · Neuron · doi:10.1016/j.neuron.2019.01.056 · Cited by 570
Preclinical Alzheimer's disease and its outcome: a longitudinal cohort study
Vos, S. J., Xiong, C., Visser, P. J., Jasielec, M. S., Hassenstab, J., Grant, E. A., Cairns, N. J., Morris, J. C., Holtzman, D. M., & Fagan, A. M. (2013) · The Lancet Neurology · doi:10.1016/s1474-4422(13)70194-7 · Cited by 564
Self-citationThe road to restoring neural circuits for the treatment of Alzheimer's disease
Canter, R. G., Penney, J., & Tsai, L.-H. (2016) · Nature · doi:10.1038/nature20412 · Cited by 565
Clinical presentation of chronic traumatic encephalopathy
Stern, R. A., Daneshvar, D. H., Baugh, C. M., Seichepine, D. R., Montenigro, P. H., Riley, D. O., Fritts, N. G., Stamm, J. M., Robbins, C. A., McHale, L., et al. (2013) · Neurology · doi:10.1212/wnl.0b013e3182a55f7f · Cited by 564
ApoE4 Accelerates Early Seeding of Amyloid Pathology
Liu, C.-C., Zhao, N., Fu, Y., Wang, N., Linares, C., Tsai, C.-W., & Bu, G. (2017) · Neuron · doi:10.1016/j.neuron.2017.11.013 · Cited by 451
YKL-40: A Novel Prognostic Fluid Biomarker for Preclinical Alzheimer's Disease
Craig-Schapiro, R., Perrin, R. J., Roe, C. M., Xiong, C., Carter, D., Cairns, N. J., Mintun, M. A., Peskind, E. R., Li, G., Galasko, D. R., et al. (2010) · Biological Psychiatry · doi:10.1016/j.biopsych.2010.08.025 · Cited by 504
Self-citationResting state functional connectivity in preclinical Alzheimer’s disease
Sheline, Y. I., & Raichle, M. E. (2013) · Biological Psychiatry · doi:10.1016/j.biopsych.2012.11.028 · Cited by 509
Morris, J. C., Roe, C. M., Grant, E. A., Head, D., Storandt, M., Goate, A. M., Fagan, A. M., Holtzman, D. M., & Mintun, M. A. (2009) · Archives of Neurology · doi:10.1001/archneurol.2009.269 · Cited by 476
Self-citationJack, C. R., Wiste, H. J., Vemuri, P., Weigand, S. D., Senjem, M. L., Zeng, G., Bernstein, M. A., Gunter, J. L., Pankratz, V. S., Aisen, P. S., et al. (2010) · Brain · doi:10.1093/brain/awq277 · Cited by 531
Smoking and increased Alzheimer's disease risk: A review of potential mechanisms
Durazzo, T. C., Mattsson, N., Weiner, M. W., & Initiative, A. D. N. (2014) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2014.04.009 · Cited by 501
Imaging tau and amyloid-β proteinopathies in Alzheimer disease and other conditions
Villemagne, V. L., Doré, V., Burnham, S. C., Masters, C. L., & Rowe, C. C. (2018) · Nature Reviews Neurology · doi:10.1038/nrneurol.2018.9 · Cited by 447
Sheline, Y. I., Morris, J. C., Snyder, A. Z., Price, J. L., Yan, Z., D’Angelo, G., Liu, C., Dixit, S., Benzinger, T. L. S., Fagan, A. M., et al. (2010) · Journal of Neuroscience · doi:10.1523/jneurosci.3987-10.2010 · Cited by 444
Self-citationReitz, C., Jun, G., Naj, A., Rajbhandary, R., Vardarajan, B. N., Wang, L.-S., Valladares, O., Lin, C.-F., Larson, E. B., Graff-Radford, N. R., et al. (2013) · JAMA · doi:10.1001/jama.2013.2973 · Cited by 431
Self-citationAlzheimer’s disease: insights into pathology, molecular mechanisms, and therapy
Zheng, Q., & Wang, X. (2024) · Protein & Cell · doi:10.1093/procel/pwae026 · Cited by 483
β-Amyloid burden in healthy aging: Regional distribution and cognitive consequences
