The DOI matches its Crossref record; 75 of the 75 references it cites were found in a registry or an index.
Stages of the Pathologic Process in Alzheimer Disease: Age Categories From 1 to 100 Years
Abstract
Two thousand three hundred and thirty two nonselected brains from 1- to 100-year-old individuals were examined using immunocytochemistry (AT8) and Gallyas silver staining for abnormal tau; immunocytochemistry (4G8) and Campbell-Switzer staining were used for the detection ofβ-amyloid. A total of 342 cases was negative in the Gallyas stain but when restaged for AT8 only 10 were immunonegative. Fifty-eight cases had subcortical tau predominantly in the locus coeruleus, but there was no abnormal cortical tau (subcortical Stages a-c). Cortical involvement (abnormal tau in neurites) was identified first in the transentorhinal region (Stage 1a, 38 cases). Transentorhinal pyramidal cells displayed pretangle material (Stage 1b, 236 cases). Pretangles gradually became argyrophilic neurofibrillary tangles (NFTs) that progressed in parallel with NFT Stages I to VI. Pretangles restricted to subcortical sites were seen chiefly at younger ages. Of the total cases, 1,031 (44.2%) had β-amyloid plaques. The first plaques occurred in the neocortex after the onset of tauopathy in the brainstem. Plaques generally developed in the 40s in 4% of all cases, culminating in their tenth decade (75%). β-amyloid plaques and NFTs were significantly correlated (p < 0.0001). These data suggest that tauopathy associated with sporadic Alzheimer disease may begin earlier than previously thought and possibly in the lower brainstem rather than in the transentorhinal region.
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
“Up to 60% of CU individuals over age 80 years have AD neuropathologic changes at autopsy or by biomarkers [60,152,212–214].”
From NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease (2018) · cites this paper as [213]
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
“screening revealed low rates of Braak 1–2 NFT stages in all three groups (Table 2), consistent with literature-based norms [3].”
From Tuberous sclerosis complex is associated with a novel human tauopathy (2023) · cites this paper as [3]
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 should be noted that tau aggregation in the brain is associated with older age and is generally uncommon in healthy young adults (Braak et al., 2011; Crary et al., 2014).”
From Tauopathy and Epilepsy Comorbidities and Underlying Mechanisms (2022) · cites this paper as Braak et al., 2011
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“It is expected that many persons die with brains that exhibit AD neuropathologic change in the preclinical phase of AD; indeed, data support the modeled expectations (44, 142).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [44]
The cited source says what the claim attributes to it.
In the citing paper
“Medial temporal and brainstem neurofibrillary changes were observed in our older TSC subjects, as expected, but at a rate comparable to that observed in the epilepsy and non-neurological control groups and age-based norms [3].”
From Tuberous sclerosis complex is associated with a novel human tauopathy (2023) · cites this paper as [3]
In the citing paper
“In individuals with autosomal dominant mutations in genes coding for amyloid precursor protein (APP) or Presenilin 119 , alterations in Aβ generation that result in early deposition of plaque initiate the disease and patients invariably develop the full spectrum of tau pathology 120,121 .”
From The amyloid hypothesis in Alzheimer disease: new insights from new therapeutics (2022) · cites this paper as [121]
In the citing paper
“NFTs first appear in layer II of the entorhinal cortex (EC) during AD onset.”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [231]
In the citing paper
“NFTs subsequently appear in interconnected anatomical regions within the brain, including the hippocampus and neocortex during neurodegenerative progression [229–231].”
From Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease (2020) · cites this paper as [231]
In the citing paper
“Furthermore, it impairs adult hippocampal neurogenesis in mice and affects cortical thickness, brain activity, and mitochondrial function well before significant Aβ accumulation in the human brains [74–76].”
From Apolipoprotein E4, inhibitory network dysfunction, and Alzheimer’s disease (2019) · cites this paper as [76]
In the citing paper
“Most of all, this binary threshold does not reflect the reality of amyloid β and tau pathology, which is continuous and present at a minimal extent in almost all people older than 70 years,17 with important discrepancies between pathology burden and clinical symptoms at intermediate extents (panel 2).”
From Clinical diagnosis of Alzheimer’s disease: Recommendations of the International Working Group (2021) · cites this paper as [17]
In the citing paper
“For tau biomarkers, there is also a strong discrepancy between neuropathological identification (in post-mortem studies, the presence of tau Braak stages I–II is almost universal after age 70 years)17,19 and in-vivo measures of tau aggregates on PET (36% of individuals are tau positive after the age of 70 years23).”
