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Sequence of Deposition of Heterogeneous Amyloid β-Peptides and APO E in Down Syndrome: Implications for Initial Events in Amyloid Plaque Formation
Open accessAbstract
Patients with trisomy 21 [Down syndrome (DS)] progressively develop amyloid beta-protein (A beta) deposits and then other features of Alzheimer's disease (AD), apparently due to increased gene dosage and thus expression of the beta-amyloid precursor protein. Because the neuropathological phenotype in older DS subjects closely resembles that of AD, the examination of DS brains of increasing age provides a unique model of the progression of AD. Here, we characterized the deposition of several A beta peptides and apolipoprotein E in formalin-fixed brain sections from 29 DS subjects between 3 and 73 years old. Amyloid plaque number and the percentage of cortical area they occupied were quantified by computerized image analysis. A beta ending at amino acid 42 (A beta 42) was the earliest form of A beta deposited in DS cortex. It was observed in 7 of 16 young (3-30 years) subjects, with the earliest deposition occurring at age 12. A beta ending at residue 40 (A beta 40) was not detected until approximately age 30, a time when degenerating neurites around A beta immunoreactive (IR) plaques were first observed, and the frequency of A beta 40 IR plaques then rose with age. Even in old (51-73 years) DS subjects, A beta 42 IR plaques were always more abundant than A beta 40 IR plaques. A beta peptides starting at aspartate 1 or pyroglutamate 3 were detected in small subsets of compacted, neuritic plaques beginning around age 30 and rose with age, the latter species always exceeding the former. Thus, the N-termini of the A beta 42 peptides abundantly deposited in very young DS subjects remain unknown. Apo E was detectable in a small subset of A beta 42 IR plaques beginning at age 12 and rose steadily with age; it clearly followed the deposition of A beta. Our analysis of very young DS brains suggests that amyloid plaque formation begins with A beta 42-ending peptides, and the number and percentage of cortical area of A beta 42 plaques increase very little with advancing age, while other heterogeneous A beta species and Apo E progressively accrue onto plaques containing A beta 42.
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“As previously reported [39], APOE staining resembles the pattern of amyloid-β plaque pathology in DSAD and EOAD cases, with minimal staining in HA cases (Supplementary Fig. 9).”
From Apolipoprotein E abundance is elevated in the brains of individuals with Down syndrome–Alzheimer’s disease (2025) · cites this paper as [39]
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“Consistent with the known sequestration of APOE within amyloid-β plaques [39], which we also observe in this study, the differences in amyloid-β plaques in DSAD that affect the sequestration of APOE may contribute to the differences in APOE abundance we observe.”
From Apolipoprotein E abundance is elevated in the brains of individuals with Down syndrome–Alzheimer’s disease (2025) · cites this paper as [39]
In the citing paper
“Down syndrome (DS) patients with trisomy-21 having extra copy of APP gene develop typical Alzheimer’s neuropathology including amyloid plaques and neurofibrillary tangles.35–37”
From Amyloid β-based therapy for Alzheimer’s disease: Challenges, successes and future (2023) · cites this paper as [37]
In the citing paper
“the earliest Aβ42 in plaques appears to be N-truncated [98].”
From Intraneuronal β-amyloid accumulation and synapse pathology in Alzheimer’s disease (2010) · cites this paper as [98]
In the citing paper
“N-terminal Aβ1-x/βCTF-specific antibodies also fail to label N-truncated Aβ42 peptides that appear to be particularly important in AD [60, 98, 157, 158, 206].”
From Intraneuronal β-amyloid accumulation and synapse pathology in Alzheimer’s disease (2010) · cites this paper as [98]
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Self-citationThe pattern of amyloid accumulation in the brains of adults with Down syndrome
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BackgroundKumar‐Singh, S., Pirici, D. N., McGowan, E. M., Serneels, S., Ceuterick, C., Hardy, J., Duff, K., Dickson, D. W., & Broeckhoven, C. V. (2005) · American Journal Of Pathology · doi:10.1016/s0002-9440(10)62995-1 · Cited by 180
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Self-citationAneuploid neurons are functionally active and integrated into brain circuitry
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“Immunohistochemical studies in cases with Down syndrome demonstrated plaque-Aβ starting at Asp-1 or pyroGlu-3 [48].”