Rodrigue, K. M., Kennedy, K. M., Devous, M. D., Rieck, J. R., Hebrank, A. C., Diaz-Arrastia, R., Mathews, D., & Park, D. C. (2012) · Neurology · doi:10.1212/wnl.0b013e318245d295 · Cited by 419
Brain β-amyloid load approaches a plateau
Jack, C. R., Wiste, H. J., Lesnick, T. G., Weigand, S. D., Knopman, D. S., Vemuri, P., Pankratz, V. S., Senjem, M. L., Gunter, J. L., Mielke, M. M., et al. (2013) · Neurology · doi:10.1212/wnl.0b013e3182840bbe · Cited by 406
Palmqvist, S., Mattsson, N., Hansson, O., & Initiative, F. T. A. D. N. (2016) · Brain · doi:10.1093/brain/aww015 · Cited by 400
Spatial correlation between brain aerobic glycolysis and amyloid-β (Aβ) deposition
Vlassenko, A. G., Vaishnavi, S. N., Couture, L., Sacco, D., Shannon, B. J., Mach, R. H., Morris, J. C., Raichle, M. E., & Mintun, M. A. (2010) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1010461107 · Cited by 404
Self-citationComparing positron emission tomography imaging and cerebrospinal fluid measurements of β‐amyloid
Landau, S. M., Lu, M., Joshi, A. D., Pontecorvo, M., Mintun, M. A., Trojanowski, J. Q., Shaw, L. M., Jagust, W. J., & Initiative, F. T. A. D. N. (2013) · Annals of Neurology · doi:10.1002/ana.23908 · Cited by 401
Self-citationApolipoprotein E in Alzheimer's Disease: An Update
Yu, J.-T., Tan, L., & Hardy, J. (2014) · Annual Review of Neuroscience · doi:10.1146/annurev-neuro-071013-014300 · Cited by 394
Joshi, A. D., Pontecorvo, M. J., Clark, C. M., Carpenter, A. P., Jennings, D. L., Sadowsky, C., Adler, L. P., Kovnat, K. D., Seibyl, J. P., Arora, A., et al. (2012) · Journal of Nuclear Medicine · doi:10.2967/jnumed.111.090340 · Cited by 401
Self-citationAge, Sex, andAPOEε4 Effects on Memory, Brain Structure, and β-Amyloid Across the Adult Life Span
Jack, C. R., Wiste, H. J., Weigand, S. D., Knopman, D. S., Vemuri, P., Mielke, M. M., Lowe, V. J., Senjem, M. L., Gunter, J. L., Machulda, M. M., et al. (2015) · JAMA Neurology · doi:10.1001/jamaneurol.2014.4821 · Cited by 412
Brain PET in the Diagnosis of Alzheimer’s Disease
Marcus, C. V., Mena, E., & Subramaniam, R. M. (2014) · Clinical Nuclear Medicine · doi:10.1097/rlu.0000000000000547 · Cited by 405
Buckley, R. F., Mormino, E. C., Rabin, J. S., Hohman, T. J., Landau, S., Hanseeuw, B. J., Jacobs, H. I. L., Papp, K. V., Amariglio, R. E., Properzi, M. J., et al. (2019) · JAMA Neurology · doi:10.1001/jamaneurol.2018.4693 · Cited by 373
Cirrito, J. R., Disabato, B. M., Restivo, J. L., Verges, D. K., Goebel, W. D., Sathyan, A., Hayreh, D., D'Angelo, G., Benzinger, T., Yoon, H., et al. (2011) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1107411108 · Cited by 377
Self-citationPalmqvist, S., Zetterberg, H., Blennow, K., Vestberg, S., Andreasson, U., Brooks, D. J., Owenius, R., Hägerström, D., Wollmer, P., Minthon, L., et al. (2014) · JAMA Neurology · doi:10.1001/jamaneurol.2014.1358 · Cited by 368
Fleisher, A. S. (2011) · Archives of Neurology · doi:10.1001/archneurol.2011.150 · Cited by 364
Sex-Specific Association of Apolipoprotein E With Cerebrospinal Fluid Levels of Tau