From Clinical diagnosis of Alzheimer’s disease: Recommendations of the International Working Group (2021) · cites this paper as [17]
In the citing paper
“The concordance of genetics and Aβ deposition is aligned with CPC studies that indicate that AβPs may be a temporally “upstream” feature of the neocortical disease, with the caveats that brainstem and medial temporal lobe pretangles and NFTs are seen in subjects without Aβ deposition in all age categories (33, 39, 44).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [44]
In the citing paper
“In contrast to NFTs, AβPs are extracellular (45, 46) and are found in a high proportion of all elderly persons but are not universal (44, 47, 48).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [44]
In the citing paper
“Recently, it has been reported that NFTs are also very common in certain brainstem nuclei in subjects without dementia (39-44).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [44]
In the citing paper
“Neurofibrillary pathology is observed in the human brain long before Aβ plaques develop (39, 44, 300).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [44]
In the citing paper
“Neuritic plaques seem to develop after diffuse AβPs and NFTs (44).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [44]
In the citing paper
“At 40 years, all individuals studied by Braak and Del Tredici (39) and Braak et al (44) exhibited at least initial neurofibrillary pathology in the brainstem (Fig. 5).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [44]
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
Neuropathological stageing of Alzheimer-related changes.
Braak, H., & Braak, E. (1991) · Acta Neuropathologica · doi:10.1007/bf00308809 · Cited by 16,123 · cited 2×
“The first lesions were usually seen in the transentorhinal region (2).”
BackgroundSelf-citationThe 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
Staging of brain pathology related to sporadic Parkinson’s disease
Braak, H., Tredici, K. D., Rüb, U., de Vos, R. A. I., Jansen Steur, E. N. H., & Braak, E. (2003) · Neurobiology of Aging · doi:10.1016/s0197-4580(02)00065-9 · Cited by 10,777
Self-citationHypothetical model of dynamic biomarkers of the Alzheimer's pathological cascade
Jack, C. R., Knopman, D. S., Jagust, W. J., Shaw, L. M., Aisen, P. S., Weiner, M. W., Petersen, R. C., & Trojanowski, J. Q. (2010) · The Lancet Neurology · doi:10.1016/s1474-4422(09)70299-6 · Cited by 4,806
Aston-Jones, G., & Cohen, J. D. (2005) · Annual Review of Neuroscience · doi:10.1146/annurev.neuro.28.061604.135709 · Cited by 4,472
Phases of Aβ-deposition in the human brain and its relevance for the development of AD
Thal, D. R., Rüb, U., Orantes, M., & Braak, H. (2002) · Neurology · doi:10.1212/wnl.58.12.1791 · Cited by 3,490
Self-citationBraak, H., Alafuzoff, I., Arzberger, T., Kretzschmar, H., & Del Tredici, K. (2006) · Acta Neuropathologica · doi:10.1007/s00401-006-0127-z · Cited by 3,172
Self-citationA Century of Alzheimer's Disease
Goedert, M., & Spillantini, M. G. (2006) · Science · doi:10.1126/science.1132814 · Cited by 2,153
The locus coeruleus and noradrenergic modulation of cognition
Sara, S. J. (2009) · Nature Reviews Neuroscience · doi:10.1038/nrn2573 · Cited by 1,848
Frequency of Stages of Alzheimer-Related Lesions in Different Age Categories
Braak, H., & Braak, E. (1997) · Neurobiology of Aging · doi:10.1016/s0197-4580(97)00056-0 · Cited by 1,656
Self-citationEnhanced neurofibrillary degeneration in transgenic mice expressing mutant tau and APP
Lewis, J., Dickson, D. W., Lin, W.-L., Chisholm, L., Corral, A., Jones, G., Yen, S.-H., Sahara, N., Skipper, L., Yager, D., et al. (2001) · Science · doi:10.1126/science.1058189 · Cited by 1,611
Formation of Neurofibrillary Tangles in P301L Tau Transgenic Mice Induced by Aβ42 Fibrils
Götz, J., Chen, F., van Dorpe, J., & Nitsch, R. M. (2001) · Science · doi:10.1126/science.1062097 · Cited by 1,526
Neural mechanisms of ageing and cognitive decline
