The DOI matches its Crossref record; 117 of the 119 references it cites were found in a registry or an index.
Hypothetical model of dynamic biomarkers of the Alzheimer's pathological cascade
Open accessAbstract
Currently available evidence strongly supports the position that the initiating event in Alzheimer's disease (AD) is related to abnormal processing of beta-amyloid (Abeta) peptide, ultimately leading to formation of Abeta plaques in the brain. This process occurs while individuals are still cognitively normal. Biomarkers of brain beta-amyloidosis are reductions in CSF Abeta(42) and increased amyloid PET tracer retention. After a lag period, which varies from patient to patient, neuronal dysfunction and neurodegeneration become the dominant pathological processes. Biomarkers of neuronal injury and neurodegeneration are increased CSF tau and structural MRI measures of cerebral atrophy. Neurodegeneration is accompanied by synaptic dysfunction, which is indicated by decreased fluorodeoxyglucose uptake on PET. We propose a model that relates disease stage to AD biomarkers in which Abeta biomarkers become abnormal first, before neurodegenerative biomarkers and cognitive symptoms, and neurodegenerative biomarkers become abnormal later, and correlate with clinical symptom severity.
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
“Studies of non-demented elderly cohorts overall report approximately 20–40% are PIB-positive [67, 68, 71–78].”
From Brain aging, Alzheimer's disease, and mitochondria (2011) · cites this paper as [76]
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
“These investigations have established that volumetric decline occurs initially in medial temporal lobe grey matter, following tau protein deposition, and is closely correlated to cognitive decline.”
From White matter microstructural abnormality precedes cortical volumetric decline in Alzheimer’s disease: evidence from data-driven disease progression modelling (2022) · cites this paper as Jack Jr. et al 2010
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
“On the regional level, abnormality is evident in medial temporal lobe areas first (hippocampus and entorhinal cortex), then in lateral temporal lobe areas (mid-temporal gyrus and fusiform gyrus) and finally in frontal lobe areas (Jack Jr. et al 2010, Young et al 2014).”
From White matter microstructural abnormality precedes cortical volumetric decline in Alzheimer’s disease: evidence from data-driven disease progression modelling (2022) · cites this paper as Jack Jr. et al 2010
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
“because measures of all biomarkers studied to date have considerable overlap with those found other types of dementia (as well the cognitively normal elderly population), it remains difficult to determine whether or not cognitive impairment is due to AD or another more dominant and concurrent process.”
From Accuracy of the Clinical Diagnosis of Alzheimer Disease at National Institute on Aging Alzheimer Disease Centers, 2005–2010 (2012) · cites this paper as [1]
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
“it is Tau pathology and synapse loss that temporally correlate with cognitive impairment and precede overt neurodegeneration (Jack et al., 2010; Scheff et al., 2006; Spires-Jones and Hyman, 2014”
From Changes in the Synaptic Proteome in Tauopathy and Rescue of Tau-Induced Synapse Loss by C1q Antibodies (2018) · cites this paper as Jack et al., 2010
Experimental — accuracy not yet measured
The cited source says what the claim attributes to it.
In the citing paper
“Amyloid accumulation probably starts many years before the onset of symptoms,2,26,27 and initiation of anti-amyloid treatment only after dementia develops may be too late to affect the clinical course of the disease.28”
From Two Phase 3 Trials of Bapineuzumab in Mild-to-Moderate Alzheimer's Disease (2014) · cites this paper as [26]
The cited source says what the claim attributes to it.
In the citing paper
“Firstly, cognitive decline is more closely correlated to neurodegeneration than tau accumulation (Jack Jr. et al 2010).”
From White matter microstructural abnormality precedes cortical volumetric decline in Alzheimer’s disease: evidence from data-driven disease progression modelling (2022) · cites this paper as Jack Jr. et al 2010
The cited source says what the claim attributes to it.
In the citing paper
“Alzheimer’s disease (AD) is characterized by deposition of hallmark pathological peptides and neurodegeneration that progress across partially overlapping neuroanatomical and temporal axes1,2.”
From Integrated multimodal cell atlas of Alzheimer’s disease (2024) · cites this paper as [2]
In the citing paper
“Autosomal dominant mutations to the MAPT (tau) gene lead to neuronal tangle pathology and frontotemporal dementia but not to amyloid plaques 122,123 , suggesting that tau pathology does not induce Aβ pathology.”
From The amyloid hypothesis in Alzheimer disease: new insights from new therapeutics (2022) · cites this paper as [123]
In the citing paper
“Amyloid plaques appear a decade or two before clinical symptoms of AD, but it is tau pathology and synapse loss that correlate best with cognitive impairment during disease progression (Jack et al., 2010).”