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“Ab40 and Ab42 were detected with C-terminus specific antibodies (Supplementary Table 1) after precipitation of AbN3pE and phosphorylated Ab to clarify whether these post-translational modifications occur in both Ab peptides, Ab40 and Ab42.”
InfluentialSelf-citationBar‐Am, O., Weinreb, O., Amit, T., & Youdim, M. B. H. (2005) · The FASEB Journal · doi:10.1096/fj.05-3794fje · Cited by 165
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“It has been suggested that deposition of amyloid in very young individuals with DS may have occurred in relationship to an institutionalized residential background [23].”
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Trisomy of human chromosome 21 enhances amyloid-β deposition independently of an extra copy of APP
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“By the age of 40, people who have Down syndrome will also have universally developed neuro- fibrillary tangles in a pattern broadly similar to that of Alzheimer’s disease in the general population (Mann, 1988; Lemere et al., 1996; Leverenz and Raskind, 1998).”
BackgroundResultInfluentialPomara, N., Bruno, D., Sarreal, A. S., Hernando, R. T., Nierenberg, J. J., Petkova, E., Sidtis, J. J., Wısnıewskı, T., Mehta, P. D., Praticò, D., et al. (2012) · American Journal of Psychiatry · doi:10.1176/appi.ajp.2011.11081153 · Cited by 143
“Amyloid beta 42 in particular is known to be deposited early in plaques (13) and is believed to be the initial trigger in Alzheimer’s low e r C SF A m y lo id Be ta Pep tid e s and H ighe r F2 -isop ro stane s in Co gn itive ly in tac t e ld e rly ind iv idua ls W ith M a jo r D ep re ssive D iso rde r”
Self-citationAlzheimer's Disease Amyloid-β Links Lens and Brain Pathology in Down Syndrome
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“However, we also observed variability in age-dependent phenotypic expression of Ab molecular pathology in the lens that comports with analogous variability in the brain of subjects with DS [34,51].”
β-secretase inhibitor; a promising novel therapeutic drug in Alzheimer’s disease
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“In 2010, the total worldwide costs of dementia were estimated at $604 billion (Wilmo and Martin, 2010).”
BackgroundEvolution of neuroinflammation across the lifespan of individuals with Down syndrome
Flores-Aguilar, L., Iulita, M. F., Kovecses, O., Torres, M. D., Levi, S. M., Zhang, Y., Askenazi, M., Wisniewski, T., Busciglio, J., & Cuello, A. C. (2020) · Brain · doi:10.1093/brain/awaa326 · Cited by 138
“This is followed by the formation of diffuse amyloid plaques during childhood (8–12 years old) (Lemere et al., 1996; Gyure et al., 2001; Mori et al., 2002) and later by mature amyloid plaques, which are commonly present in 30-year-old individuals with Down syndrome (Handen et al., 2012; Lao et al.,…”
BackgroundSelf-citationAlzheimer disease therapy: Can the amyloid cascade be halted?
Golde, T. E. (2003) · Journal of Clinical Investigation · doi:10.1172/jci17527 · Cited by 164
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“Anti-A antibodies were used to immunolabel AD cortical plaques on paraffi n-embedded, formalin-fi xed sections as previously described (Wiener et al., 2000; Lemere et al., 1996 ) using immunized mouse sera diluted 1:100 in TBS (150 mM NaCl, 50 mM Tris) as primary antibodies.”
Self-citationAlzheimer disease therapy: Can the amyloid cascade be halted?
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Self-citationThe amyloid plaque proteome in early onset Alzheimer’s disease and Down syndrome
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Self-citationFAD mutant PS-1 gene-targeted mice: increased Aβ42 and Aβ deposition without APP overproduction
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“Amyloid pathology has been observed as early as 15 years of age in postmortem brain samples from individuals with DS [4].”
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“The underlying reasons for this are not clear, but are presumably related to the triplication of the APP gene, as well as the tau kinase DYRK1A gene (Woods et al., 2001) on chromosome 21 (Beyreuther et al., 1993; Burger and Vogel, 1973; Lemere et al., 1996; Rumble et al., 1989).”
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“ronal accumulation of A 42 precedes plaque formation (19) and may be the important step in extracellular amyloid deposition in human brain (28, 32, 33).”
