The DOI matches its Crossref record; 52 of the 52 references it cites were found in a registry or an index.
Accelerated Amyloid Deposition in the Brains of Transgenic Mice Coexpressing Mutant Presenilin 1 and Amyloid Precursor Proteins
Open accessAbstract
Missense mutations in two related genes, termed presenilin 1 (PS1) and presenilin 2 (PS2), cause dementia in a subset of early-onset familial Alzheimer's disease (FAD) pedigrees. In a variety of experimental in vitro and in vivo settings, FAD-linked presenilin variants influence the processing of the amyloid precursor protein (APP), leading to elevated levels of the highly fibrillogenic Abeta1-42 peptides that are preferentially deposited in the brains of Alzheimer Disease (AD) patients. In this report, we demonstrate that transgenic animals that coexpress a FAD-linked human PS1 variant (A246E) and a chimeric mouse/human APP harboring mutations linked to Swedish FAD kindreds (APP swe) develop numerous amyloid deposits much earlier than age-matched mice expressing APP swe and wild-type Hu PS1 or APP swe alone. These results provide evidence for the view that one pathogenic mechanism by which FAD-linked mutant PS1 causes AD is to accelerate the rate of beta-amyloid deposition in brain.
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“However, APP mice develop dystrophic neurites immediately around plaques (50), suggesting that this neuronal pathology is independent of cell death.”
From Attenuating astrocyte activation accelerates plaque pathogenesis in APP/PS1 mice (2013) · cites this paper as [50]
In the citing paper
“However, such studies have not definitively identified which Aβ species are responsible for seeding amyloid deposition in either the parenchyma or vasculature.”
From Aβ42 Is Essential for Parenchymal and Vascular Amyloid Deposition in Mice (2005) · cites this paper as Borchelt et al., 1997
In the citing paper
“Increasing relative Aβ42 levels lowers the age when deposition first occurs, increases the amount of diffuse Aβ, and promotes parenchymal versus cerebrovascular deposition.”
From Aβ42 Is Essential for Parenchymal and Vascular Amyloid Deposition in Mice (2005) · cites this paper as Borchelt et al., 1997
In the citing paper
“These genetic findings led to several transgenic mouse models that successfully recapitulated Aβ plaque formation, increasing support for the hypothesis (Table 1) [23–29].”
From Systems-based proteomics to resolve the biology of Alzheimer’s disease beyond amyloid and tau (2021) · cites this paper as [24]
Citations
Cites
1 retracted
Familial Alzheimer's disease associated with S182 codon 286 mutation
Chapman, J., Asherov, A., Wang, N., Treves, T. A., Korczyn, A. D., & Goldfarb, L. G. (1995) · The Lancet · doi:10.1016/s0140-6736(95)91723-3 · Cited by 25
RetractedMcKhann, 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
Self-citationGoate, A., Chartier-Harlin, M.-C., Mullan, M., Brown, J., Crawford, F., Fidani, L., Giuffra, L., Haynes, A., Irving, N., James, L., et al. (1991) · Nature · doi:10.1038/349704a0 · Cited by 4,659
Correlative Memory Deficits, Aβ Elevation, and Amyloid Plaques in Transgenic Mice
Hsiao, K., Chapman, P., Nilsen, S., Eckman, C., Harigaya, Y., Younkin, S., Yang, F., & Cole, G. (1996) · Science · doi:10.1126/science.274.5284.99 · Cited by 4,210