Hohman, T. J., Dumitrescu, L., Barnes, L. L., Thambisetty, M., Beecham, G., Kunkle, B., Gifford, K. A., Bush, W. S., Chibnik, L. B., Mukherjee, S., et al. (2018) · JAMA Neurology · doi:10.1001/jamaneurol.2018.0821 · Cited by 340
Chételat, G., Joie, R. L., Villain, N., Perrotin, A., Sayette, V. D. L., Eustache, F., & Vandenberghe, R. R. (2013) · NeuroImage Clinical · doi:10.1016/j.nicl.2013.02.006 · Cited by 363
Amyloid‐β associated cortical thinning in clinically normal elderly
Becker, J. A., Hedden, T., Carmasin, J., Maye, J., Rentz, D. M., Putcha, D., Fischl, B., Greve, D. N., Marshall, G. A., Salloway, S., et al. (2011) · Annals of Neurology · doi:10.1002/ana.22333 · Cited by 342
Association of Lifetime Cognitive Engagement and Low β-Amyloid Deposition
Marks, S. M. (2012) · Archives of Neurology · doi:10.1001/archneurol.2011.2748 · Cited by 359
Exercise and Alzheimer’s disease biomarkers in cognitively normal older adults
Liang, K. Y., Mintun, M. A., Fagan, A. M., Goate, A. M., Bugg, J. M., Holtzman, D. M., Morris, J. C., & Head, D. (2010) · Annals of Neurology · doi:10.1002/ana.22096 · Cited by 340
Self-citationAmyloid-Beta Protein Clearance and Degradation (ABCD) Pathways and their Role in Alzheimer’s Disease
Baranello, R., Bharani, K., Padmaraju, V., Chopra, N., Lahiri, D., Greig, N., Pappolla, M., & Sambamurti, K. (2015) · Current Alzheimer Research · doi:10.2174/1567205012666141218140953 · Cited by 331
Vulnerable Neural Systems and the Borderland of Brain Aging and Neurodegeneration
Jagust, W. J. (2013) · Neuron · doi:10.1016/j.neuron.2013.01.002 · Cited by 335
Sex differences in Alzheimer risk: Brain imaging of endocrine vs chronologic aging
Mosconi, L., Berti, V., Quinn, C., McHugh, P., Petrongolo, G., Varsavsky, I., Osorio, R. S., Pupi, A., Vallabhajosula, S., Isaacson, R. S., et al. (2017) · Neurology · doi:10.1212/wnl.0000000000004425 · Cited by 319
Johnson, K. A., Minoshima, S., Bohnen, N. I., Donohoe, K. J., Foster, N. L., Herscovitch, P., Karlawish, J. H., Rowe, C. C., Carrillo, M. C., Hartley, D. M., et al. (2013) · Journal of Nuclear Medicine · doi:10.2967/jnumed.113.120618 · Cited by 329
Apolipoprotein E4 effects in Alzheimer’s disease are mediated by synaptotoxic oligomeric amyloid-β
Koffie, R. M., Hashimoto, T., Tai, H.-C., Kay, K. R., Serrano-Pozo, A., Joyner, D., Hou, S., Kopeikina, K. J., Frosch, M. P., Lee, V. M., et al. (2012) · Brain · doi:10.1093/brain/aws127 · Cited by 327
Self-citationJack, C. R., Wiste, H. J., Weigand, S. D., Rocca, W. A., Knopman, D. S., Mielke, M. M., Lowe, V. J., Senjem, M. L., Gunter, J. L., Preboske, G. M., et al. (2014) · The Lancet Neurology · doi:10.1016/s1474-4422(14)70194-2 · Cited by 358
ApoE Cascade Hypothesis in the pathogenesis of Alzheimer’s disease and related dementias
Martens, Y. A., Zhao, N., Liu, C.-C., Kanekiyo, T., Yang, A. J., Goate, A. M., Holtzman, D. M., & Bu, G. (2022) · Neuron · doi:10.1016/j.neuron.2022.03.004 · Cited by 316
Self-citationPrevalence Estimates of Amyloid Abnormality Across the Alzheimer Disease Clinical Spectrum
Jansen, W. J., Janssen, O., Tijms, B. M., Vos, S. J. B., Ossenkoppele, R., Visser, P. J., Amyloid Biomarker Study Group, Aarsland, D., Alcolea, D., Altomare, D., et al. (2022) · JAMA Neurology · doi:10.1001/jamaneurol.2021.5216 · Cited by 290