From Microglia in Alzheimer’s disease (2018) · cites this paper as Jack et al., 2010
In the citing paper
“Extensive biomarker and imaging studies indicate that amyloid-β aggregation is the earliest pathological event in Alzheimer’s disease, followed at a later stage by pathological changes of tau aggregation extending beyond the limbic system to the neocortex, which correlates with brain atrophy and cognitive decline2,3.”
From Interplay between innate immunity and Alzheimer disease: APOE and TREM2 in the spotlight (2018) · cites this paper as [2]
In the citing paper
“Their timeline states that in individuals who develop AD, Aβ plaque deposition and reduced CSF Aβ occur first. Next, CSF tau levels rise. These changes manifest years before clinical signs or symptoms develop. Later on hippocampal atrophy appears, followed shortly thereafter by memory decline and eventually dementia. Full progression from Aβ changes to clinical decline takes approximately 10 to 20”
From The Alzheimer’s disease mitochondrial cascade hypothesis: progress and perspectives (2014) · cites this paper as [205]
In the citing paper
“Plaque formation rates also vary over time [217]. After a period of rapid accumulation, plaque deposition gradually slows and by the time symptoms manifest plaque deposition is essentially done [20, 205, 218].”
From The Alzheimer’s disease mitochondrial cascade hypothesis: progress and perspectives (2014) · cites this paper as [205]
In the citing paper
“data argue symptoms generally manifest only after plaques stop forming (Figure 5) [205, 216, 217].”
From The Alzheimer’s disease mitochondrial cascade hypothesis: progress and perspectives (2014) · cites this paper as [205]
In the citing paper
“As people meeting preclinical AD criteria may remain cognitively stable for many years [205, 214], these trials will take a long time to complete.”
From The Alzheimer’s disease mitochondrial cascade hypothesis: progress and perspectives (2014) · cites this paper as [205]
In the citing paper
“The new AD biological framework and the model of pathologic AD biomarkers from Jack and colleagues 18 conceptualize a progressive sequence of measurable biochemical, neurophysiological, and neuroanatomical alterations that can be detected years before psychometrically and clinically noticeable deterioration in cognition, behavior, and function.”
From The Alzheimer’s Disease Clinical Spectrum (2019) · cites this paper as [18]
In the citing paper
“The neuropathological changes that are quintessential for AD diagnosis—namely, the development of amyloid plaques and tau tangles—are considered to develop years before onset of the cognitive changes that characterize AD dementia [26].”
From Deep proteomic network analysis of Alzheimer’s disease brain reveals alterations in RNA binding proteins and RNA splicing associated with disease (2018) · cites this paper as [26]
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
McKhann, G., Drachman, D., Folstein, M., Katzman, R., Price, D., & Stadlan, E. M. (1984) · Neurology · doi:10.1212/wnl.34.7.939 · Cited by 27,915
Neuropathological stageing of Alzheimer-related changes.
Braak, H., & Braak, E. (1991) · Acta Neuropathologica · doi:10.1007/bf00308809 · Cited by 16,123
The Amyloid Hypothesis of Alzheimer’s Disease: Progress and Problems on the Road to Therapeutics
Hardy, J., & Selkoe, D. J. (2002) · Science · doi:10.1126/science.1072994 · Cited by 13,864
Amyloid oligomers exacerbate tau pathology in a mouse model of tauopathy
Selenica, M.-L. B., Brownlow, M., Jimenez, J. P., Lee, D. C., Pena, G., Dickey, C. A., Gordon, M. N., & Morgan, D. (2013) · Neurodegenerative Diseases · doi:10.1159/000337230 · Cited by 10,359
Corder, 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 as a diagnostic entity
Petersen, R. C. (2004) · Journal of Internal Medicine · doi:10.1111/j.1365-2796.2004.01388.x · Cited by 7,864
Self-citationImaging 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
Research criteria for the diagnosis of Alzheimer's disease: revising the NINCDS–ADRDA criteria
