The DOI matches its Crossref record.
Staging of Alzheimer-Related Cortical Destruction
Abstract
The gradual intraneuronal accumulation of an insoluble fibrous material which partly consists of abnormally phosphorylated tau protein (neurofibrillary change) represents an important neuropathological hallmark of Alzheimer’s disease. Neurofibrillary tangles and neuropil threads formed from this material develop in only a few types of cortical pyramidal cells. The first changes are seen in the entorhinal cortex. The destructive process then spreads into the hippocampal formation and eventually encroaches upon the isocortex. This sequence of events permits the distinction of six stages with a progressive increase in the severity of cortical destruction. The entorhinal region serves as an important interface between the isocortex and hippocampus. This interface function is markedly impaired due to the early deterioration of the entorhinal cortex. Severe entorhinal involvement is considered to represent the morphological counterpart of clinically incipient Alzheimer’s disease. Similar changes are found in mentally impaired individuals suffering from Parkinson’s disease or progressive supranuclear palsy.
Overview
Integrity signals
Registry
Cites
Statistics
Verification
Claims the paper makes
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?
In the citing paper
“On the basis of the review of an enormous sample of cross-sectional autopsy data, the pattern of NFT development across the clinical spectrum of disease has been integrated in Braak neuropathologic staging (60, 298, 299).”
From Correlation of Alzheimer Disease Neuropathologic Changes With Cognitive Status: A Review of the Literature (2012) · cites this paper as [299]
Citations
Cited by
Sorted by citations
Items 401–500 of 838
Verdurand, M., Chauveau, F., Daoust, A., Morel, A., Bonnefoi, F., Liger, F., Bérod, A., & Zimmer, L. (2015) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2015.12.008 · Cited by 33
“These apparently conflicting results may have arisen from the different techniques and M AN US CR IP T AC CE PT ED “markers” used (radiotracers, antibodies), the various stages of the disease (Braak et al., 1993) as well as the particular subregions of the medial temporal lobe assessed.”
InfluentialGenomics and CSF analyses implicate thyroid hormone in hippocampal sclerosis of aging
Initiative, A. D. N., Nelson, P. T., Katsumata, Y., Nho, K. T., Artiushin, S., Jicha, G. A., Wang, W., Abner, E. L., Saykin, A. J., Kukull, W. A., et al. (2016) · Acta Neuropathologica · doi:10.1007/s00401-016-1641-2 · Cited by 31
“Both cohorts were selected, such that the groups with and without HS pathology would have comparable AD-type pathology (by Braak NFT stages [10]), PMI, cognitive status [final Mini-Mental State Exam (MMSE) scores], and length of time the samples were stored in the −80 °C freezer before being analyzed in the current st…”
Rammes, G., Seeser, F., Mattusch, K., Zhu, K., Haas, L. T., Kummer, M. P., Heneka, M. T., Herms, J. W., & Parsons, C. G. (2018) · Neuropharmacology · doi:10.1016/j.neuropharm.2018.07.021 · Cited by 30
“At early stages of the disease, the entorhinal cortex and hippocampus are particularly affected and this is associated with deficits in cognition/memory (Braak et al., 1993).”
Insights into Aβ and Presenilin from a Canine Model of Human Brain Aging
Head, E., & Torp, R. (2002) · Neurobiology of Disease · doi:10.1006/nbdi.2002.0476 · Cited by 32
Nicholas, T., Duvvuri, S., Leurent, C., Raunig, D. L., Rapp, T. L., Iredale, P., Rowinski, C., Carr, R. A., Roberts, P., Spiros, Ä., et al. (2013) · Advances in Alzheimer s Disease · doi:10.4236/aad.2013.23012 · Cited by 31
Association between neurite metrics and tau/inflammatory pathology in Alzheimer's disease
Sone, D., Shigemoto, Y., Ogawa, M., Maikusa, N., Okita, K., Takano, H., Kato, K., Sato, N., & Matsuda, H. (2020) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1002/dad2.12125 · Cited by 33
Hippocampal and entorhinal cortex volume decline in cognitively intact elderly
Thomann, P. A., Wüstenberg, T., Nolte, H. M., Menzel, P. B., Wolf, R. C., Essig, M., & Schröder, J. (2012) · Psychiatry Research Neuroimaging · doi:10.1016/j.pscychresns.2012.06.002 · Cited by 31
“, 2002), refer to stage-related neuropathological processes (Braak et al., 1993; Van Hoesen et al., 2000) rather than to structurespecific age-related changes.”
BackgroundParsons, C. G., Ruitenberg, M., Freitag, C. E., Sroka, K., Russ, H., & Rammes, G. (2015) · Neuropharmacology · doi:10.1016/j.neuropharm.2014.12.038 · Cited by 31
Osthole Upregulates BDNF to Enhance Adult Hippocampal Neurogenesis in APP/PS1 Transgenic Mice
Liu, H., Xue, X., Shi, H., Qi, L., & Gong, D. (2015) · Biological and Pharmaceutical Bulletin · doi:10.1248/bpb.b15-00013 · Cited by 31
Hippocampal MRI volumetry in cognitively discordant monozygotic twin pairs.