Self-citationLewczuk, P., Riederer, P. F., O’Bryant, S. E., Verbeek, M. M., Dubois, B., Visser, P. J., Jellinger, K. A., Engelborghs, S., Ramírez, A., Parnetti, L., et al. (2017) · The World Journal of Biological Psychiatry · doi:10.1080/15622975.2017.1375556 · Cited by 318
Self-citationAPOE2: protective mechanism and therapeutic implications for Alzheimer’s disease
Li, Z., Shue, F., Zhao, N., Shinohara, M., & Bu, G. (2020) · Molecular Neurodegeneration · doi:10.1186/s13024-020-00413-4 · Cited by 306
Suspected non-Alzheimer disease pathophysiology — concept and controversy
Jack, C. R., Knopman, D. S., Chételat, G., Dickson, D. W., Fagan, A. M., Frisoni, G. B., Jagust, W. J., Mormino, E. C., Petersen, R. C., Sperling, R. A., et al. (2016) · Nature Reviews Neurology · doi:10.1038/nrneurol.2015.251 · Cited by 313
Self-citationExercise counteracts declining hippocampal function in aging and Alzheimer's disease
Intlekofer, K. A., & Cotman, C. W. (2012) · Neurobiology of Disease · doi:10.1016/j.nbd.2012.06.011 · Cited by 300
Apolipoprotein E: Structural Insights and Links to Alzheimer Disease Pathogenesis
Chen, Y., Strickland, M. R., Soranno, A., & Holtzman, D. M. (2021) · Neuron · doi:10.1016/j.neuron.2020.10.008 · Cited by 298
Self-citationRabinovici, G. D., Furst, A. J., Alkalay, A., Racine, C. A., O’Neil, J. P., Janabi, M., Baker, S. L., Agarwal, N., Bonasera, S. J., Mormino, E. C., et al. (2010) · Brain · doi:10.1093/brain/awp326 · Cited by 289
Fernández-Calle, R., Konings, S. C., Frontiñán-Rubio, J., García-Revilla, J., Camprubí-Ferrer, L., Svensson, M., Martinson, I., Boza-Serrano, A., Venero, J. L., Nielsen, H. M., et al. (2022) · Molecular Neurodegeneration · doi:10.1186/s13024-022-00566-4 · Cited by 278
Head (2012) · doi:10.1001/archneurol.2011.845 · Cited by 267
Clearance of cerebral Aβ in Alzheimer’s disease: reassessing the role of microglia and monocytes
Zuroff, L. R., Daley, D. A., Black, K. L., & Koronyo‐Hamaoui, M. (2017) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-017-2463-7 · Cited by 292
Cullen, N. C., Leuzy, A., Janelidze, S., Palmqvist, S., Svenningsson, A. L., Stomrud, E., Dage, J. L., Mattsson, N., & Hansson, O. (2021) · Nature Communications · doi:10.1038/s41467-021-23746-0 · Cited by 282
Cerebrospinal Fluid Aβ 42/40 Corresponds Better than Aβ 42 to Amyloid PET in Alzheimer’s Disease
Lewczuk, P., Matzen, A., Blennow, K., Parnetti, L., Molinuevo, J. L., Eusebi, P., Kornhuber, J., Morris, J. C., & Fagan, A. M. (2016) · Journal of Alzheimer’s Disease · doi:10.3233/jad-160722 · Cited by 253
Self-citationInsulin resistance predicts brain amyloid deposition in late middle‐aged adults
Willette, A. A., Johnson, S. C., Birdsill, A. C., Sager, M. A., Christian, B., Baker, L. D., Craft, S., Oh, J. M., Statz, E. H., Hermann, B. P., et al. (2014) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2014.03.011 · Cited by 267
Face-name associative memory performance is related to amyloid burden in normal elderly
Rentz, D. M., Amariglio, R. E., Becker, J. A., Frey, M., Olson, L. E., Frishe, K., Carmasin, J. S., Maye, J. E., Johnson, K. A., & Sperling, R. A. (2011) · Neuropsychologia · doi:10.1016/j.neuropsychologia.2011.06.006 · Cited by 285
