Cited by 1,023Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

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Accelerated Amyloid Deposition in the Brains of Transgenic Mice Coexpressing Mutant Presenilin 1 and Amyloid Precursor Proteins

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Borchelt, David R, Ratovitski, Tamara, van Lare, Judy, Lee, Michael K, Gonzales, Vicki, Jenkins, Nancy A, Copeland, Neal G, Price, Donald L, Sisodia, Sangram S·1997·Neuron

DOI 10.1016/s0896-6273(00)80974-5

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Abstract

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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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
ORCID: Borchelt, David R
Ratovitski, Tamara
Lee, Michael K
Jenkins, Nancy A
Sisodia, Sangram S
Venue: Neuron
Publisher: Elsevier BV
Published: 1997-10
Volume: 19
Issue: 4
Pages: 939-945
ISSN: 0896-6273 (ISSN-L)
DOI: 10.1016/s0896-6273(00)80974-5
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: cc-by-nc-nd
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
creativecommons.org/licenses/by-nc-nd/4.0/ (vor, 1288 d)
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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Accelerated Amyloid Deposition in the Brains of Transgenic Mice Coexpressing Mutant Presenilin 1 and Amyloid Precursor Proteins

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