Cloning of a gene bearing missense mutations in early-onset familial Alzheimer's disease
Sherrington, R., Rogaev, E. I., Liang, Y., Rogaeva, E. A., Levesque, G., Ikeda, M., Chi, H., Lin, C., Li, G., Holman, K., et al. (1995) · Nature · doi:10.1038/375754a0 · Cited by 4,051
Scheuner, D., Eckman, C., Jensen, M., Song, X., Citron, M., Suzuki, N., Bird, T. D., Hardy, J., Hutton, M., Kukull, W., et al. (1996) · Nature Medicine · doi:10.1038/nm0896-864 · Cited by 2,599
Candidate gene for the chromosome 1 familial Alzheimer’s disease locus
Levy-Lahad, E., Wasco, W., Poorkaj, P., Romano, D. M., Oshima, J., Pettingell, W. H., Yu, C.-E., Jondro, P. D., Schmidt, S. D., Wang, K., et al. (1995) · Science · doi:10.1126/science.7638622 · Cited by 2,577
Alzheimer-type neuropathology in transgenic mice overexpressing V717F β-amyloid precursor protein
Games, D., Adams, D., Alessandrini, R., Barbour, R., Borthelette, P., Blackwell, C., Carr, T., Clemens, J., Donaldson, T., Gillespie, F., et al. (1995) · Nature · doi:10.1038/373523a0 · Cited by 2,516
Self-citationRogaev, E. I., Sherrington, R., Rogaeva, E. A., Levesque, G., Ikeda, M., Liang, Y., Chi, H., Lin, C., Holman, K., Tsuda, T., et al. (1995) · Nature · doi:10.1038/376775a0 · Cited by 2,052
Jarrett, J. T., Berger, E. P., & Lansbury, P. T. (1993) · Biochemistry · doi:10.1021/bi00069a001 · Cited by 2,022
Amyloid β-peptide is produced by cultured cells during normal metabolism
Haass, C., Schlossmacher, M. G., Hung, A. Y., Vigo-Pelfrey, C., Mellon, A., Ostaszewski, B. L., Lieberburg, I., Koo, E. H., Schenk, D., Teplow, D. B., et al. (1992) · Nature · doi:10.1038/359322a0 · Cited by 1,921
Iwatsubo, T., Odaka, A., Suzuki, N., Mizusawa, H., Nukina, N., & Ihara, Y. (1994) · Neuron · doi:10.1016/0896-6273(94)90458-8 · Cited by 1,774
Citron, M., Oltersdorf, T., Haass, C., McConlogue, L., Hung, A. Y., Seubert, P., Vigo-Pelfrey, C., Lieberburg, I., & Selkoe, D. J. (1992) · Nature · doi:10.1038/360672a0 · Cited by 1,757
Mullan, M., Crawford, F., Axelman, K., Houlden, H., Lilius, L., Winblad, B., & Lannfelt, L. (1992) · Nature Genetics · doi:10.1038/ng0892-345 · Cited by 1,513
Increased amyloid-β42(43) in brains of mice expressing mutant presenilin 1
Duff, K., Eckman, C., Zehr, C., Yu, X., Prada, C.-M., Pérez‐Tur, J., Hutton, M., Buée, L., Harigaya, Y., Yager, D., et al. (1996) · Nature · doi:10.1038/383710a0 · Cited by 1,486
Borchelt, D. R., Thinakaran, G., Eckman, C. B., Lee, M. K., Davenport, F., Ratovitsky, T., Prada, C.-M., Kim, G., Seekins, S., Yager, D., et al. (1996) · Neuron · doi:10.1016/s0896-6273(00)80230-5 · Cited by 1,478
Self-citationSuzuki, N., Cheung, T. T., Cai, X.-D., Odaka, A., Otvos, L., Eckman, C., Golde, T. E., & Younkin, S. G. (1994) · Science · doi:10.1126/science.8191290 · Cited by 1,471
Production of the Alzheimer Amyloid β Protein by Normal Proteolytic Processing
Shoji, M., Golde, T. E., Ghiso, J., Cheung, T. T., Estus, S., Shaffer, L. M., Cai, X.-D., McKay, D. M., Tintner, R., Frangione, B., et al. (1992) · Science · doi:10.1126/science.1439760 · Cited by 1,447
The Clinical Diagnosis of Alzheimer's Disease
Wade, J. P. H., Mirsen, T. R., Hachinski, V. C., Fisman, M., Lau, C. S., & Merskey, H. (1987) · Archives of Neurology · doi:10.1001/archneur.1987.00520130016010 · Cited by 1,416