Quantitative Analysis of PiB-PET with FreeSurfer ROIs
Su, Y., D'Angelo, G. M., Vlassenko, A. G., Zhou, G., Snyder, A. Z., Marcus, D. S., Blazey, T. M., Christensen, J. J., Vora, S., Morris, J. C., et al. (2013) · PLoS ONE · doi:10.1371/journal.pone.0073377 · Cited by 246
“Binding potentials (BPND) are calculated using Logan graphical analysis [12] with cerebellar cortex as the reference region [4,11,13].”
BackgroundMethodSelf-citationMild cognitive impairment: pathology and mechanisms
Mufson, E. J., Binder, L. I., Counts, S., DeKosky, S. T., deToledo‐Morrell, L., Ginsberg, S. D., Ikonomović, M. D., Perez, S. E., & Scheff, S. W. (2011) · Acta Neuropathologica · doi:10.1007/s00401-011-0884-1 · Cited by 268
APOE mediated neuroinflammation and neurodegeneration in Alzheimer’s disease
Parhizkar, S., & Holtzman, D. M. (2022) · Seminars in Immunology · doi:10.1016/j.smim.2022.101594 · Cited by 255
Self-citationUngar, L., Altmann, A., & Greicius, M. D. (2014) · Brain Imaging and Behavior · doi:10.1007/s11682-013-9272-x · Cited by 246
EEG evidence of compensatory mechanisms in preclinical Alzheimer’s disease
Gaubert, S., Raimondo, F., Houot, M., Corsi, M., Naccache, L., Sitt, J. D., Hermann, B., Oudiette, D., Gagliardi, G. P., Habert, M., et al. (2019) · Brain · doi:10.1093/brain/awz150 · Cited by 243
Amyloid imaging and CSF biomarkers in predicting cognitive impairment up to 7.5 years later
Roe, C. M., Fagan, A. M., Grant, E. A., Hassenstab, J., Moulder, K. L., Maue Dreyfus, D., Sutphen, C. L., Benzinger, T. L. S., Mintun, M. A., Holtzman, D. M., et al. (2013) · Neurology · doi:10.1212/wnl.0b013e3182918ca6 · Cited by 222
Self-citationTakeda, S., Sato, N., & Morishita, R. (2014) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2014.00171 · Cited by 236
Biomarkers for the Early Detection and Progression of Alzheimer's Disease
Counts, S. E., Ikonomovic, M. D., Mercado, N., Vega, I. E., & Mufson, E. J. (2017) · Neurotherapeutics · doi:10.1007/s13311-016-0481-z · Cited by 224
Effect of APOE ε4 Status on Intrinsic Network Connectivity in Cognitively Normal Elderly Subjects
Machulda, M. M., Jones, D. T., Vemuri, P., McDade, E., Avula, R. T. V., Przybelski, S. A., Boeve, B. F., Knopman, D. S., Petersen, R. C., & Jack, C. R. (2011) · Archives of Neurology · doi:10.1001/archneurol.2011.108 · Cited by 229
Amyloid deposition in Parkinson's disease and cognitive impairment: A systematic review
Petrou, M., Dwamena, B. A., Foerster, B. R., MacEachern, M. P., Bohnen, N. I., Müller, M. L., Albin, R. L., & Frey, K. A. (2015) · Movement Disorders · doi:10.1002/mds.26191 · Cited by 208
Lifespan brain activity, β-amyloid, and Alzheimer's disease
Jagust, W. J., & Mormino, E. C. (2011) · Trends in Cognitive Sciences · doi:10.1016/j.tics.2011.09.004 · Cited by 221
“However, elevated Aβ deposition is uncommon prior to age 50 (in 3 studies, only 6 out of 60 carriers younger than 50 had evidence for detectable quantities of elevated Aβ [27–29], while elevated Aβ amongst APOE4 carriers after age 50 is present across multiple studies [27,28,30]).”