Dubois, B., Feldman, H. H., Jacova, C., DeKosky, S. T., Barberger-Gateau, P., Cummings, J., Delacourte, A., Galasko, D., Gauthier, S., Jicha, G., et al. (2007) · The Lancet Neurology · doi:10.1016/s1474-4422(07)70178-3 · Cited by 4,411
Terry, R. D., Masliah, E., Salmon, D. P., Butters, N., DeTeresa, R., Hill, R., Hansen, L. A., & Katzman, R. (1991) · Annals of Neurology · doi:10.1002/ana.410300410 · Cited by 4,397
Interplay between Cortical Spreading Depolarization and Seizures
Kramer, D. R., Fujii, T., Ohiorhenuan, I. E., & Liu, C. Y. (2017) · Stereotactic and Functional Neurosurgery · doi:10.1159/000452841 · Cited by 3,721
Cited by
Sorted by citations
Items 101–200 of 1,077
Clinical utility of cerebrospinal fluid biomarkers in the diagnosis of early Alzheimer's disease
Blennow, K., Dubois, B., Fagan, A. M., Lewczuk, P., de Leon, M. J., & Hampel, H. J. (2014) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2014.02.004 · Cited by 473
Amyloid biomarkers in Alzheimer's disease
Blennow, K., Mattsson, N., Schöll, M., Hansson, O., & Zetterberg, H. (2015) · Trends in Pharmacological Sciences · doi:10.1016/j.tips.2015.03.002 · Cited by 470
Alzheimer’s disease: insights into pathology, molecular mechanisms, and therapy
Zheng, Q., & Wang, X. (2024) · Protein & Cell · doi:10.1093/procel/pwae026 · Cited by 483
The amyloid cascade-inflammatory hypothesis of Alzheimer disease: implications for therapy
McGeer, P. L., & McGeer, E. G. (2013) · Acta Neuropathologica · doi:10.1007/s00401-013-1177-7 · Cited by 467
Wu, T., Dejanovic, B., Gandham, V. D., Gogineni, A., Edmonds, R., Schauer, S., Srinivasan, K., Huntley, M. A., Wang, Y., Wang, T.-M., et al. (2019) · Cell Reports · doi:10.1016/j.celrep.2019.07.060 · Cited by 466
Circadian rest-activity pattern changes in aging and preclinical Alzheimer disease
Musiek, E. S., Bhimasani, M., Zangrilli, M. A., Morris, J. C., Holtzman, D. M., & Ju, Y.-E. S. (2018) · JAMA Neurology · doi:10.1001/jamaneurol.2017.4719 · Cited by 465
de Paula, V. D. J. R., Radanovic, M., Diniz, B. S., & Forlenza, O. V. (2012) · Sub-cellular biochemistry/Subcellular biochemistry · doi:10.1007/978-94-007-5416-4_14 · Cited by 466
Mustapic, M., Eitan, E., Werner, J. K., Berkowitz, S. T., Lazaropoulos, M. P., Tran, J., Goetzl, E. J., & Kapogiannis, D. (2017) · Frontiers in Neuroscience · doi:10.3389/fnins.2017.00278 · Cited by 441
Biomarker Changes during 20 Years Preceding Alzheimer’s Disease
Jia, J., Ning, Y., Chen, M., Wang, S., Yang, H., Li, F., Ding, J., Li, Y., Zhao, B., Lyu, J., et al. (2024) · New England Journal of Medicine · doi:10.1056/nejmoa2310168 · Cited by 455
Veitch, D. P., Weiner, M. W., Aisen, P. S., Beckett, L. A., Cairns, N. J., Green, R. C., Harvey, D., Jack, C. R., Jagust, W., Morris, J. C., et al. (2019) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2018.08.005 · Cited by 454
Self-citationGray, J. P., Müller, V. I., Eickhoff, S. B., & Fox, P. T. (2020) · American Journal of Psychiatry · doi:10.1176/appi.ajp.2019.19050560 · Cited by 449
ATR-FTIR: A “rejuvenated” tool to investigate amyloid proteins
Sarroukh, R., Goormaghtigh, E., Ruysschaert, J., & Raussens, V. (2013) · Biochimica et Biophysica Acta (BBA) - Biomembranes · doi:10.1016/j.bbamem.2013.04.012 · Cited by 449
Stancu, I.-C., Cremers, N., Vanrusselt, H., Couturier, J., Vanoosthuyse, A., Kessels, S., Lodder, C., Brône, B., Huaux, F., Octave, J.-N., et al. (2019) · Acta Neuropathologica · doi:10.1007/s00401-018-01957-y · Cited by 447
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
Shi, J., Zheng, X., Li, Y., Zhang, Q., & Ying, S. (2018) · IEEE Journal of Biomedical and Health Informatics · doi:10.1109/jbhi.2017.2655720 · Cited by 444
A Plaque-Specific Antibody Clears Existing β-amyloid Plaques in Alzheimer's Disease Mice
DeMattos, R. B., Lu, J., Tang, Y., Racke, M. M., DeLong, C. A., Tzaferis, J. A., Hole, J. T., Forster, B. M., McDonnell, P. C., Liu, F., et al. (2012) · Neuron · doi:10.1016/j.neuron.2012.10.029 · Cited by 442
In vivo staging of regional amyloid deposition
Grothe, M. J., Barthel, H., Sepulcre, J., Dyrba, M., Sabri, O., Teipel, S. J., Initiative, F. T. A. D. N., Initiative, A. D. N., Weiner, M., Aisen, P., et al. (2017) · Neurology · doi:10.1212/wnl.0000000000004643 · Cited by 440