Bishop, N. A., Lu, T., & Yankner, B. A. (2010) · Nature · doi:10.1038/nature08983 · Cited by 1,323
Zarow, C., Lyness, S. A., Mortimer, J. A., & Chui, H. C. (2003) · Archives of Neurology · doi:10.1001/archneur.60.3.337 · Cited by 1,003
Arizona Parkinson’s Disease Consortium, Beach, T. G., Adler, C. H., Sue, L. I., Vedders, L., Lue, L., White III, C. L., Akiyama, H., Caviness, J. N., Shill, H. A., et al. (2010) · Acta Neuropathologica · doi:10.1007/s00401-010-0664-3 · Cited by 911
Stamer, K., Vogel, R., Thies, E., Mandelkow, E., & Mandelkow, E.-M. (2002) · The Journal of Cell Biology · doi:10.1083/jcb.200108057 · Cited by 885
The pathological process underlying Alzheimer’s disease in individuals under thirty
Braak, H., & Del Tredici, K. (2011) · Acta Neuropathologica · doi:10.1007/s00401-010-0789-4 · Cited by 812
Self-citationOddo, S., Billings, L., Kesslak, J. P., Cribbs, D. H., & LaFerla, F. M. (2004) · Neuron · doi:10.1016/j.neuron.2004.07.003 · Cited by 780
Braak, F., Braak, H., & Mandelkow, E. (1994) · Acta Neuropathologica · doi:10.1007/bf00293315 · Cited by 769
Self-citationProdromal Alzheimer's disease: successive emergence of the clinical symptoms
Amieva, H., Le Goff, M., Millet, X., Orgogozo, J. M., Pérès, K., Barberger‐Gateau, P., Jacqmin‐Gadda, H., & Dartigues, J. F. (2008) · Annals of Neurology · doi:10.1002/ana.21509 · Cited by 737
Yankner, B. A., Lu, T., & Loerch, P. (2008) · Annual Review of Pathology: Mechanisms of Disease · doi:10.1146/annurev.pathmechdis.2.010506.092044 · Cited by 677
Neuropathology and Cognitive Impairment in Alzheimer Disease: A Complex but Coherent Relationship
Nelson, P. T., Braak, H., & Markesbery, W. R. (2009) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/nen.0b013e3181919a48 · Cited by 643
Self-citationSeeding of Normal Tau by Pathological Tau Conformers Drives Pathogenesis of Alzheimer-like Tangles
Guo, J. L., & Lee, V. M.-Y. (2011) · Journal of Biological Chemistry · doi:10.1074/jbc.m110.209296 · Cited by 636
Mechanisms of tau-induced neurodegeneration
Iqbal, K., Liu, F., Gong, C.-X., Alonso, A. D. C., & Grundke-Iqbal, I. (2009) · Acta Neuropathologica · doi:10.1007/s00401-009-0486-3 · Cited by 628
Demonstration of amyloid deposits and neurofibrillary changes in whole brain sections
Braak, H., & Braak, E. (1991) · Brain Pathology · doi:10.1111/j.1750-3639.1991.tb00661.x · Cited by 598
Self-citationLemere, C. A., Blusztajn, J. K., Yamaguchi, H., Wisniewski, T., Saido, T. C., & Selkoe, D. J. (1996) · Neurobiology of Disease · doi:10.1006/nbdi.1996.0003 · Cited by 584
The propagation of prion-like protein inclusions in neurodegenerative diseases
Goedert, M., Clavaguera, F., & Tolnay, M. (2010) · Trends in Neurosciences · doi:10.1016/j.tins.2010.04.003 · Cited by 472
Alafuzoff, I., Arzberger, T., Al‐Sarraj, S., Bodi, I., Bogdanovic, N., Braak, H., Bugiani, O., Del‐Tredici, K., Ferrer, I., Gelpi, E., et al. (2008) · Brain Pathology · doi:10.1111/j.1750-3639.2008.00147.x · Cited by 467
Self-citationThe neuropathology of aminergic nuclei in Alzheimer's disease
Zweig, R. M., Ross, C. A., Hedreen, J. C., Steele, C., Cardillo, J. E., Whitehouse, P. J., Folstein, M. F., & Price, D. L. (1988) · Annals of Neurology · doi:10.1002/ana.410240210 · Cited by 446
Goedert, M., Jakes, R., Crowther, R. A., Six, J., Lübke, U., Vandermeeren, M., Cras, P., Trojanowski, J. Q., & Lee, V. M. (1993) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.90.11.5066 · Cited by 446
Reimagining Alzheimer's Disease—An Age-Based Hypothesis
Herrup, K. (2010) · Journal of Neuroscience · doi:10.1523/jneurosci.4521-10.2010 · Cited by 408
Grudzien, A., Shaw, P., Weintraub, S., Bigio, E., Mash, D. C., & Mesulam, M. M. (2007) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2006.02.007 · Cited by 396
Reassessing the amyloid cascade hypothesis of Alzheimer's disease
Pimplikar, S. W. (2008) · The International Journal of Biochemistry & Cell Biology · doi:10.1016/j.biocel.2008.12.015 · Cited by 389
Alzheimer’s pathogenesis: is there neuron-to-neuron propagation?