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“This hypothesis is further supported by previous findings that amyloid plaques do not increase in size or number in the already aged brain (Hyman et al., 1995; Lemere et al., 1996).”
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“], whereas As42/43 deposits in senile plaques precede the As40 deposition [ ,”
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“diffuse [35,73] and fibrillar Aβ deposits [73] represent additional evidence of the selective overexpression of genes throughout the entire lifespan of patients with DS.”
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“This finding and the fact that patients with trisomy 21 (Down's syndrome) develop the classical neuropathological features of Alzheimer's disease in their forties (Giaccone et al., 1989; Lemere et al., 1996; Mann, 1989) led to a specific search for families with autosomal dominant Alzheimer's disease with genetic link…”
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“For instance, many studies in transgenic models have demonstrated that Aβ accumulates first intraneuronally, before amyloid plaques appear [8-13]; a finding that has been validated in postmortem AD and Down syndrome (DS) brains [14-20].”
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“In addition, the triplication of tau kinases, such as DYRK1A and RCAN1, which act in parallel with aberrant mTOR pathway activation, contributes to increased tau phosphorylation and NFT formation [72, 75, 76].”
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“Interestingly, there are reports of diffuse SPs in 8- to 12-year-old persons with DS [9,10], in whom the onset of dementia appears later, after 50 years of age, suggesting a prodromal period in which clinical signs are undetectable or minimal [11].”
BackgroundPyroglutamate and Isoaspartate modified Amyloid-Beta in ageing and Alzheimer’s disease
Moro, M. L., Phillips, A. S., Gaimster, K., Paul, C., Mudher, A. K., Nicoll, J. A. R., & Boche, D. (2018) · Acta Neuropathologica Communications · doi:10.1186/s40478-017-0505-x · Cited by 97
“containing pE3-Aβ were not detectable in DS cases under 27 years old, while they were present in older cases [16].”
BackgroundCellular Receptors of Amyloid β Oligomers (AβOs) in Alzheimer’s Disease
Mroczko, B., Groblewska, M., Litman-Zawadzka, A., Kornhuber, J., & Lewczuk, P. (2018) · International Journal of Molecular Sciences · doi:10.3390/ijms19071884 · Cited by 97
Zhen, W., Han, H., Anguiano, M., Lemere, C. A., Cho, C., & Lansbury, P. T. (1999) · Journal of Medicinal Chemistry · doi:10.1021/jm990103w · Cited by 96
Self-citationMechanisms of amyloid plaque pathogenesis
Fiala, J. C. (2007) · Acta Neuropathologica · doi:10.1007/s00401-007-0284-8 · Cited by 99
AFM-Based Single Molecule Techniques: Unraveling the Amyloid Pathogenic Species
Ruggeri, F. S., Habchi, J., Cerreta, A., & Dietler, G. (2016) · Current Pharmaceutical Design · doi:10.2174/1381612822666160518141911 · Cited by 92
“However, several studies have showed that the number and size of plaques in post mortem AD brains do not correlate with the severity of the pathology and that amyloid plaques were found in the cortex of cognitively normal elder people [84, 85].”
BackgroundLiu, K., Solano, I., Mann, D. M. A., Lemere, C. A., Mercken, M. H., Trojanowski, J. Q., & Lee, V. M. ‐. (2006) · Acta Neuropathologica · doi:10.1007/s00401-006-0077-5 · Cited by 96
“For example, posttranslationally modiWed pyroA 3-42 has been shown to be most abundant in aVected brain regions of AD and DS patients [12, 16, 19, 20, 31].”
BackgroundSelf-citationCerebral amyloid angiopathy: pathogenetic mechanisms and link to dense amyloid plaques
Kumar‐Singh, S. (2008) · Genes Brain & Behavior · doi:10.1111/j.1601-183x.2007.00380.x · Cited by 101
“Similarly, Down’s syndrome patients, also with three copies of APP, are detected to have CAA as young as 30 years, and the severity of CAA increases with age (Lemere et al. 1996).”
