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Persistent Amyloidosis following Suppression of Aβ Production in a Transgenic Model of Alzheimer Disease
Open accessAbstract
BACKGROUND: The proteases (secretases) that cleave amyloid-beta (Abeta) peptide from the amyloid precursor protein (APP) have been the focus of considerable investigation in the development of treatments for Alzheimer disease. The prediction has been that reducing Abeta production in the brain, even after the onset of clinical symptoms and the development of associated pathology, will facilitate the repair of damaged tissue and removal of amyloid lesions. However, no long-term studies using animal models of amyloid pathology have yet been performed to test this hypothesis. METHODS AND FINDINGS: We have generated a transgenic mouse model that genetically mimics the arrest of Abeta production expected from treatment with secretase inhibitors. These mice overexpress mutant APP from a vector that can be regulated by doxycycline. Under normal conditions, high-level expression of APP quickly induces fulminant amyloid pathology. We show that doxycycline administration inhibits transgenic APP expression by greater than 95% and reduces Abeta production to levels found in nontransgenic mice. Suppression of transgenic Abeta synthesis in this model abruptly halts the progression of amyloid pathology. However, formation and disaggregation of amyloid deposits appear to be in disequilibrium as the plaques require far longer to disperse than to assemble. Mice in which APP synthesis was suppressed for as long as 6 mo after the formation of Abeta deposits retain a considerable amyloid load, with little sign of active clearance. CONCLUSION: This study demonstrates that amyloid lesions in transgenic mice are highly stable structures in vivo that are slow to disaggregate. Our findings suggest that arresting Abeta production in patients with Alzheimer disease should halt the progression of pathology, but that early treatment may be imperative, as it appears that amyloid deposits, once formed, will require additional intervention to clear.
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“Despite this response, however, Aβ clearance and plaque modulation/dynamics is unaffected10–12”
From Sustained microglial depletion with CSF1R inhibitor impairs parenchymal plaque development in an Alzheimer’s disease model (2019) · cites this paper as [12]
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Metadata
- Authors
- Jankowsky, J. L., Slunt, H. H., Gonzales, V., Savonenko, A. V., Wen, J. C., Jenkins, N. A., Copeland, N. G., Younkin, L. H., Lester, H. A., Younkin, S. G., & Borchelt, D. R.
- Affiliations
- California Institute of Technology (US)
- Johns Hopkins University (US)
- National Cancer Institute (US)
- Mayo Clinic (US)
- Corresponding author
- Jankowsky, Joanna L
- Borchelt, David R
- Venue
- PLoS Medicine
- Publisher
- Public Library of Science (PLoS)
- Published
- 2005-11-15
- Volume
- 2
- Issue
- 12
- Pages
- e355
- ISSN
- 1549-1277 (ISSN-L)
- 1549-1676
- PMC
- PMC1283364
- OpenAlex
- W2152864425
- Cited by
- 237
- References
- 67
- Citations by year
- 2026: 3 · 2025: 6 · 2024: 23 · 2023: 10 · 2022: 14 · 2021: 7 · 2020: 5 · 2019: 9 · 2018: 9 · 2017: 14 · 2016: 19 · 2015: 9 · 2014: 13 · 2013: 8 · 2012: 16
- FWCI
- 6.19
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Locations
- PLoS Medicine (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- CaltechAUTHORS (California Institute of Technology) (acceptedVersion)
- CaltechAUTHORS (California Institute of Technology) (submittedVersion, cc-by)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Figshare (submittedVersion, cc-by)
- Funders
- Alzheimer's Association
- Johns Hopkins University
- National Alliance for Research on Schizophrenia and Depression
- Rose Hills Foundation
- National Institute on Aging (K01 AG26144-01, P50 AGO5146-20, K01AG026144, P01AG015453, P50AG005146, R01AG006656)
- National Cancer Institute
- National Institute of Neurological Disorders and Stroke (R01NS047225)
- 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, amyloid-beta, amyloid plaques, amyloidosis, amyloid precursor protein, secretase inhibitors, transgenic mouse model, amyloid clearance
- MeSH terms
- Alzheimer Disease, Animals, Humans, Mice, Inbred C57BL, Mice, Transgenic, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Gene Expression Profiling, Mice, Plaque, Amyloid
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.
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