Järvenpää, T., Laakso, M. P., Rossi, R., Koskenvuo, M., Kaprio, J. A., Räihä, I. J., Kurki, T. J. I., Laine, M., Frisoni, G. B., & Rinne, J. (2004) · PubMed Central · Cited by 30
Liu, Z., Shi, D., Cai, Y. Q., Li, A., Lan, G., Sun, P., Liu, L., Zhu, Y., Yang, J., Zhou, Y., et al. (2024) · Alzheimer s Research & Therapy · doi:10.1186/s13195-024-01458-z · Cited by 38
“Extracellular β-amyloid (Aβ) plaques and neurofibrillary tau tangles are the two key hallmarks of AD [3].”
BackgroundYotter, R. A., Doshi, J. J., Clark, V., Sojkova, J., Zhou, Y., Wong, D. F., Ferrucci, L., Resnick, S. M., & Davatzikos, C. A. (2013) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2013.05.030 · Cited by 29
“As shown in a large series of post-mortem brains studied by Braak and Braak (Braak and Braak, 1997b), the progression of amyloid plaque deposition (both diffuse and neuritic) follows characteristic spatially unique stages rather than uniform deposition throughout the brain.”
BackgroundMethodInfluentialBrain effective connectivity modeling for alzheimer's disease by sparse gaussian bayesian network
Huang, S., Li, J., Ye, J., Fleisher, A., Chen, K., Wu, T., & Reiman, E. M. (2011) · ACM SIGKDD Conference on Knowledge Discovery and Data Mining (KDD) · doi:10.1145/2020408.2020562 · Cited by 29
“A possible interpretation is that these are neocortical regions associated with amyloid deposition and early FDG hypometabolism in AD [34-37, 41-42].”
BackgroundPort‐to‐port delivery: Mobilization of toxic sphingolipids via extracellular vesicles
Scesa, G., Moyano, A. L., Bongarzone, E. R., & Givogri, M. I. (2016) · Journal of Neuroscience Research · doi:10.1002/jnr.23798 · Cited by 30
“These conditions are almost invariably affected by a progressive spreading of insoluble material, with spreading patterns remarkably similar among patients (Braak et al., 1993; Braak et al., 2003; Guo and Lee, 2014).”
BackgroundAlzheimer's disease and synapse Loss: What can we learn from induced pluripotent stem Cells?
Rodríguez-Jiménez, F. J., Ureña‐Peralta, J. R., Jendelová, P., & Erceg, S. (2023) · Journal of Advanced Research · doi:10.1016/j.jare.2023.01.006 · Cited by 33
“Integration of activity across distant brain regions (including the hippocampus) provides insight into the intrinsic connectivity networks (ICNs), particularly the DMN as the most well-characterized ICN [54,55].”
BackgroundHaley, A. P., Knight‐Scott, J., Fuchs, K. L., Simnad, V. I., & Manning, C. A. (2004) · Neuroscience Letters · doi:10.1016/j.neulet.2004.01.031 · Cited by 29
The structure of human tau-tubulin kinase 1 both in the apo form and in complex with an inhibitor
Kiefer, S. E., Chang, C., Kimura, S., Gao, M., Xie, D., Zhang, Y., Zhang, G., Gill, M. B., Mastalerz, H. A., Thompson, L. A., et al. (2014) · Acta Crystallographica Section F Structural Biology Communications · doi:10.1107/s2053230x14000144 · Cited by 31
“The most prevalent tauopathy, Alzheimer’s disease (AD), spreads in a neuroanatomically specific manner, with progressive deposition of insoluble amyloid-containing plaques and insoluble neurofibrillary tangles (NFTs) that contain hyperphosphorylated tau (Braak et al., 1993; Holtzman et al., 2012).”
BackgroundThe MUC6/AP2A2 Locus and Its Relevance to Alzheimer’s Disease: A Review
Nelson, P. T., Fardo, D. W., & Katsumata, Y. (2020) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/nlaa024 · Cited by 28
Olfactory impairment in men and mice related to aging and amyloid-induced pathology
Tzeng, W.-Y., Figarella, K., & Garaschuk, O. (2021) · Pflügers Archiv - European Journal of Physiology · doi:10.1007/s00424-021-02527-0 · Cited by 29
“Besides, AD pathology is well-known to involve the hippocampus [15], thus impacting memory formation as well as information transmission and reception [167].”