Citron, M., Westaway, D., Xia, W., Carlson, G., Diehl, T., Levesque, G., Johnson-wood, K., Lee, M., Seubert, P., Davis, A., et al. (1997) · Nature Medicine · doi:10.1038/nm0197-67 · Cited by 1,271
Self-citationIdentification, biogenesis, and localization of precursors of Alzheimer's disease A4 amyloid protein
Weidemann, A., König, G., Bunke, D., Fischer, P. Q., Salbaum, J. M., Masters, C. L., & Beyreuther, K. T. (1989) · Cell · doi:10.1016/0092-8674(89)90177-3 · Cited by 1,233
Chartier-Harlin, M.-C., Crawford, F., Houlden, H., Warren, A., Hughes, D., Fidani, L., Goate, A., Rossor, M., Roques, P., Hardy, J., et al. (1991) · Nature · doi:10.1038/353844a0 · Cited by 1,214
Endoproteolysis of Presenilin 1 and Accumulation of Processed Derivatives In Vivo
Thinakaran, G., Borchelt, D., Lee, M. K., Slunt, H. H., Spitzer, L., Kim, G. J., Ratovitski, T., Davenport, F., Nordstedt, C., Seeger, M., et al. (1996) · Neuron · doi:10.1016/s0896-6273(00)80291-3 · Cited by 1,025
Self-citationGenetic Linkage Evidence for a Familial Alzheimer's Disease Locus on Chromosome 14
Schellenberg, G. D., Bird, T. D., Wijsman, E. M., Orr, H. T., Anderson, L., Nemens, E. J., White, J. A., Bonnycastle, L. L., Weber, J. L., Alonso, M. E., et al. (1992) · Science · doi:10.1126/science.1411576 · Cited by 957
Release of Excess Amyloid β Protein from a Mutant Amyloid β Protein Precursor
Cai, X.-D., Golde, T. E., & Younkin, S. G. (1993) · Science · doi:10.1126/science.8424174 · Cited by 913
Alzheimer's Disease--Genotypes, Phenotype, and Treatments
Selkoe, D. J. (1997) · Science · doi:10.1126/science.275.5300.630 · Cited by 879
Senile dementia of the Alzheimer type
Terry, R. D., & Katzman, R. (1983) · Annals of Neurology · doi:10.1002/ana.410140502 · Cited by 839
Amyloid β Protein (Aβ) in Alzheimeri's Disease Brain
Gravina, S. A., Ho, L., Eckman, C. B., Long, K. E., Otvos, L., Younkin, L. H., Suzuki, N., & Younkin, S. G. (1995) · Journal of Biological Chemistry · doi:10.1074/jbc.270.13.7013 · Cited by 676
Lemere, 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
Clark, R. F., Hutton, M., Fuldner, M., Froelich, S., Karran, E., Talbot, C., Crook, R., Lendon, C., Prihar, G., He, C., et al. (1995) · Nature Genetics · doi:10.1038/ng1095-219 · Cited by 474
Genetic evidence for a novel familial Alzheimer's disease locus on chromosome 14
George‐Hyslop, P. S., Haines, J. L., Rogaev, E. I., Mortilla, M., Vaula, G., Pericak‐Vance, M. A., Foncin, J. P., Montesi, M. P., Bruni, A. C., Sorbi, S., et al. (1992) · Nature Genetics · doi:10.1038/ng1292-330 · Cited by 467
Amyloid β protein (Aβ) deposition: Aβ42(43) precedes Aβ40 in down Syndrome
Iwatsubo, T., Mann, D. M. A., Odaka, A., Suzuki, N., & Ihara, Y. (1995) · Annals of Neurology · doi:10.1002/ana.410370305 · Cited by 386
Tomita, T., Maruyama, K., Saido, T. C., Kume, H., Shinozaki, K., Tokuhiro, S., Capell, A., Walter, J., Grünberg, J., Haass, C., et al. (1997) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.94.5.2025 · Cited by 385
Haass, C., Hung, A. Y., Selkoe, D. J., & Teplow, D. B. (1994) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(17)32503-6 · Cited by 319
A vector for expressing foreign genes in the brains and hearts of transgenic mice