Self-citationTrushina, E., Dutta, T., Persson, X.-M. T., Mielke, M. M., & Petersen, R. C. (2013) · PLoS ONE · doi:10.1371/journal.pone.0063644 · Cited by 438
Self-citationAn early and late peak in microglial activation in Alzheimer’s disease trajectory
Fan, Z., Brooks, D. J., Okello, A., & Edison, P. (2017) · Brain · doi:10.1093/brain/aww349 · Cited by 438
Longitudinal Change in CSF Biomarkers in Autosomal-Dominant Alzheimer’s Disease
Fagan, A. M., Xiong, C., Jasielec, M. S., Bateman, R. J., Goate, A. M., Benzinger, T. L. S., Ghetti, B., Martins, R. N., Masters, C. L., Mayeux, R., et al. (2014) · Science Translational Medicine · doi:10.1126/scitranslmed.3007901 · Cited by 434
Brain amyloid-β oligomers in ageing and Alzheimer’s disease
Lesné, S., Sherman, M. A., Grant, M. K. O., Kuskowski, M. A., Schneider, J. A., Bennett, D. A., & Ashe, K. H. (2013) · Brain · doi:10.1093/brain/awt062 · Cited by 430
Targeting protein aggregation for the treatment of degenerative diseases
Eisele, Y. S., Monteiro, C., Fearns, C., Encalada, S. E., Wiseman, R. L., Powers, E. T., & Kelly, J. W. (2015) · Nature Reviews Drug Discovery · doi:10.1038/nrd4593 · Cited by 426
Olfactory and other sensory impairments in Alzheimer disease
Murphy, C. (2019) · Nature Reviews Neurology · doi:10.1038/s41582-018-0097-5 · Cited by 425
Power, M. C., Adar, S. D., Yanosky, J. D., & Weuve, J. (2016) · NeuroToxicology · doi:10.1016/j.neuro.2016.06.004 · Cited by 422
Alzheimer's disease: connecting findings from graph theoretical studies of brain networks
Tijms, B. M., Wink, A. M., de Haan, W., van der Flier, W. M., Stam, C. J., Scheltens, P., & Barkhof, F. (2013) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2013.02.020 · Cited by 416
National estimates of the prevalence of Alzheimer's disease in the United States
Brookmeyer, R., Evans, D. A., Hebert, L. E., Langa, K. M., Heeringa, S. G., Plassman, B. L., & Kukull, W. A. (2011) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2010.11.007 · Cited by 416
Kobayashi, Y., Sugahara, H., Shimada, K., Mitsuyama, E., Kuhara, T., Yasuoka, A., Kondo, T., Abe, K., & Xiao, J. (2017) · Scientific Reports · doi:10.1038/s41598-017-13368-2 · Cited by 411
Villeneuve, S., Rabinovici, G. D., Cohn-Sheehy, B. I., Madison, C., Ayakta, N., Ghosh, P. M., La Joie, R., Arthur-Bentil, S. K., Vogel, J. W., Marks, S. M., et al. (2015) · Brain · doi:10.1093/brain/awv112 · Cited by 408
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
Self-citationResting-state fMRI changes in Alzheimer's disease and mild cognitive impairment
Binnewijzend, M. A. A., Schoonheim, M. M., Sanz‐Arigita, E., Wink, A. M., van der Flier, W. M., Tolboom, N., Adriaanse, S. M., Damoiseaux, J. S., Scheltens, P., van Berckel, B. N. M., et al. (2011) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2011.07.003 · Cited by 407
Forecasting the prevalence of preclinical and clinical Alzheimer's disease in the United States
Brookmeyer, R., Abdalla, N., Kawas, C. H., & Corrada, M. M. (2018) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2017.10.009 · Cited by 406
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
Self-citationZhang, B., Carroll, J., Trojanowski, J. Q., Yao, Y., Iba, M., Potuzak, J. S., Hogan, A.-M. L., Xie, S. X., Ballatore, C., Smith, A. B., et al. (2012) · The Journal of Neuroscience · doi:10.1523/jneurosci.4922-11.2012 · Cited by 401
Self-citationJoshi, 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
Palmqvist, S., Mattsson, N., Hansson, O., & Initiative, F. T. A. D. N. (2016) · Brain · doi:10.1093/brain/aww015 · Cited by 400
Integrated multimodal cell atlas of Alzheimer’s disease
Gabitto, M. I., Travaglini, K. J., Rachleff, V. M., Kaplan, E. S., Long, B., Ariza, J., Ding, Y., Mahoney, J. T., Dee, N., Goldy, J., et al. (2024) · Nature Neuroscience · doi:10.1038/s41593-024-01774-5 · Cited by 397
“Next, we validated our results by: (1) assessing the supertype prediction probabilities across disease severity and (2) constructing supertype-specific signature scores based on differentially expressed genes in reference data (Methods) and comparing them across disease severity.”
