The DOI matches its Crossref record; 40 of the 40 references it cites were found in a registry or an index.
Familial Alzheimer's Disease–Linked Presenilin 1 Variants Elevate Aβ1–42/1–40 Ratio In Vitro and In Vivo
Open accessAbstract
Mutations in the presenilin 1 (PS1) and presenilin 2 genes cosegregate with the majority of early-onset familial Alzheimer's disease (FAD) pedigrees. We now document that the Abeta1-42(43)/Abeta1-40 ratio in the conditioned media of independent N2a cell lines expressing three FAD-linked PS1 variants is uniformly elevated relative to cells expressing similar levels of wild-type PS1. Similarly, the Abeta1-42(43)/Abeta1-40 ratio is elevated in the brains of young transgenic animals coexpressing a chimeric amyloid precursor protein (APP) and an FAD-linked PS1 variant compared with brains of transgenic mice expressing APP alone or transgenic mice coexpressing wild-type human PS1 and APP. These studies provide compelling support for the view that one mechanism by which these mutant PS1 cause AD is by increasing the extracellular concentration of Abeta peptides terminating at 42(43), species that foster Abeta deposition.
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“each of these genetic forms of AD either selectively increases the extracellular concentration of A42 (Suzuki et al., 1994;Borchelt et al., 1996;Duff et al., 1996;Scheuner et al., 1996;Citron et al., 1997) or increases both A42 and A40 (Cai et al., 1993;Citron et al., 1994;Scheuner et al., 1996).”
From Age-Dependent Changes in Brain, CSF, and Plasma Amyloid β Protein in the Tg2576 Transgenic Mouse Model of Alzheimer's Disease (2001) · cites this paper as Borchelt et al., 1996
In the citing paper
“In FAD, metabolic effects of mutations promote increased levels of total Aβ, or increased Aβ42 to Aβ40 ratio (Borchelt et al., 1996; Citron et al., 1992), conditions that favor oligomerization.”
From The Aβ oligomer hypothesis for synapse failure and memory loss in Alzheimer’s disease (2011) · cites this paper as Borchelt et al., 1996
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1 retracted
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Self-citationCandidate gene for the chromosome 1 familial Alzheimer’s disease locus
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Chen, Q., Kimura, H., & Schubert, D. (2002) · The Journal of Cell Biology · doi:10.1083/jcb.200110151 · Cited by 63
Campos-Peña, V., Toral-Rios, D., Becerril-Pérez, F., Sánchez-Torres, C., Delgado-Namorado, Y., Torres-Ossorio, E., Franco-Bocanegra, D., & Carvajal, K. (2017) · Antioxidants & Redox Signaling · doi:10.1089/ars.2016.6768 · Cited by 58
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Parnell, M., Guo, L., Abdi, M., & Cordeiro, M. F. (2012) · International Journal of Alzheimer s Disease · doi:10.1155/2012/786494 · Cited by 56
Synaptic contact number and size in stratum radiatum CA1 of APP/PS1ΔE9 transgenic mice
West, M. J., Bach, G., Søderman, A., & Jensen, J. L. (2009) · Neurobiology of Aging · doi:10.1016/j.neurobiolaging.2008.01.009 · Cited by 48
Ayton, S., & Bush, A. I. (2021) · Ageing Research Reviews · doi:10.1016/j.arr.2020.101212 · Cited by 45
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Amyloid β Protein in Plasma as a Diagnostic Marker for Alzheimer’s Disease
Iwatsubo, T. (1998) · Neurobiology of Aging · doi:10.1016/s0197-4580(98)00015-3 · Cited by 37
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Aβ43 levels determine the onset of pathological amyloid deposition
Tambini, M. D., Yin, T., Yesiltepe, M., Breuillaud, L., Zehntner, S. P., d'Abramo, C., Giliberto, L., & D'Adamio, L. (2023) · Journal of Biological Chemistry · doi:10.1016/j.jbc.2023.104868 · Cited by 8
The roles of GxxxG motif and gamma-secretase components in APP processing
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Metadata
- Authors
- Borchelt, D. R., Thinakaran, G., Eckman, C. B., Lee, M. K., Davenport, F., Ratovitsky, T., Prada, C.-M., Kim, G., Seekins, S., Yager, D., Slunt, H. H., Wang, R., Seeger, M., Levey, A. I., Gandy, S. E., Copeland, N. G., Jenkins, N. A., Price, D. L., Younkin, S. G., & Sisodia, S. S.
- Affiliations
- Johns Hopkins University (US)
- Mayo Clinic in Florida (US)
- Rockefeller University (US)
- Cornell University (US)
- Emory University (US)
- Frederick National Laboratory for Cancer Research (US)
- Corresponding author
- Sisodia, Sangram S.
- ORCID
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 1996-11
- Volume
- 17
- Issue
- 5
- Pages
- 1005-1013
- ISSN
- 0896-6273 (ISSN-L)
- OpenAlex
- W2095745901
- Cited by
- 1,478
- References
- 40
- Citations by year
- 2026: 2 · 2025: 20 · 2024: 28 · 2023: 23 · 2022: 26 · 2021: 32 · 2020: 45 · 2019: 27 · 2018: 26 · 2017: 51 · 2016: 47 · 2015: 43 · 2014: 42 · 2013: 43 · 2012: 53
- FWCI
- 53.49
- 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 (AG05689, P50AG005146, F32AG005689, 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
- familial Alzheimer's disease, presenilin 1, PS1 mutations, amyloid-beta 42, amyloid precursor protein, transgenic mice, N2a cells, conditioned medium, amyloid deposition
- MeSH terms
- Alzheimer Disease, Animals, Brain Chemistry, Humans, Membrane Proteins, Mice, Transgenic, Mutation, Neuroblastoma, Recombinant Fusion Proteins, Transfection, Tumor Cells, Cultured, Gene Expression, Amyloid beta-Protein Precursor, Culture Media, Conditioned, Mice, Presenilin-1
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