Braak, H., & Tredici, K. D. (2011) · Acta Neuropathologica · doi:10.1007/s00401-011-0825-z · Cited by 375
Self-citationNeurons May Live for Decades with Neurofibrillary Tangles
Morsch, R., Simon, W., & Coleman, P. D. (1999) · Journal of Neuropathology and Experimental Neurology · doi:10.1097/00005072-199902000-00008 · Cited by 370
Sequence of Aβ-protein deposition in the human medial temporal lobe
Thal, D. R., Rüb, U., Schultz, C., Sassin, I., Ghebremedhin, E., Del Tredici, K., Braak, E., & Braak, H. (2000) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/59.8.733 · Cited by 370
Self-citationNelson, P. T., Head, E., Schmitt, F. A., Davis, P. R., Neltner, J. H., Jicha, G. A., Abner, E. L., Smith, C. D., Van Eldik, L. J., Kryscio, R. J., et al. (2011) · Acta Neuropathologica · doi:10.1007/s00401-011-0826-y · Cited by 365
Reactive Oxygen Species: Stuck in the Middle of Neurodegeneration
Patten, D. A., Germain, M., Kelly, M., & Slack, R. S. (2010) · Journal of Alzheimer s Disease · doi:10.3233/jad-2010-100498 · Cited by 286
Ferrer, I., Santpere, G., & van Leeuwen, F. W. (2008) · Brain · doi:10.1093/brain/awm305 · Cited by 263
Spatial and temporal relationships between plaques and tangles in Alzheimer-pathology
Schönheit, B., Zarski, R., & Ohm, T. G. (2004) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2003.09.009 · Cited by 262
Grinberg, L. T., Rüb, U., Ferretti, R. E. L., Nitríni, R., Farfel, J. M., Polichiso, L., Gierga, K., Jacob‐Filho, W., Heinsen, H., & Brazilian Brain Bank Study Group (2009) · Neuropathology and Applied Neurobiology · doi:10.1111/j.1365-2990.2008.00997.x · Cited by 247
Structural Principles of Tau and the Paired Helical Filaments of Alzheimer's Disease
Mandelkow, E., Von Bergen, M., Biernat, J., & Mandelkow, E. (2007) · Brain Pathology · doi:10.1111/j.1750-3639.2007.00053.x · Cited by 243
Braak, H., & Braak, E. (1987) · Neuroscience Letters · doi:10.1016/0304-3940(87)90204-7 · Cited by 236
Self-citationOhm, T. G., Müller, H., Braak, H., & Böhl, J. (1995) · Neuroscience · doi:10.1016/0306-4522(95)90397-p · Cited by 222
Self-citationMartínez, A., Portero‐Otín, M., Pamplona, R., & Ferrer, I. (2009) · Brain Pathology · doi:10.1111/j.1750-3639.2009.00326.x · Cited by 217
Leverenz, J. B., & Raskind, M. A. (1998) · Experimental Neurology · doi:10.1006/exnr.1997.6777 · Cited by 214
Pearson, J., Goldstein, M., MARKEY, K., & Brandeis, L. (1983) · Neuroscience · doi:10.1016/0306-4522(83)90023-4 · Cited by 213
Tau protein, the paired helical filament and Alzheimer's disease
Goedert, M., Klug, A., & Crowther, R. A. (2006) · Journal of Alzheimer s Disease · doi:10.3233/jad-2006-9s323 · Cited by 205
Alzheimer's disease: Neurofibrillary tangles in nuclei that project to the cerebral cortex
German, D. C., White, C. L., & Sparkman, D. R. (1987) · Neuroscience · doi:10.1016/0306-4522(87)90123-0 · Cited by 204
Cholinergic Neuronal and Axonal Abnormalities Are Present Early in Aging and in Alzheimer Disease
Geula, C., Nagykery, N. G., Nicholas, A., & Wu, C. (2008) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/nen.0b013e31816a1df3 · Cited by 204
Does Alzheimer's disease begin in the brainstem?