Regional variability of imaging biomarkers in autosomal dominant Alzheimer's disease
Benzinger, T. L. S., Blazey, T., Jack, C. R., Koeppe, R. A., Su, Y., Xiong, C., Raichle, M. E., Snyder, A. Z., Ances, B. M., Bateman, R. J., et al. (2013) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1317918110 · Cited by 391
Self-citationMendez, M. F. (2017) · Neurologic Clinics · doi:10.1016/j.ncl.2017.01.005 · Cited by 389
Preventing Alzheimer’s Disease
Selkoe, D. J. (2012) · Science · doi:10.1126/science.1228541 · Cited by 391
Reduced non–rapid eye movement sleep is associated with tau pathology in early Alzheimer’s disease
Lucey, B. P., McCullough, A. A., Landsness, E. C., Toedebusch, C. D., McLeland, J., Zaza, A., Fagan, A. M., McCue, L. M., Xiong, C., Morris, J. C., et al. (2019) · Science Translational Medicine · doi:10.1126/scitranslmed.aau6550 · Cited by 386
Distinguishing Alzheimer’s disease from other major forms of dementia
Karantzoulis, S., & Galvin, J. E. (2011) · Expert Review of Neurotherapeutics · doi:10.1586/ern.11.155 · Cited by 385
Gut microbiome composition may be an indicator of preclinical Alzheimer’s disease
Ferreiro, A. L., Choi, J., Ryou, J., Newcomer, E. P., Thompson, R., Bollinger, R. M., Hall-Moore, C. M., Ndao, I. M., Sax, L., Benzinger, T. L. S., et al. (2023) · Science Translational Medicine · doi:10.1126/scitranslmed.abo2984 · Cited by 384
La Joie, R., Perrotin, A., Barré, L., Hommet, C., Mézenge, F., Ibazizene, M., Camus, V., Abbas, A., Landeau, B., Guilloteau, D., et al. (2012) · The Journal of Neuroscience · doi:10.1523/jneurosci.2170-12.2012 · Cited by 374
Zhao, J., Fu, Y., Yamazaki, Y., Ren, Y., Davis, M. D., Liu, C.-C., Lu, W., Wang, X., Chen, K., Cherukuri, Y., et al. (2020) · Nature Communications · doi:10.1038/s41467-020-19264-0 · Cited by 374
The Dynamics of Cortical and Hippocampal Atrophy in Alzheimer Disease
Sabuncu, M. R. (2011) · Archives of Neurology · doi:10.1001/archneurol.2011.167 · Cited by 339
Intraneuronal β-amyloid accumulation and synapse pathology in Alzheimer’s disease
Gouras, G. K., Tampellini, D., Takahashi, R. H., & Capetillo-Zarate, E. (2010) · Acta Neuropathologica · doi:10.1007/s00401-010-0679-9 · Cited by 372
Koepsell, T. D., & Monsell, S. E. (2012) · Neurology · doi:10.1212/wnl.0b013e31826e26b7 · Cited by 369
Palmqvist, 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
Walczak, Ł. J., & Herbet, M. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22179290 · Cited by 376
Decreased brain stiffness in Alzheimer's disease determined by magnetic resonance elastography
Murphy, M. C., Huston, J., Jack, C. R., Glaser, K. J., Manduca, A., Felmlee, J. P., & Ehman, R. L. (2011) · Journal of Magnetic Resonance Imaging · doi:10.1002/jmri.22707 · Cited by 364
Self-citationChételat, 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
Neurodegenerative Diseases: Expanding the Prion Concept
Walker, L. C., & Jucker, M. (2015) · Annual Review of Neuroscience · doi:10.1146/annurev-neuro-071714-033828 · Cited by 361
Statistical analysis of longitudinal neuroimage data with Linear Mixed Effects models
Bernal-Rusiel, J. L., Greve, D. N., Reuter, M., Fischl, B., & Sabuncu, M. R. (2013) · NeuroImage · doi:10.1016/j.neuroimage.2012.10.065 · Cited by 360
Neuroimaging markers for the prediction and early diagnosis of Alzheimer's disease dementia
Ewers, M., Sperling, R. A., Klunk, W. E., Weiner, M. W., & Hampel, H. J. (2011) · Trends in Neurosciences · doi:10.1016/j.tins.2011.05.005 · Cited by 360
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
Self-citationPontecorvo, M. J., Devous, M. D., Navitsky, M., Lu, M., Salloway, S., Schaerf, F. W., Jennings, D., Arora, A. K., McGeehan, A., Lim, N. C., et al. (2017) · Brain · doi:10.1093/brain/aww334 · Cited by 357
Modifiable factors that alter the size of the hippocampus with ageing