Borchelt, D. R., Davis, J., Fischer, M., Lee, M. K., Slunt, H. H., Ratovitsky, T., Regard, J., Copeland, N. G., Jenkins, N. A., Sisodia, S. S., et al. (1996) · Genetic Analysis: Biomolecular Engineering · doi:10.1016/s1050-3862(96)00167-2 · Cited by 317
Self-citationAlzheimer's disease associated with mutations in presenilin 2 is rare and variably penetrant
Sherrington, R. (1996) · Human Molecular Genetics · doi:10.1093/hmg/5.7.985 · Cited by 313
Sisodia, S., Koo, E., Hoffman, P., Perry, G. L., & Price, D. (1993) · Journal of Neuroscience · doi:10.1523/jneurosci.13-07-03136.1993 · Cited by 284
Self-citationNaruse, S., Igarashi, S., Aoki, K., Kaneko, K., Iihara, K., Miyatake, T., Kobayashi, H., Inuzuka, T., Shimizu, T., Kojima, T., et al. (1991) · The Lancet · doi:10.1016/0140-6736(91)91612-x · Cited by 281
A mutation in Alzheimerʼs disease destroying a splice acceptor site in the presenilin-1 gene
Pérez‐Tur, J., Froelich, S., Prihar, G., Crook, R., Baker, M., Duff, K., Wragg, M. A., Busfield, F., Lendon, C. L., Clark, R. F., et al. (1995) · Neuroreport · doi:10.1097/00001756-199512000-00071 · Cited by 264
Iwatsubo, T., Saido, T. C., Mann, D. M. A., Lee, V. M.-Y., & Trojanowski, J. Q. (1996) · Europe PMC (PubMed Central) · Cited by 248
Wısnıewskı, T., Ghiso, J. A., & Frangione, B. (1991) · Biochemical and Biophysical Research Communications · doi:10.1016/0006-291x(91)91706-i · Cited by 248
Mann, D. M. A., Iwatsubo, T., Ihara, Y., Cairns, N. J., Lantos, P. L., Bogdanović, N., Lannfelt, L., Winblad, B. G., Maat–Schieman, M. L. C., & Rossor, M. N. (1996) · Europe PMC (PubMed Central) · Cited by 184
Molecular genetic analysis of familial early-onset Alzheimer's disease linked to chromosome 14q24.3
Cruts, M., Backhovens, H., Wang, S., Gassen, G. V., Theuns, J., Jonghe, C. D., Wehnert, A., Voecht, J. D., Winter, G. D., Cras, P. P., et al. (1995) · Human Molecular Genetics · doi:10.1093/hmg/4.12.2363 · Cited by 180
Genetic dissection of Alzheimer disease, a heterogeneous disorder.
Schellenberg, G. D. (1995) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.92.19.8552 · Cited by 178
(1994) · PubMed Central · Cited by 169
Self-citationHyperaccumulation of FAD-linked presenilin 1 variants in vivo
Lee, M. K., Borchelt, D., Kim, G. J., Thinakaran, G., Slunt, H. H., Ratovitski, T., Martin, L. J., Kittur, A., Gandy, S., Levey, A. I., et al. (1997) · Nature Medicine · doi:10.1038/nm0797-756 · Cited by 148
Self-citationBarelli, H., Lebeau, A., Vizzavona, J., Delaère, P., Chevallier, N., Drouot, C., Marambaud, P., Ancolio, K., Buxbaum, J. D., Khorkova, O., et al. (1997) · Molecular Medicine · doi:10.1007/bf03401708 · Cited by 143
Borchelt, D. R., Koliatsos, V. E., Guarnieri, M., Pardo, C. A., Sisodia, S. S., & Price, D. L. (1994) · Journal of Biological Chemistry · doi:10.1016/s0021-9258(17)36683-8 · Cited by 132
Self-citationFamilial Alzheimer's chromosome 14 mutations
Wasco, W., Pettingell, W. P., Jondro, P. D., Schmidt, S. D., Gurubhagavatula, S., Rodes, L., Di-Blasi, T., Romano, D., Guénette, S. Y., Kovacs, D. M., et al. (1995) · Nature Medicine · doi:10.1038/nm0995-848a · Cited by 109
Campion, D., Brice, A., Dumanchin‐Njock, C., Puel, M., Baulac, M., Sayette, V. D. L., Mannequin, D., Duyckaerts, C. J., Michon, A., Martin, C., et al. (1996) · Neuroreport · doi:10.1097/00001756-199607080-00009 · Cited by 74