BackgroundSavonenko, A. V., Melnikova, T., Wang, Y., Ravert, H. T., Gao, Y., Koppel, J. L., Lee, D., Pletniková, O., Cho, E., Sayyida, N., et al. (2015) · PLoS ONE · doi:10.1371/journal.pone.0129618 · Cited by 97
Patil, S. P., Maki, S., Khedkar, S. A., Rigby, A. C., & Chan, C. (2010) · Journal of Natural Products · doi:10.1021/np900633j · Cited by 92
Visualization of cell-to-cell transmission of mutant huntingtin oligomers
Herrera, F., Tenreiro, S., Miller‐Fleming, L., & Outeiro, T. F. (2011) · PLoS Currents · doi:10.1371/currents.rrn1210 · Cited by 94
Węgiel, J., Kuchna, I., Nowicki, K., Frackowiak, J., Mazur‐Kolecka, B., Imaki, H., Wegiel, J., Mehta, P. D., Silverman, W. P., Reisberg, ., et al. (2007) · Acta Neuropathologica · doi:10.1007/s00401-006-0191-4 · Cited by 89
“Overexpression of APP, overproduction of A, and early intracellular accumulation of A [ 33 ] have been considered the foundation for early onset of AD pathology and functional deterioration in adults with Down syndrome (DS) in their 40’s [22, 39, 63].”
BackgroundSelf-citationEvidence of Tau Hyperphosphorylation and Dystrophic Microglia in the Common Marmoset
Rodríguez-Callejas, J. D., Fuchs, E., & Perez‐Cruz, C. (2016) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2016.00315 · Cited by 94
Opposite roles of apolipoprotein E in normal brains and in Alzheimer’s disease
Russo, C., Angelini, G., Dapino, D., Piccini, A., Piombo, G., Schettini, G., Chen, S., Teller, J. K., Zaccheo, D., Gambetti, P. L., et al. (1998) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.95.26.15598 · Cited by 93
Reversal of Protein Aggregation Provides Evidence for Multiple Aggregated States
Calamai, M., Canale, C., Relini, A., Stefani, M., Chiti, F., & Dobson, C. M. (2004) · Journal of Molecular Biology · doi:10.1016/j.jmb.2004.11.067 · Cited by 92
Cerebral amyloid angiopathy in Down syndrome and sporadic and autosomal‐dominant Alzheimer's disease
Carmona‐Iragui, M., Balasa, M., Benejam, B., Alcolea, D. A., Fernández, S., Videla, L., Sala, I., Sánchez‐Saudinós, M. B., Morenas‐Rodríguez, E., Nogué, R. R., et al. (2017) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2017.03.007 · Cited by 93
“It is difficult to sort out the contribution of vascular Aβ42 deposition from parenchymal plaque deposition except with neuropathological analysis of the post-mortem brain, which was not available in this study [32,33].”
Lao, P. J., Betthauser, T. J., Hillmer, A. T., Price, J. C., Klunk, W. E., Mihaila, I., Higgins, A. T., Bulova, P. D., Hartley, S. L., Hardison, R. M., et al. (2015) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2015.05.013 · Cited by 89
“The DS population, similar to individuals with autosomal dominant Alzheimer’s disease, exhibits a higher ratio of amyloid-b42 to amyloid-b40, where amyloid-b42 is the form that is more likely to aggregate into amyloid plaques [33].”
BackgroundHead, E., Lott, I. T., Patterson, D. W., Doran, E. W., & Haier, R. J. (2007) · Journal of Alzheimer s Disease · doi:10.3233/jad-2007-11110 · Cited by 91
β‐Amyloid (Aβ)42(43), Aβ42, Aβ40 and apoE immunostaining of plaques in fatal head injury
Horsburgh, K. J., Cole, G. M., Yang, F., Savage, M. J., Greenberg, B., Gentleman, S. M., Graham, D. I., & Nicoll, J. A. R. (2000) · Neuropathology and Applied Neurobiology · doi:10.1046/j.1365-2990.2000.026002124.x · Cited by 88
RETRACTED AND REPLACED: Nerve growth factor metabolic dysfunction in Down’s syndrome brains
Iulita, M. F., Carmo, S. D., Ower, A. K., Fortress, A. M., Aguilar, L. F., Hanna, M., Wısnıewskı, T., Granholm, A., Buhusi, M. C., Busciglio, J. A., et al. (2014) · Brain · doi:10.1093/brain/awt372 · Cited by 94
“Amyloid-b peptides progressively deposit in Down’s syndrome brains from early life (Lemere et al., 1996; Mori et al., 2002) and recent studies have shown accumulation of Pittsburgh compound B-positive amyloid plaques in subjects with Down’s syndrome already in their 30 s (Handen et al., 2012).”