BackgroundChronic Traumatic Encephalopathy and Neurodegeneration in Contact Sports and American Football
Zuckerman, S. L., Brett, B. L., Jeckell, A. S., Yengo-Kahn, A. M., & Solomon, G. S. (2018) · Journal of Alzheimer s Disease · doi:10.3233/jad-180218 · Cited by 30
“Second, these data will be collected longitudinally over an extended period (decades), which will help establish the natural history and correlate signs and symptoms to neuropathologic findings if they exist following the methodology of Braak et al.’s landmark work with AD [119–122].”
Somatostatin and the pathophysiology of Alzheimer’s disease
Almeida, V. N. (2024) · Ageing Research Reviews · doi:10.1016/j.arr.2024.102270 · Cited by 31
Besga, A., Ortiz, L. O., Fernández, A., Maestú, F., Arrazola, J., Gil‐Gregorio, P., Fuentes, M. E., & Ortiz, T. (2010) · Alzheimer Disease & Associated Disorders · doi:10.1097/wad.0b013e3181aba730 · Cited by 28
“The implication of visual association cortex in the AD is well known.(35) Thus, 2 longitudinal studies have supported the concept that AD is a chronic process beginning many years before the clinical expression of dementia.”
BackgroundOlofsson, J., Larsson, M. U., Roa, C., Wilson, D. A., & Laukka, E. J. (2019) · Behavior Genetics · doi:10.1007/s10519-019-09980-9 · Cited by 27
Gatt, A. P., Lee, H. A., Williams, G. H., Thuret, S., & Ballard, C. G. (2019) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2018.12.016 · Cited by 28
Neuronal histaminergic system in aging and age-related neurodegenerative disorders
Shan, L., Swaab, D. F., & Bao, A. (2012) · Experimental Gerontology · doi:10.1016/j.exger.2012.08.002 · Cited by 28
“in Braak stage 3 (Braak et al., 1993).”
BackgroundRay, S., Hossain, S. M. M., Khatun, L., & Mukhopadhyay, A. (2017) · BMC Bioinformatics · doi:10.1186/s12859-017-1946-8 · Cited by 27
“Other brain regions such as the “middle temporal gyrus” (MTG) and the “posterior cingulate cortex” (PC) get affected later during progression of the disease [10, 11].”
BackgroundSchöberl, F., Zwergal, A., & Brandt, T. (2020) · Frontiers in Neural Circuits · doi:10.3389/fncir.2020.00006 · Cited by 29
“This paradigm can be used to depict navigation-induced brain activations because the cerebral glucose utilization is weighted to the 10 min following [18F]FDG injection and is integrative due to intracellular trapping of the tracer (adapted from Irving et al., 2018b; permission from the journal obtained). hippocampus,…”
BackgroundInfluentialNassif, C., Kawles, A., Ayala, I. A. D. L., Minogue, G., Gill, N. P., Shepard, R. A., Zouridakis, A., Keszycki, R. M., Zhang, H., Mao, Q., et al. (2022) · Journal of Neuroscience · doi:10.1523/jneurosci.0679-22.2022 · Cited by 28
Amyloid and Tau Pathology in Normal Cognitive Aging
Reas, E. T. (2017) · Journal of Neuroscience · doi:10.1523/jneurosci.1388-17.2017 · Cited by 25
“Similar changes to the hippocampus appear relatively early in AD, but they occur downstream of morphological and functional neural changes that appear first in the entorhinal cortex, subsequently spreading to limbic circuits and eventually throughout the cortex (Braak et al., 1993).”
BackgroundGuan, H., Liu, T., Jiang, J., Tao, D., Zhang, J., Niu, H., Zhu, W., Wang, Y., Cheng, J., Kochan, N. A., et al. (2017) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2017.00309 · Cited by 30
Pait, M. C., Kaye, S. D., Su, Y., Kumar, A., Singh, S., Gironda, S. C., Vincent, S., Anwar, M., Carroll, C. M., Snipes, J. A., et al. (2024) · Journal of Extracellular Vesicles · doi:10.1002/jev2.12398 · Cited by 29
Fawzi, S. F., Menze, E. T., & Tadros, M. G. (2019) · Behavioural Brain Research · doi:10.1016/j.bbr.2019.112314 · Cited by 26
Zheng, L., Vinters, H. V., Mack, W. J., Weiner, M. W., Chui, H. C., & for the IVD program project (2015) · Journal of Cerebral Blood Flow & Metabolism · doi:10.1038/jcbfm.2015.152 · Cited by 27
Martín, M., Sasson, Y., Crivelli, L., et al. (2012) · Neurología · doi:10.1016/j.nrl.2012.04.013 · Cited by 26
Rammes, G., Gravius, A., Ruitenberg, M., Wegener, N., Chambon, C., Sroka, K., Jeggo, R., Staniaszek, L. E., Spanswick, D. C., O‘Hare, E., et al. (2015) · Neuropharmacology · doi:10.1016/j.neuropharm.2014.12.037 · Cited by 51