Fotuhi, M., Do, D., & Jack, C. R. (2012) · Nature Reviews Neurology · doi:10.1038/nrneurol.2012.27 · Cited by 356
Self-citationGomar, J. J. (2011) · Archives of General Psychiatry · doi:10.1001/archgenpsychiatry.2011.96 · Cited by 353
Developing the ATX(N) classification for use across the Alzheimer disease continuum
Hampel, H. J., Cummings, J. L., Blennow, K., Gao, P., Jack, C. R., & Vergallo, A. (2021) · Nature Reviews Neurology · doi:10.1038/s41582-021-00520-w · Cited by 351
Self-citationWeiner, M. W., Veitch, D. P., Aisen, P. S., Beckett, L. A., Cairns, N. J., Cedarbaum, J., Green, R. C., Harvey, D., Jack, C. R., Jagust, W., et al. (2015) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2014.11.001 · Cited by 348
Self-citationBasal forebrain degeneration precedes and predicts the cortical spread of Alzheimer’s pathology
Schmitz, T. W., Spreng, R. N., Initiative, T. A. D. N., Weiner, M. W., Aisen, P. S. S., Petersen, R. C., Jack, C. R., Jagust, W. J., Trojanowki, J. Q., Toga, A. W., et al. (2016) · Nature Communications · doi:10.1038/ncomms13249 · Cited by 345
Self-citationMormino, E. C., Smiljic, A., Hayenga, A. O., Onami, S. H., Greicius, M. D., Rabinovici, G. D., Janabi, M., Baker, S. L., Yen, I. V., Madison, C. M., et al. (2011) · Cerebral Cortex · doi:10.1093/cercor/bhr025 · Cited by 344
Self-citationdel Campo, M., Mollenhauer, B., Bertolotto, A., Engelborghs, S., Hampel, H., Simonsen, A. H., Kapaki, E., Kruse, N., Le Bastard, N., Lehmann, S., et al. (2012) · Biomarkers in Medicine · doi:10.2217/bmm.12.46 · Cited by 343
Beecham, G. W., Hamilton, K., Naj, A. C., Martin, E. R., Huentelman, M., Myers, A. J., Corneveaux, J. J., Hardy, J., Vonsattel, J.-P., Younkin, S. G., et al. (2014) · PLoS Genetics · doi:10.1371/journal.pgen.1004606 · Cited by 343
Self-citationAmyloid‐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
The complexity of Alzheimer’s disease: an evolving puzzle
Ferrari, C., & Sorbi, S. (2021) · Physiological Reviews · doi:10.1152/physrev.00015.2020 · Cited by 343
18F-THK523: a novel in vivo tau imaging ligand for Alzheimer's disease
Fodero‐Tavoletti, M. T., Okamura, N., Furumoto, S., Mulligan, R. S., Connor, A. R., McLean, C., Cao, D., Rigopoulos, A., Cartwright, G. A., O'Keefe, G. J., et al. (2011) · Brain · doi:10.1093/brain/awr038 · Cited by 340
Cognitive symptoms of Alzheimer’s disease: clinical management and prevention
Joe, E., & Ringman, J. M. (2019) · BMJ · doi:10.1136/bmj.l6217 · Cited by 339
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
Self-citationImpact of sleep on the risk of cognitive decline and dementia
Spira, A. P., Chen-Edinboro, L. P., Wu, M. N., & Yaffe, K. S. (2014) · Current Opinion in Psychiatry · doi:10.1097/yco.0000000000000106 · Cited by 331
The future of blood‐based biomarkers for Alzheimer's disease
Henriksen, K., O’Bryant, S. E., Hampel, H. J., Trojanowski, J. Q., Montine, T. J., Jeromin, A., Blennow, K., Lönneborg, A., Wyss‐Coray, T., Soares, H. D., et al. (2013) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2013.01.013 · Cited by 327
Self-citationWeiner, M. W., Veitch, D. P., Aisen, P. S. S., Beckett, L. A., Cairns, N. J., Green, R. C., Harvey, D. J., Jack, C. R., Jagust, W. J., Morris, J. C., et al. (2017) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2016.11.007 · Cited by 325
Self-citationBrunden, K. R., Zhang, B., Carroll, J., Yao, Y., Potuzak, J. S., Hogan, A.-M. L., Iba, M., James, M. J., Xie, S. X., Ballatore, C., et al. (2010) · The Journal of Neuroscience · doi:10.1523/jneurosci.3059-10.2010 · Cited by 320
Self-citationPhagocytosis in the Brain: Homeostasis and Disease
Galloway, D. A., Phillips, A. E. M., Owen, D. R., & Moore, C. S. (2019) · Frontiers in Immunology · doi:10.3389/fimmu.2019.00790 · Cited by 319
Accelerating Cortical Thinning: Unique to Dementia or Universal in Aging?