BackgroundSelf-citationRetractedNeuroimaging and other modalities to assess Alzheimer's disease in Down syndrome
Neale, N., Padilla, C., Fonseca, L. M., Holland, T., & Zaman, S. H. (2017) · NeuroImage Clinical · doi:10.1016/j.nicl.2017.10.022 · Cited by 91
“…the current amyloid ligands available are useful tools for detecting AD, one drawback is their limited ability to detect non-neuritic amyloid plaques that may occur in a prodromal or early stage of dementia (Cairns et al., 2009; Ikonomovic et al., 2008; Iwatsubo et al., 1995; Lemere et al., 1996).”
BackgroundAnderson, A. J., Stoltzner, S., Lai, F., Su, J. H., & Nixon, R. A. (2000) · Neurobiology of Aging · doi:10.1016/s0197-4580(00)00126-3 · Cited by 88
Solans, A., Estivill, X., & de la Luna, S. (2000) · Cytogenetic and Genome Research · doi:10.1159/000015608 · Cited by 87
“In DS patients, excessive accumulation of Aß42 can be detected in diffuse plaques as early as age 12 yr, whereas Aß42 appears in the plaques later on, at around 30 yr of age (Mann et al., 1995; Lemere et al., 1996).”
BackgroundRafii, M. S., Wishnek, H., Brewer, J. B., Donohue, M., Ness, S. L., Mobley, W. C., Aisen, P. S. S., & Rissman, R. A. (2015) · Frontiers in Behavioral Neuroscience · doi:10.3389/fnbeh.2015.00239 · Cited by 84
“Furthermore, as seen in familial and sporadic AD, presence of the Apolipoprotein E (ApoE) ε4 allele is generally associated with greater accumulation of Aβ plaques in the brains of adults with DS (Hyman et al., 1995; Lemere et al., 1996).”
BackgroundFrost, J. L., Liu, B., Kleinschmidt, M., Schilling, S., Demuth, H., & Lemere, C. A. (2012) · Neurodegenerative Diseases · doi:10.1159/000335913 · Cited by 82
Self-citationProteomics Study of Peripheral Blood Mononuclear Cells in Down Syndrome Children
Lanzillotta, C., Greco, V., Valentini, D., Villani, A., Folgiero, V., Caforio, M., Locatelli, F., Pagnotta, S. E., Barone, E., Urbani, A., et al. (2020) · Antioxidants · doi:10.3390/antiox9111112 · Cited by 85
Savonenko, A. V., Xu, G. M., Price, D. L., Borchelt, D. R., & Markowska, A. L. (2003) · Neurobiology of Disease · doi:10.1016/s0969-9961(02)00012-8 · Cited by 63
Schlenzig, D., Rönicke, R., Cynis, H., Ludwig, H., Scheel, E., Reymann, K. G., Saido, T. C., Hause, G., Schilling, S., & Demuth, H. (2012) · Journal of Neurochemistry · doi:10.1111/j.1471-4159.2012.07707.x · Cited by 83
Self-citationHook, G., Yu, J., Toneff, T., Kindy, M. S., & HOOK, V. Y. H. (2014) · Journal of Alzheimer s Disease · doi:10.3233/jad-131370 · Cited by 87
“The pGlu-A (3-42) species is a dominant fraction of the A in brains of AD and Down syndrome patients, who develop an age-accelerated AD pathology [9–14].”
Complement in Alzheimer's disease: opportunities for modulating protective and pathogenic events
Tenner, A. (2001) · Neurobiology of Aging · doi:10.1016/s0197-4580(01)00301-3 · Cited by 81
Evidence of intraneuronal Aβ accumulation preceding tau pathology in the entorhinal cortex
Welikovitch, L. A., Carmo, S. D., Maglóczky, Z., Szocsics, P., Lőke, J., Freund, T. F., & Cuello, A. C. (2018) · Acta Neuropathologica · doi:10.1007/s00401-018-1922-z · Cited by 84
Murine models of Alzheimer's disease and their use in developing immunotherapies
Wısnıewskı, T., & Sigurdsson, E. M. (2010) · Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease · doi:10.1016/j.bbadis.2010.05.004 · Cited by 84
“(2) Down's syndrome, where there is an extra copy of the APP gene due to trisomy 21, is associated with AD-related pathology at a very early age [9].”