Event-based prospective memory failure in amnestic mild cognitive impairment
da Costa, A. L. C., Perri, R., Zabberoni, S., Barban, F., Caltagirone, C., & Carlesimo, G. A. (2011) · Neuropsychologia · doi:10.1016/j.neuropsychologia.2011.03.016 · Cited by 29
Hasani, S. A., Mayeli, M., Salehi, M. A., & Parizi, R. B. (2021) · Dementia and Geriatric Cognitive Disorders Extra · doi:10.1159/000516164 · Cited by 26
EEG Resting-State Functional Networks in Amnestic Mild Cognitive Impairment
Caravaglios, G., Muscoso, E. G., Blandino, V., Maria, G. D., Gangitano, M., Graziano, F., Guajana, F., & Piccoli, T. (2022) · Clinical EEG and Neuroscience · doi:10.1177/15500594221110036 · Cited by 38
MicroRNA in situ hybridization in the human entorhinal and transentorhinal cortex
Nelson, P. T. (2010) · Frontiers in Human Neuroscience · doi:10.3389/neuro.09.007.2010 · Cited by 24
“Most clinico-pathological correlation studies indicate that cortical NFT density, assessed by Braak staging (Braak et al., 1993) or other means, is the parameter best correlated with the severity of AD cognitive impairment (Arriagada et al., 1992; Nelson et al., 2007b, 2008a,b, 2009b; Sonnen et…”
InfluentialGefen, T. D., Kawles, A., Makowski‐Woidan, B., Engelmeyer, J., Ayala, I. A. D. L., Abbassian, P., Zhang, H., Weıntraub, S., Flanagan, M. E., Mao, Q., et al. (2021) · Cerebral Cortex · doi:10.1093/cercor/bhaa409 · Cited by 25
“Braak staging according to published guidelines (Braak and Braak 1991; Braak et al. 1993) was also determined in each case to identify NFT”
MethodWhen the Amnestic Mild Cognitive Impairment Disappears
Perri, R., Carlesimo, G. A., Serra, L., & Caltagirone, C. (2009) · Cognitive and Behavioral Neurology · doi:10.1097/wnn.0b013e3181a7225c · Cited by 25
“In light of previous evidence of the high rate of conversion to AD in a-MCI patients,1,13 in the MCI group the presence of an enduring impairment in all aspects of episodic memory functioning, seems very likely to reflect involvement of the mesial temporal structures from the degenerative process characteristic of AD.…”
BackgroundInfluentialCharacterization of neuronal cell death induced by complement activation
Shen, Y., Halperin, J. A., Benzaquen, L. R., & Lee, C. (1997) · Brain Research Protocols · doi:10.1016/s1385-299x(96)00026-8 · Cited by 26
Bipolar disorder and neurophysiologic mechanisms
McCrea, S. M. (2008) · Neuropsychiatric Disease and Treatment · doi:10.2147/ndt.s4329 · Cited by 26
Classification-Biased Apparent Brain Age for the Prediction of Alzheimer's Disease
Varzandian, A., Razo, M. A. S., Sanders, M., Atmakuru, A., & Fatta, G. D. (2021) · Frontiers in Neuroscience · doi:10.3389/fnins.2021.673120 · Cited by 25
Traikapi, A., Kalli, I., Kyriakou, A., Stylianou, E., Symeou, R. T., Kardama, A., Christou, Y. P., Phylactou, P., & Konstantinou, N. (2022) · Journal of Neuropsychology · doi:10.1111/jnp.12299 · Cited by 24
Bagheri, S., Rashno, M., Salehi, I., Karimi, S. A., Raoufi, S., & Komaki, A. (2022) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2023.175714 · Cited by 25
The functional and structural changes in the hippocampus of COVID-19 patients
Nouraeinejad, A. (2023) · Acta Neurologica Belgica · doi:10.1007/s13760-023-02291-1 · Cited by 28
“This is also supported by the finding that the hippocampus is one of the earliest areas to be distressed in Alzheimer's disease [103].”
ResultPosture recognition in Alzheimer’s disease
Mozaz, M., Garaigordobil, M., Rothi, L. J. G., Anderson, J., Crucian, G. P., & Heilman, K. M. (2006) · Brain and Cognition · doi:10.1016/j.bandc.2006.06.003 · Cited by 24
Diabetic encephalopathy: the role of oxidative stress and inflammation in type 2 diabetes
Reis, F., Soares, Nunes, & Pereira, F. C. (2012) · International Journal of Interferon Cytokine and Mediator Research · doi:10.2147/ijicmr.s29322 · Cited by 26
“90,91 Moreover, it is associated with consistent pathological findings, including intracellular neurofibrillary tangles (an accumulation of insoluble fibrous material, partly composed of an abnormally hyperphosphorylated form of tau protein) and extracellular senile plaques, mainly composed of…”
Alzheimer's disease and semantic deficits: A feature-listing study.