Fjell, A. M., Westlye, L. T., Grydeland, H., Amlien, I. K., Espeseth, T., Reinvang, I., Raz, N., Dale, A. M., Walhovd, K. B., & Initiative, A. D. N. (2012) · Cerebral Cortex · doi:10.1093/cercor/bhs379 · Cited by 318
NPTX2 and cognitive dysfunction in Alzheimer’s Disease
Xiao, M.-F., Xu, D., Craig, M. T., Pelkey, K. A., Chien, C.-C., Shi, Y., Zhang, J., Resnick, S., Pletnikova, O., Salmon, D., et al. (2017) · eLife · doi:10.7554/elife.23798 · Cited by 316
Lewczuk, 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-citationHadoux, X., Hui, F., Lim, J. K. H., Masters, C. L., Pébay, A., Chevalier, S., Ha, J. J., Loi, S. M., Fowler, C. J., Rowe, C. C., et al. (2019) · Nature Communications · doi:10.1038/s41467-019-12242-1 · Cited by 315
The amyloid cascade hypothesis: an updated critical review
Kepp, K. P., Robakis, N. K. R. K., Høilund‐Carlsen, P. F., Sensi, S. L., & Vissel, B. (2023) · Brain · doi:10.1093/brain/awad159 · Cited by 315
Fyn inhibition rescues established memory and synapse loss in Alzheimer mice
Kaufman, A. C., Salazar, S. V., Haas, L. T., Yang, J., Kostylev, M. A., Jeng, A. T., Robinson, S. A., Gunther, E. C., van Dyck, C. H., Nygaard, H. B., et al. (2015) · Annals of Neurology · doi:10.1002/ana.24394 · Cited by 314
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-citationLiss, J. L., Seleri Assunção, S., Cummings, J., Atri, A., Geldmacher, D. S., Candela, S. F., Devanand, D. P., Fillit, H. M., Susman, J., Mintzer, J., et al. (2021) · Journal of Internal Medicine · doi:10.1111/joim.13244 · Cited by 312
Depression—an underrecognized target for prevention of dementia in Alzheimer’s disease
Dafsari, F. S., & Jessen, F. (2020) · Translational Psychiatry · doi:10.1038/s41398-020-0839-1 · Cited by 312
The role of CREB signaling in Alzheimer’s disease and other cognitive disorders
Saura, C. A., & Valero, J. (2011) · revneuro · doi:10.1515/rns.2011.018 · Cited by 312
Efficacy of Souvenaid in Mild Alzheimer's Disease: Results from a Randomized, Controlled Trial
Scheltens, P., Twisk, J. W. R., Blesa, R., Scarpini, E. A., Arnim, C. A. F. V., Bongers, A., Harrison, J., Willemsen‐Swinkels, S. H. N., Stam, C. J., de Waal, H., et al. (2012) · Journal of Alzheimer s Disease · doi:10.3233/jad-2012-121189 · Cited by 314
Brain microbleeds and Alzheimer’s disease: innocent observation or key player?
Cordonnier, C., & van der Flier, W. M. (2011) · Brain · doi:10.1093/brain/awq321 · Cited by 310
Fibre-specific white matter reductions in Alzheimer’s disease and mild cognitive impairment
Mito, R., Raffelt, D., Dhollander, T., Vaughan, D. N., Tournier, J.-D., Salvado, O., Brodtmann, A., Rowe, C. C., Villemagne, V. L., & Connelly, A. (2018) · Brain · doi:10.1093/brain/awx355 · Cited by 309
Update on the biomarker core of the Alzheimer's Disease Neuroimaging Initiative subjects
Trojanowski, J. Q., Vandeerstichele, H., Korecka, M., Clark, C. M., Aisen, P. S. S., Petersen, R. C., Blennow, K., Soares, H. D., Simon, A. J., Lewczuk, P., et al. (2010) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2010.03.008 · Cited by 309
Self-citationPlasma neurofilament light as a potential biomarker of neurodegeneration in Alzheimer’s disease
Lewczuk, P., Ermann, N., Andréasson, U., Schultheis, C., Podhorná, J., Spitzer, P., Maler, J. M., Kornhuber, J., Blennow, K., & Zetterberg, H. (2018) · Alzheimer s Research & Therapy · doi:10.1186/s13195-018-0404-9 · Cited by 309
Early Adult to Midlife Cardiovascular Risk Factors and Cognitive Function
Yaffe, K., Vittinghoff, E., Pletcher, M. J., Hoang, T. D., Launer, L. J., Whitmer, R. A., Coker, L. H., & Sidney, S. (2014) · Circulation · doi:10.1161/circulationaha.113.004798 · Cited by 308
A data-driven model of biomarker changes in sporadic Alzheimer’s disease
Young, A. L., Oxtoby, N. P., Daga, P., Cash, D. M., Fox, N. C., Ourselin, S., Schott, J. M., & Alexander, D. C. (2014) · Brain · doi:10.1093/brain/awu176 · Cited by 308
Brain aging, Alzheimer's disease, and mitochondria
Swerdlow, R. H. (2011) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2011.08.012 · Cited by 306
“This is based on studies that suggest fi brillar A β deposition or low CSF A β either can or does precede the other changes [76,89].”