Simic, G., Stanic, G., Mladinov, M., Jovanov‐Milosevic, N., Kostovic, I., & Hof, P. R. (2009) · Neuropathology and Applied Neurobiology · doi:10.1111/j.1365-2990.2009.01038.x · Cited by 204
Evolution of Alzheimer's disease-related cytoskeletal changes in the basal nucleus of Meynert
Sassin, I., Schultz, C., Thal, D. R., Rüb, U., Arai, K., Braak, E., & Braak, H. (2000) · Acta Neuropathologica · doi:10.1007/s004019900178 · Cited by 193
Self-citationTrojanowski, J. Q., & LEE, V. M. ‐. (2000) · Annals of the New York Academy of Sciences · doi:10.1111/j.1749-6632.2000.tb05561.x · Cited by 184
Functional Consequences of Locus Coeruleus Degeneration in Alzheimers Disease
Weinshenker, D. (2008) · Current Alzheimer Research · doi:10.2174/156720508784533286 · Cited by 180
Quantitative neuropathological changes in presymptomatic Huntington's disease
Gómez‐Tortosa, E., MacDonald, M. E., Friend, J. C., Taylor, S. A., Weiler, L., Cupples, L. A., Srinidhi, J., Gusella, J. F., Bird, E. D., Vonsattel, J., et al. (2001) · Annals of Neurology · doi:10.1002/1531-8249(200101)49:1 · Cited by 174
Disruption of microtubule network by Alzheimer abnormally hyperphosphorylated tau
Li, B., Chohan, M. O., Grundke, I., & Iqbal, K. (2007) · Acta Neuropathologica · doi:10.1007/s00401-007-0207-8 · Cited by 173
Cowan, C. M., Bossing, T., Page, A., Shepherd, D., & Mudher, A. (2010) · Acta Neuropathologica · doi:10.1007/s00401-010-0716-8 · Cited by 156
Why Pleiotropic Interventions are Needed for Alzheimer's Disease
Frautschy, S. A., & Cole, G. M. (2010) · Molecular Neurobiology · doi:10.1007/s12035-010-8137-1 · Cited by 152
The amyloid cascade hypothesis
Korczyn, A. D. (2008) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2007.11.008 · Cited by 136
Propofol Directly Increases Tau Phosphorylation
Whittington, R. A., Virág, L., Marcouiller, F., Papon, M.-A., Khoury, N. B. E., Julien, C., Morin, F., Emala, C. W., & Planel, E. (2011) · PLoS ONE · doi:10.1371/journal.pone.0016648 · Cited by 133
Mechanism of Tau-Induced Neurodegeneration in Alzheimer Disease and Related Tauopathies
Alonso, A. D. C., Li, B., Grundke, I., & Iqbal, K. (2008) · Current Alzheimer Research · doi:10.2174/156720508785132307 · Cited by 128
Neuropathology of non-Alzheimer degenerative disorders.
(2009) · PubMed Central · Cited by 117
Hertz, L. (1989) · Brain Research Reviews · doi:10.1016/0165-0173(89)90017-9 · Cited by 107
Spatial, Temporal and Numeric Analysis of Alzheimer Changes in the Nucleus Coeruleus
Busch, C., Bohl, J. R. E., & Ohm, T. G. (1997) · Neurobiology of Aging · doi:10.1016/s0197-4580(97)00035-3 · Cited by 105
Alzheimer?s disease: intraneuronal alterations precede insoluble amyloid-$beta; formation
Braak, H., & Tredici, K. D. (2004) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2003.12.015 · Cited by 93
Self-citationHaglund, M., Sjöbeck, M., & Englund, E. M. (2006) · Neuropathology · doi:10.1111/j.1440-1789.2006.00725.x · Cited by 81
Hyman, B. T., & Gómez‐Isla, T. (1994) · Neurobiology of Aging · doi:10.1016/0197-4580(94)90031-0 · Cited by 74
Pikkarainen, M., MARTIKAINEN, P. M., & Alafuzoff, I. I. (2009) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/nen.0b013e3181c6c13d · Cited by 68
Transition of Tau Protein from Disordered to Misordered in Alzheimer’s Disease
Kovačech, B., Škrabana, R., & Novák, M. (2010) · Neurodegenerative Diseases · doi:10.1159/000283478 · Cited by 51
Tolnay, M., & Probst, A. (2008) · Handbook of clinical neurology · doi:10.1016/s0072-9752(07)01251-1 · Cited by 41
Duration of neurofibrillary changes in the hippocampal pyramidal neurons
Bobinski, M., Węgiel, J., Tarnawski, M. J., Bobinski, M., de Leon, M. J., Reisberg, ., Miller, D. C., & Wı́sniewski, H. M. (1998) · Brain Research · doi:10.1016/s0006-8993(98)00441-7 · Cited by 38
Muresan, Z. L., & Mureşan, V. (2008) · Neurodegenerative Diseases · doi:10.1159/000113716 · Cited by 30
Del Tredici, K., & Braak, H. (2008) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2008.04.016 · Cited by 27 · cited 1×
“Thus, advanced age per se is not a precondition for the formation of the ADassociated tau lesions; rather, there is now strong evidence that the pathologic process underlying AD is not ‘‘age-dependent’’ but an uncommonly slowly progressive one that frequently extends into old age (55).”