Mutation analysis of presenilin 1 gene in Alzheimer's disease
Boteva, K., Vitek, M. P., Mitsuda, H., de Silva, H., Xu, P.-T., Small, G. W., & Gilbert, J. R. (1996) · The Lancet · doi:10.1016/s0140-6736(96)90261-5 · Cited by 57
Nakano, I., & Hirano, A. (1987) · Journal of Neuropathology & Experimental Neurology · doi:10.1097/00005072-198701000-00004 · Cited by 43
Research works printed but not linked: 2
- Barelli, 1997, Characterization of new polyclonal antibodies specific for 40 and 42 amino acid-long amyloid β peptides, Mol. Med, in press
- Kim, 1990, Detection and quantitation of amyloid β-peptide with 2 monoclonal antibodies, Neurosci. Res. Commun, 7, 113
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Oakley, H., Cole, S. L., Logan, S., Maus, E., Shao, P., Craft, J., Guillozet-Bongaarts, A., Ohno, M., Disterhoft, J., Van Eldik, L., et al. (2006) · The Journal of Neuroscience · doi:10.1523/jneurosci.1202-06.2006 · Cited by 3,530
“Previous studies have shown that mice coexpressing FAD mutant APP and PS1 transgenes exhibit additive increases in A 42 production (Borchelt et al., 1996, 1997; Citron et al., 1997; Holcomb et al., 1998), although rarely have more than two A 42-elevating FAD mutations been combined in transgenic…”
BackgroundMucke, L., Masliah, E., Yu, G.-Q., Mallory, M., Rockenstein, E. M., Tatsuno, G., Hu, K., Kholodenko, D., Johnson-Wood, K., & McConlogue, L. (2000) · The Journal of Neuroscience · doi:10.1523/jneurosci.20-11-04050.2000 · Cited by 1,856
APP Processing and Synaptic Function
Kamenetz, F., Tomita, T., Hsieh, H., Seabrook, G., Borchelt, D., Iwatsubo, T., Sisodia, S., & Malinow, R. (2003) · Neuron · doi:10.1016/s0896-6273(03)00124-7 · Cited by 1,644
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
Metadata
- Authors
- Borchelt, D. R., Ratovitski, T., van Lare, J., Lee, M. K., Gonzales, V., Jenkins, N. A., Copeland, N. G., Price, D. L., & Sisodia, S. S.
- Affiliations
- Johns Hopkins University (US)
- Frederick National Laboratory for Cancer Research (US)
- Corresponding author
- Borchelt, David R
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 1997-10
- Volume
- 19
- Issue
- 4
- Pages
- 939-945
- ISSN
- 0896-6273 (ISSN-L)
- OpenAlex
- W2062214806
- Cited by
- 1,023
- References
- 52
- Citations by year
- 2026: 9 · 2025: 13 · 2024: 16 · 2023: 17 · 2022: 18 · 2021: 36 · 2020: 35 · 2019: 25 · 2018: 30 · 2017: 38 · 2016: 29 · 2015: 38 · 2014: 33 · 2013: 44 · 2012: 46
- FWCI
- 17.54
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Neuron (publishedVersion, cc-by-nc-nd)
- PubMed (publishedVersion)
- Funders
- National Institute on Aging (AG 14248, P50AG005146, P01AG014248, AG 05146)
- National Institute of Neurological Disorders and Stroke (NS-20471)
- 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
- presenilin 1, presenilin 2, amyloid precursor protein, familial Alzheimer's disease, amyloid-beta deposition, transgenic mice, amyloid-beta 42, amyloidosis, Alzheimer's disease pathogenesis
- MeSH terms
- Aging, Alzheimer Disease, Amyloid, Animals, Brain, Family, Humans, Membrane Proteins, Mice, Transgenic, Pedigree, Recombinant Fusion Proteins, Sweden, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Mice, Presenilin-1
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