Perri, R., Zannino, G. D., Caltagirone, C., & Carlesimo, G. A. (2012) · Neuropsychology · doi:10.1037/a0029302 · Cited by 24
Heinemann, S. D., Posimo, J. M., Mason, D. M., Hutchison, D. F., & Leak, R. K. (2016) · Hippocampus · doi:10.1002/hipo.22580 · Cited by 24
“Furthermore, Parkinson’s and Alzheimer’s disease both involve dense protein aggregations (Braak et al., 1993; Braak and Braak, 1995; Braak et al., 2000a,b,2002,2003).”
BackgroundAshby, E. L., Kierzkowska, M., Hull, J., Kehoe, P. G., Hutson, S. M., & Conway, M. E. (2016) · Neurochemical Research · doi:10.1007/s11064-016-1855-7 · Cited by 23
“In addition to specific neuropathology observed post-mortem (such as deposition of amyloid plaques and neurofibrillary tangles), several neurotransmitter profiles are compromised in AD brain, such as the cholinergic system and glutamate [2, 3].”
β-Amyloid (Aβ) deposition in elderly non-demented patients and patients with Alzheimer's disease
Armstrong, R. A. (1994) · Neuroscience Letters · doi:10.1016/0304-3940(94)90289-5 · Cited by 24
Wiescholleck, V., André, M. A. E., & Manahan‐Vaughan, D. (2013) · Hippocampus · doi:10.1002/hipo.22220 · Cited by 22
“The hippocampus is indeed considered the brain structure that is most severely involved in aging-related cognitive decline, as well as in age-related pathology, such as Alzheimer’s disease (Braak et al., 1993; Driscoll et al., 2003).”
BackgroundMartín, M., Sasson, Y., Crivelli, L., et al. (2013) · Neurología (English Edition) · doi:10.1016/j.nrleng.2012.04.014 · Cited by 23
Shape-Attributes of Brain Structures as Biomarkers for Alzheimer’s Disease
Glozman, T., Solomon, J., Pestilli, F., Guibas, L. J., & Initiative, A. D. N. (2016) · Journal of Alzheimer s Disease · doi:10.3233/jad-160900 · Cited by 23
“The hippocampus is one of the earliest structures to be affected [2].”
BackgroundPhosphorylated Amyloid-β: the Toxic Intermediate in Alzheimer’s Disease Neurodegeneration
Milton, N. G. N. (2006) · Springer eBooks · doi:10.1007/0-387-23226-5_20 · Cited by 23
Armstrong, R. A., Lantos, P. L., & Cairns, N. J. (2007) · Journal of Neural Transmission · doi:10.1007/s00702-007-0796-3 · Cited by 23
“Braak staging (Braak et al. 1993) for cortical destruction based on NFT suggested with one exception (Case F), cases were Braak stage 1 or 2.”
BackgroundMethodGenetic Epidemiology of Alzheimer Disease
Mayeux, R. P. (2006) · Alzheimer Disease & Associated Disorders · doi:10.1097/00002093-200607001-00008 · Cited by 25
“There is an accompanying loss of neurons and synapses throughout the brain but particularly in the hippocampus, and there is neuropil thread protein deposits and granulovacuolar degeneration in hippocampal cells.(2,3) The fundamental pathogenic mechanisms responsible for the development of these degenerative changes a…”
BackgroundDifferential phosphorylation of tau proteins during kitten brain development and Alzheimer's disease
Riederer, B. M., Mourton-Gilles, C., Frey, P., Delacourte, A., & Probst, A. (2001) · Journal of Neurocytology · doi:10.1023/a:1011991207942 · Cited by 22
“As for the choice of the human entorhinal cortex, this region is among the first one to develop Alzheimer-like features with the number of tangles correlating well with the severity of the disease (Braak et al., 1993).”
BackgroundAdvances in PET Imaging of Degenerative, Cerebrovascular, and Traumatic Causes of Dementia
Eisenmenger, L. B., Huo, E. J., Hoffman, J. M., Minoshima, S., Matesan, M. C., Lewis, D. H., Lopresti, B. J., Mathis, C. A., Okonkwo, D. O., & Mountz, J. M. (2015) · Seminars in Nuclear Medicine · doi:10.1053/j.semnuclmed.2015.09.003 · Cited by 21
Episodic Memory Decline and Healthy Aging ☆
Wang, W., Daselaar, S. M., & Cabeza, R. E. L. (2017) · Elsevier eBooks · doi:10.1016/b978-0-12-809324-5.21093-6 · Cited by 26
van Ameijde, J., Crespo, R., Janson, R., Juraszek, J., Siregar, B., Verveen, H., Sprengers, I., Nahar, T., Hoozemans, J. J. M., Steinbacher, S., et al. (2018) · Acta Neuropathologica Communications · doi:10.1186/s40478-018-0562-9 · Cited by 21
Gyanwali, B., Shaik, M. A., Tan, C. S., Vrooman, H. A., Venketasubramanian, N., Chen, C., & Hilal, S. (2019) · Aging · doi:10.18632/aging.102478 · Cited by 23
López‐Cuenca, I., Salobrar‐García, E., Sánchez-Puebla, L., Espejel, E., del Arco, L. G., Rojas, P., Elvira‐Hurtado, L., Fernández‐Albarral, J. A., Ramírez‐Toraño, F., Barabash, A., et al. (2022) · Journal of Clinical Medicine · doi:10.3390/jcm11113248 · Cited by 21
“These results suggest that it would be of great interest to study cognitively healthy subjects because changes related to neurodegenerative disease may appear decades before the onset of cognitive symptoms [28,29], and these functional and structural features may be useful for future diagnostic procedures [1].”