BackgroundAmyloid burden and neural function in people at risk for Alzheimer's Disease
Johnson, S. C., Christian, B. T., Okonkwo, O. C., Oh, J. M., Harding, S., Xu, G., Hillmer, A. T., Wooten, D. W., Murali, D., Barnhart, T. E., et al. (2014) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2013.09.028 · Cited by 218
Sex and gender differences in cognitive resilience to aging and Alzheimer's disease
Arenaza‐Urquijo, E. M., Boyle, R., Casaletto, K., Anstey, K. J., Vila‐Castelar, C., Colverson, A., Palpatzis, E., Eissman, J. M., Kheng Siang Ng, T., Raghavan, S., et al. (2024) · Alzheimer's & Dementia · doi:10.1002/alz.13844 · Cited by 223
Cerebrospinal fluid APOE levels: an endophenotype for genetic studies for Alzheimer's disease
Cruchaga, C., Kauwe, J. S. K., Nowotny, P., Bales, K., Pickering, E. H., Mayo, K., Bertelsen, S., Hinrichs, A., Fagan, A. M., Holtzman, D. M., et al. (2012) · Human Molecular Genetics · doi:10.1093/hmg/dds296 · Cited by 207
Self-citationHuynh, T.-P. V., Davis, A. A., Ulrich, J. D., & Holtzman, D. M. (2017) · Journal of Lipid Research · doi:10.1194/jlr.r075481 · Cited by 210
Self-citationMorris, J. C., Aisen, P. S. S., Bateman, R. J., Benzinger, T. L. S., Cairns, N. J., Fagan, A. M., Ghetti, B. F., Goate, A., Holtzman, D. M., Klunk, W. E., et al. (2012) · Clinical Investigation · doi:10.4155/cli.12.93 · Cited by 211
Self-citationGenome-wide association study of CSF biomarkers Aβ 1-42 , t-tau, and p-tau 181p in the ADNI cohort
Kim, S., Swaminathan, S., Shen, L., Risacher, S. L., Nho, K., Foroud, T., Shaw, L. M., Trojanowski, J. Q., Potkin, S. G., Huentelman, M. J., et al. (2011) · Neurology · doi:10.1212/wnl.0b013e318204a397 · Cited by 206
Fleisher, A. S., Chen, K., Liu, X., Ayutyanont, N., Roontiva, A., Thiyyagura, P., Protas, H., Joshi, A. D., Sabbagh, M., Sadowsky, C. H., et al. (2013) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2012.04.017 · Cited by 202
Self-citationEarly detection of Alzheimer's disease using PiB and FDG PET
Cohen, A. D., & Klunk, W. E. (2014) · Neurobiology of Disease · doi:10.1016/j.nbd.2014.05.001 · Cited by 216
Amyloid-first and neurodegeneration-first profiles characterize incident amyloid PET positivity
Jack, C. R., Wiste, H. J., Weigand, S. D., Knopman, D. S., Lowe, V. J., Vemuri, P., Mielke, M. M., Jones, D. T., Senjem, M. L., Gunter, J. L., et al. (2013) · Neurology · doi:10.1212/01.wnl.0000435556.21319.e4 · Cited by 203
Kim, J., Jiang, H., Park, S., Eltorai, A. E. M., Stewart, F. R., Yoon, H., Basak, J. M., Finn, M. B., & Holtzman, D. M. (2011) · The Journal of Neuroscience · doi:10.1523/jneurosci.3773-11.2011 · Cited by 204
Self-citation
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
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review