BackgroundSelf-citationMolecular and cellular pathways towards and away from Alzheimer’s disease
Mattson, M. P. (2006) · Springer eBooks · doi:10.1007/978-3-540-37652-1_47 · Cited by 5
The Amyloid Hypothesis: history and alternatives
Hardy, J. (2006) · Springer eBooks · doi:10.1007/978-3-540-37652-1_15 · Cited by 4
Cited by
Sorted by citations
NIA‐AA Research Framework: Toward a biological definition of Alzheimer's disease
Jack, C. R., Bennett, D. A., Blennow, K., Carrillo, M. C., Dunn, B., Haeberlein, S. B., Holtzman, D. M., Jagust, W., Jessen, F., Karlawish, J., et al. (2018) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2018.02.018 · Cited by 10,537
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
2023 Alzheimer's disease facts and figures
(2023) · Alzheimer's & Dementia · doi:10.1002/alz.13016 · Cited by 3,212
Hyman, B. T., Phelps, C. H., Beach, T. G., Bigio, E. H., Cairns, N. J., Carrillo, M. C., Dickson, D. W., Duyckaerts, C., Frosch, M. P., Masliah, E., et al. (2012) · Alzheimer's & Dementia · doi:10.1016/j.jalz.2011.10.007 · Cited by 3,092
Self-citationKnopman, D. S., Amieva, H., Petersen, R. C., Chételat, G., Holtzman, D. M., Hyman, B. T., Nixon, R. A., & Jones, D. T. (2021) · Nature Reviews Disease Primers · doi:10.1038/s41572-021-00269-y · Cited by 2,606
Metadata
- Authors
- Braak, H., Thal, D. R., Ghebremedhin, E., & Del Tredici, K.
- Affiliations
- The University of Queensland (AU)
- Corresponding author
- Braak, Heiko
- Venue
- Journal of Neuropathology & Experimental Neurology
- Publisher
- Oxford University Press (OUP)
- Published
- 2011-11
- Volume
- 70
- Issue
- 11
- Pages
- 960-969
- ISSN
- 0022-3069 (ISSN-L)
- 1554-6578
- OpenAlex
- W1993023011
- Cited by
- 2,194
- References
- 75
- Citations by year
- 2026: 152 · 2025: 192 · 2024: 260 · 2023: 233 · 2022: 192 · 2021: 235 · 2020: 182 · 2019: 144 · 2018: 121 · 2017: 110 · 2016: 100 · 2015: 85 · 2014: 78 · 2013: 65 · 2012: 42
- FWCI
- 41.00
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neuropathology & Experimental Neurology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Alzheimer Forschung Initiative (10810)
- Deutsche Forschungsgemeinschaft (TH624 4–1)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, pathological staging, tauopathy, neurofibrillary tangles, amyloid plaques, locus coeruleus, brainstem, sporadic Alzheimer's disease, AT8 antibody
- MeSH terms
- Adolescent, Adult, Aged, Aged, 80 and over, Alzheimer Disease, Brain, Child, Child, Preschool, Female, Humans, Infant, Male, Middle Aged, Neurons, Cohort Studies, Amyloid beta-Peptides, Silver Staining, Neurofibrillary Tangles, tau Proteins, Disease Progression, Statistics, Nonparametric, Young Adult
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