BackgroundMalter, J. S. (2022) · Translational research · doi:10.1016/j.trsl.2022.09.003 · Cited by 23
Risacher, S. L., & Apostolova, L. G. (2023) · CONTINUUM Lifelong Learning in Neurology · doi:10.1212/con.0000000000001248 · Cited by 25
Deep Learning on Brain Cortical Thickness Data for Disease Classification
Menikdiwela, M., Nguyen, C. V., & Shaw, M. E. (2018) · International Conference on Digital Image Computing: Techniques and Applications (DICTA) · doi:10.1109/dicta.2018.8615775 · Cited by 25
“[1] also proposed that the depositions of abnormal proteins between nerve cells cause this problem.”
BackgroundBaker, J. E., Pietrzak, R. H., Laws, S. M., Ames, D. J., Villemagne, V. L., Rowe, C. C., Masters, C. L., Maruff, P. T., & Lim, Y. Y. (2019) · Neuropsychology · doi:10.1037/neu0000561 · Cited by 22
Good, T. J., Villafuerte, J. W., Ryan, J. D., Grady, C. L., & Barense, M. D. (2020) · eNeuro · doi:10.1523/eneuro.0290-19.2020 · Cited by 22
“Importantly, the effect was most robust in the MTL, where AD pathology is known to begin (Braak and Braak, 1991; Braak et al., 1993), and where this sample of ostensibly healthy older adults showed reduction in gray matter volume (Olsen et al.”
BackgroundInfluentialCheung, E. Y., Shea, Y. F., Chiu, P. K. C., Kwan, J. S. K., & Mak, H. K. (2021) · Life · doi:10.3390/life11101108 · Cited by 22
“The trend suggested that mild deposition of amyloid induces functional connectivity increases to compensate the loss of function [58].”
BackgroundMarsland, P., Vore, A. S., DaPrano, E. M., Paluch, J. M., Blackwell, A. A., Varlinskaya, E. I., & Deak, T. (2022) · Alcohol · doi:10.1016/j.alcohol.2022.08.013 · Cited by 19
Switching On/Off Amyloid Plaque Formation in Transgenic Animal Models of Alzheimer’s Disease
Kozin, S. A., Kechko, O. I., Adzhubei, A. A., Makarov, A. А., & Mitkevich, V. A. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms25010072 · Cited by 21
“These pathomorphological features are observed in certain areas of the brain [5,6], but are particularly common in the hippocampus, an area of the brain critical for learning and memory, where amyloid plaques, neurofibril-lary tangles and neuropil threads appear at the earliest stages of AD [7,8].”
BackgroundHaase, L., Wang, M., Green, E., & Murphy, C. (2011) · Human Brain Mapping · doi:10.1002/hbm.21451 · Cited by 22
“In addition, although speculative, the failure to find a cohesive functional connectivity model, may be a function of the prodromal neuropathological processes that are associated with the presence of the e4 allele, which first disrupt connections between structures that subserve memory functioning [e.g., entorhinal c…”
BackgroundSpatial gene expression analysis of neuroanatomical differences in mouse models
Fernandes, D., Ellegood, J., Askalan, R., Blakely, R., DiCicco-Bloom, E. M., Egan, S. E., Osborne, L. R., Powell, C. M., Raznahan, A., Robins, D. M., et al. (2017) · NeuroImage · doi:10.1016/j.neuroimage.2017.08.065 · Cited by 21
Li, H., Jia, X., Qi, Z., Fan, X., Ma, T., Pang, R., Ni, H., Li, C. R., Lu, J., & Li, K. (2018) · Frontiers in Human Neuroscience · doi:10.3389/fnhum.2018.00413 · Cited by 23
Feng, L., Watanabe, H., Molino, P. J., Wallace, G. G., Phung, S. L., Uchihashi, T., & Higgins, M. J. (2019) · Journal of Molecular Biology · doi:10.1016/j.jmb.2019.04.044 · Cited by 21
Patel, V. R., Liu, M., Worsham, C. M., & Jena, A. B. (2024) · BMJ · doi:10.1136/bmj-2024-082194 · Cited by 21
Vanherle, L., Lidington, D., Uhl, F. E., Steiner, S., Vassallo, S., Skoug, C., Duarte, J. M. N., Ramu, S., Uller, L., Desjardins, J., et al. (2022) · EBioMedicine · doi:10.1016/j.ebiom.2022.104384 · Cited by 20
Degeneration in Nucleus basalis of Meynert signals earliest stage of Alzheimer’s disease progression
Shafiee, N., Fonov, V., Dadar, M., Spreng, R. N., & Collins, D. L. (2024) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2024.03.003 · Cited by 21
“Widely accepted models suggest that Alzheimer ’ s degeneration starts in the entorhinal cortices and then spreads through the temporoparietal cortex (Braak, Braak, and Bohl, 1993).”