BackgroundBateman, R. J., Benzinger, T. L., Berry, S., Clifford, D. B., Duggan, C., Fagan, A. M., Fanning, K., Farlow, M. R., Hassenstab, J., McDade, E. M., et al. (2017) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2016.07.005 · Cited by 303
The Alzheimer's Disease Neuroimaging Initiative 2 PET Core: 2015
Jagust, W. J., Landau, S. M., Koeppe, R. A., Reiman, E. M., Chen, K., Mathis, C. A., Price, J. C., Foster, N. L., & Wang, A. Y. (2015) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2015.05.001 · Cited by 302
Self-citationAging and Alzheimer's disease: comparison and associations from molecular to system level
Xia, X., Jiang, Q., McDermott, J., & Han, J. J. (2018) · Aging Cell · doi:10.1111/acel.12802 · Cited by 301
Perrotin, A. (2012) · Archives of Neurology · doi:10.1001/archneurol.2011.666 · Cited by 300
Qualification of the analytical and clinical performance of CSF biomarker analyses in ADNI
Initiative, T. A. D. N., Shaw, L. M. J., Vanderstichele, H., Knapik-Czajka, M. E., Figurski, M., Coart, E., Blennow, K., Soares, H. D., Simon, A. J., Lewczuk, P., et al. (2011) · Acta Neuropathologica · doi:10.1007/s00401-011-0808-0 · Cited by 301
Self-citationIdentifying and Mapping Connectivity Patterns of Brain Network Hubs in Alzheimer's Disease
Dai, Z., Yan, C., Li, K., Wang, Z., Wang, J., Cao, M., Lin, Q., Shu, N., Xia, M., Bi, Y., et al. (2014) · Cerebral Cortex · doi:10.1093/cercor/bhu246 · Cited by 298
van Oostveen, W. M., & de Lange, E. C. M. (2021) · International Journal of Molecular Sciences · doi:10.3390/ijms22042110 · Cited by 297
Shinohara, M., Tachibana, M., Kanekiyo, T., & Bu, G. (2017) · Journal of Lipid Research · doi:10.1194/jlr.r075796 · Cited by 297
Metadata
- Authors
- Jack, C. R., Knopman, D. S., Jagust, W. J., Shaw, L. M., Aisen, P. S., Weiner, M. W., Petersen, R. C., & Trojanowski, J. Q.
- Affiliations
- Mayo Clinic (US)
- University of California, Berkeley (US)
- University of Pennsylvania (US)
- University of California San Diego (US)
- University of California, San Francisco (US)
- Corresponding author
- Jack, Clifford R
- ORCID
- Venue
- The Lancet Neurology
- Publisher
- Elsevier BV
- Published
- 2010-01
- Volume
- 9
- Issue
- 1
- Pages
- 119-128
- ISSN
- 1474-4422 (ISSN-L)
- PMC
- PMC2819840
- OpenAlex
- W2167840686
- Cited by
- 4,806
- References
- 119
- Citations by year
- 2026: 273 · 2025: 317 · 2024: 278 · 2023: 259 · 2022: 308 · 2021: 321 · 2020: 359 · 2019: 303 · 2018: 267 · 2017: 283 · 2016: 265 · 2015: 273 · 2014: 335 · 2013: 337 · 2012: 301
- FWCI
- 127.41
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The Lancet Neurology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institutes of Health (AG11378)
- National Institute on Aging
- 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
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, amyloid-beta, amyloid PET, tau protein, brain atrophy, FDG-PET, synaptic dysfunction, neurodegeneration, disease stage, biomarkers, cognitive decline
- MeSH terms
- Aging, Alzheimer Disease, Brain, Cognition Disorders, Humans, Magnetic Resonance Imaging, Models, Neurological, Time Factors, Signal Transduction, Biomarkers, Amyloid beta-Peptides, tau Proteins, Disease Progression, Positron-Emission Tomography, Apolipoprotein E4, 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