BackgroundSelf-citationO'Callaghan, P. W., Sandwall, E., Li, J.-P., Yu, H., Ravid, R., Guan, Z., Kuppevelt, T. H. V., Nilsson, L. N. G., Ingelsson, M., Hyman, B. T., et al. (2008) · Brain Pathology · doi:10.1111/j.1750-3639.2008.00152.x · Cited by 81
“In favor of this idea are studies of Down’s syndrome cases, where diffuse Ab42 immunoreactive plaques are the first to be observed in post-mortem brains of young patients (14, 20).”
BackgroundAnti-amyloidogenic therapies: strategies for prevention and treatment of Alzheimer’s disease
Hamaguchi, T., Ono, K., & Yamada, M. (2006) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-005-5599-9 · Cited by 83
Olofsson, A., Lindhagen‐Persson, M., Sauer-Eriksson, A. E., & Öhman, A. (2007) · Biochemical Journal · doi:10.1042/bj20061561 · Cited by 80
Cohen, A. D., McDade, E., Christian, B. T., Price, J. C., Mathis, C. A., Klunk, W. E., & Handen, B. L. (2018) · Alzheimer s & Dementia · doi:10.1016/j.jalz.2018.01.002 · Cited by 79
“Pathological studies in ADAD and DS have not identified clear differences in neurofibrillary tau deposition from LOAD, but these are restricted to those with latestage disease in all groups [2,17,32].”
BackgroundHoffmann, T., Meyer, A., Heiser, U. F., Kurat, S., Böhme, L., Kleinschmidt, M., Bühring, K. U., Hutter‐Paier, B., Farcher, M., Demuth, H., et al. (2017) · Journal of Pharmacology and Experimental Therapeutics · doi:10.1124/jpet.117.240614 · Cited by 77
“In postmortem tissue, the pE-Ab content of deposits varies between 10 and 25% or even higher, depending on the methods of Ab extraction (Näslund et al., 1994; Lemere et al., 1996; Saido et al., 1996; Kuo et al., 1997; Portelius et al., 2010;Wu et al., 2014).”
BackgroundMicroglial cells in neurodegenerative disorders.
Wojtera, M., Sikorska, B., Sobów, T., & Liberski, P. P. (2005) · PubMed · Cited by 78
Metadata
- Authors
- Lemere, C. A., Blusztajn, J. K., Yamaguchi, H., Wisniewski, T., Saido, T. C., & Selkoe, D. J.
- Affiliations
- Boston University (US)
- Gunma University (JP)
- Tokyo Metropolitan Institute of Medical Science (JP)
- Brigham and Women's Hospital (US)
- Corresponding author
- Selkoe, D.J.
- Venue
- Neurobiology of Disease
- Publisher
- Elsevier BV
- Published
- 1996-02
- Volume
- 3
- Issue
- 1
- Pages
- 16-32
- ISSN
- 0969-9961 (ISSN-L)
- OpenAlex
- W1985323612
- Cited by
- 584
- References
- 0
- Citations by year
- 2026: 8 · 2025: 17 · 2024: 24 · 2023: 12 · 2022: 17 · 2021: 27 · 2020: 20 · 2019: 18 · 2018: 18 · 2017: 18 · 2016: 17 · 2015: 21 · 2014: 22 · 2013: 15 · 2012: 17
- FWCI
- 14.67
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Neurobiology of Disease (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Foundation for Neurologic Diseases
- National Institutes of Health
- National Institute on Aging (AG 12749, AG-06173, R01AG012749)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Down syndrome and intellectual disability research
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Down syndrome, amyloid-beta, amyloid plaques, apolipoprotein E, amyloid-beta 42, Aβ40, neuritic plaques, Alzheimer's disease, amyloid precursor protein, cortical amyloid deposition
- MeSH terms
- Adolescent, Adult, Aged, Aging, Alzheimer Disease, Apolipoproteins E, Child, Child, Preschool, Down Syndrome, Female, Humans, Immunoenzyme Techniques, Male, Middle Aged, Nerve Tissue Proteins, Peptide Fragments, Staining and Labeling, Temporal Lobe, Amyloid beta-Peptides, Neurites, Amyloid beta-Protein Precursor, Neurofibrillary Tangles
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