A note on testing hypotheses for stationary processes in the frequency domain
Holger Dette, A., & Hildebrandt, T. (2011) · Journal of Multivariate Analysis · doi:10.1016/j.jmva.2011.07.002 · Cited by 19
Functional Connectivity of the Hippocampus in Early- and vs. Late-Onset Alzheimer's Disease
Park, K. H., Noh, Y., Choi, E.-J., Kim, H., Chun, S., & Son, Y. (2017) · Journal of Clinical Neurology · doi:10.3988/jcn.2017.13.4.387 · Cited by 20
Molecular and Clinical Aspects of Protein Aggregation Assays in Neurodegenerative Diseases
Villar‐Piqué, A., Schmitz, M., Candelise, N., Ventura, S., Llorens, F., & Zerr, I. (2018) · Molecular Neurobiology · doi:10.1007/s12035-018-0926-y · Cited by 22
“orated the Braak’s hypothesis of disease staging, where the appearance of pathological lesions in the brain follows a diseasespecific temporal and regional pattern [8, 9].”
BackgroundThe Potential Roles of Ghrelin in Metabolic Syndrome and Secondary Symptoms of Alzheimer’s Disease
Kim, S., Nam, Y., Shin, S. J., Park, Y., Jeon, S. G., Kim, J.-I., Kim, M., & Moon, M. (2020) · Frontiers in Neuroscience · doi:10.3389/fnins.2020.583097 · Cited by 20
Haubold, A., Peterson, B. S., & Bansal, R. (2012) · Journal of Child Psychology and Psychiatry · doi:10.1111/j.1469-7610.2012.02539.x · Cited by 20
Evidence for the involvement of TNF and NF-?B in hippocampal synaptic plasticity
Albensi, B. C., & Mattson, M. P. (2000) · Synapse · doi:10.1002/(sici)1098-2396(200002)35:2 · Cited by 527
Neuropathology of the Brainstem to Mechanistically Understand and to Treat Alzheimer’s Disease
Patthy, Á., Murai, J., Hanics, J., Pintér, A., Zahola, P., Hökfelt, T. G. M., Harkany, T., & Alpár, A. (2021) · Journal of Clinical Medicine · doi:10.3390/jcm10081555 · Cited by 17
“This said, pioneering studies found that cognitive loss parallels histopathological signs: the accumulation of β-amyloid (Aβ) (1–40) and (1–42) extracellularly [1] and neurofibrillary tangles (NFTs) composed of hyperphosphorylated tau intracellularly [2], allowing cortical staging of the pathological process [3].”
BackgroundAl‐Onaizi, M., Thériault, P., Lecordier, S., Préfontaine, P., Rivest, S., & ElAli, A. (2021) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2021.07.016 · Cited by 20
Modeling recall memory for emotional objects in Alzheimer's disease
Sundstrøm, M. (2011) · Aging Neuropsychology and Cognition · doi:10.1080/13825585.2011.567324 · Cited by 19
Pfeffer, A., Munder, T., Schreyer, S., Klein, C., Rasińska, J., Winter, Y., & Steiner, B. (2018) · Behavioural Brain Research · doi:10.1016/j.bbr.2018.03.030 · Cited by 20
Hubs of long‐distance co‐alteration characterize brain pathology
Cauda, F., Mancuso, L., Nani, A., Ficco, L., Premi, E., Manuello, J., Liloia, D., Gelmini, G., Duca, S., & Costa, T. (2020) · Human Brain Mapping · doi:10.1002/hbm.25093 · Cited by 17
“…the hippocampus may be the pathological epicenter, as well as with the observation that the left hemisphere is more affected than the right one (Braak, Braak, & Bohl, 1993; Buckner, 2005; Janke et al., 2001; Loewenstein et al., 1989; Manuello et al., 2018; Pievani, de Haan, Wu, Seeley, &…”
Stevenson, A. J., McCartney, D. L., Shireby, G. L., Hillary, R. F., King, D., Tzioras, M., Wrobel, N., McCafferty, S., Murphy, L., McColl, B. W., et al. (2022) · European Journal of Neuroscience · doi:10.1111/ejn.15661 · Cited by 20
“Age378 related decline in hippocampal volume is well established (38) and it is one of the earliest, and most 379 profoundly, affected regions in Alzheimer’s disease, suffering insidious synapse loss and neuronal 380 cell death culminating in a substantial atrophy as the disease progresses (39).”
BackgroundJiang, M. H., Vanan, S., Tu, H., Zhang, W., Zhang, Z.-W., Chia, S., Jang, S. E., Zeng, X., Yu, W., Xu, J., et al. (2020) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2020.07.031 · Cited by 19
Automated Measurement of Hippocampal Atrophy Using Fluid-Registered Serial MRI in AD and Controls
Barnes, J., Lewis, E. B., Scahill, R. I., Bartlett, J. W., Frost, C. D., Schott, J. M., Rossor, M. N., & Fox, N. C. (2007) · Journal of Computer Assisted Tomography · doi:10.1097/rct.0b013e31802f4139 · Cited by 19
Kelliny, S., Zhou, X., & Bobrovskaya, L. (2025) · Journal of Neuroscience Research · doi:10.1002/jnr.70046 · Cited by 27
“Alzheimer's disease (AD) is a severe neurodegenerative disorder characterized by gradual and progressive deficits in more than one domain of cognition, including learning and memory, attention, language, and deterioration of social skills (Braak et al. 1993).”
Immunogenomics Parameters for Patient Stratification in Alzheimer’s Disease
Huda, T. I., Diaz, M. J., Gozlan, E. C., Chobrutskiy, A., Chobrutskiy, B. I., & Blanck, G. (2022) · Journal of Alzheimer s Disease · doi:10.3233/jad-220119 · Cited by 18
“Thesestagesprogressfrom0,transentorhinal(I-II), limbic(III-IV),andendwithisocorticalstages(V-VI) [11].”
Amato, L. G., Vergani, A. A., Lassi, M., Fabbiani, C., Mazzeo, S., Burali, R., Nacmias, B., Sorbi, S., Mannella, R., Grippo, A., et al. (2024) · Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring · doi:10.1002/dad2.12526 · Cited by 17
Therapeutic Interventions Targeting Beta Amyloid Pathogenesis in an Aging Dog Model
Martin, S. B., Dowling, A. L. S., & Head, E. (2011) · Current Neuropharmacology · doi:10.2174/157015911798376217 · Cited by 19
“AD is characterized by the presence of senile plaques and neurofibrillary tangles (NFTs) in the brain [1-3].”
BackgroundMaurer, A. P., Burke, S. N., Diba, K., & Barnes, C. A. (2017) · Journal of Neuroscience · doi:10.1523/jneurosci.0531-17.2017 · Cited by 16
“Moreover, this structure is one of the first brain areas to undergo pathological alterations in preclinical Alzheimer’s disease (Braak and Braak, 1991; Braak et al., 1993; Khan et al., 2014; Hirni et al., 2016; Krumm et al., 2016).”
BackgroundLim, S., Tran, D. N., Zumkehr, J., Chen, C., Ghiaar, S., Kieu, Z., Villanueva, E., Gallup, V., Rodríguez‐Ortiz, C. J., & Kitazawa, M. (2018) · Glia · doi:10.1002/glia.23522 · Cited by 20
Metadata
- Authors
- Braak, H., Braak, E., & Bohl, J.
- Affiliations
- Goethe University Frankfurt (DE)
- ORCID
- Braak, Heiko
- Venue
- European Neurology
- Publisher
- S. Karger AG
- Published
- 2008-02-12
- Volume
- 33
- Issue
- 6
- Pages
- 403-408
- ISSN
- 0014-3022 (ISSN-L)
- 1421-9913
- OpenAlex
- W2095422335
- Cited by
- 836
- References
- 0
- Citations by year
- 2026: 15 · 2025: 27 · 2024: 29 · 2023: 34 · 2022: 38 · 2021: 32 · 2020: 35 · 2019: 33 · 2018: 30 · 2017: 40 · 2016: 35 · 2015: 47 · 2014: 36 · 2013: 39 · 2012: 35
- FWCI
- 29.38
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- European Neurology (publishedVersion)
- PubMed (publishedVersion)
- 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, cortical destruction, neurofibrillary tangles, tau protein, neuropil threads, entorhinal cortex, hippocampal formation, neocortex, disease staging, cortical pyramidal neurons, Parkinson's disease, progressive supranuclear palsy, neuropathology
- MeSH terms
- Aged, Alzheimer Disease, Brain Mapping, Cerebral Cortex, Dementia, Diagnosis, Differential, Hippocampus, Humans, Limbic System, Parkinson Disease, Supranuclear Palsy, Progressive, Neurites, Neurofibrillary Tangles
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
