Changes in Amyloid-β and Tau in the Cerebrospinal Fluid of Transgenic Mice Overexpressing Amyloid Precursor Protein
Abstract
Changes in Aβ and Tau in the CSF of APP transgenic mice mirror the temporal sequence and magnitude of changes in these proteins in the CSF of Alzheimer’s disease patients.
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Preclinical studies provide compelling evidence supporting early brain amyloidosis as a driver of tau hyperphosphorylation in AD.
“Preclinical studies provide compelling evidence supporting early brain amyloidosis as a driver of tau hyperphosphorylation in AD.14,15”
From Cerebrospinal fluid p-tau231 as an early indicator of emerging pathology in Alzheimer's disease (2022) · cites this paper as [14]
Transgenic animal experiments have shown that Aβ aggregates are associated with increased levels of soluble tau and increased tau phosphorylation.
“For example, transgenic animal experiments have shown that Aβ aggregates are associated with increased levels of soluble tau and increased tau phosphorylation (5, 6).”
From Aβ deposition is associated with increases in soluble and phosphorylated tau that precede a positive tau PET in Alzheimer's disease (2020) · cites this paper as [5]
Cell and animal experiments have verified that Aβ may induce pathologically relevant alterations in neuronal tau, including increased phosphorylation and release of tau.
“Cell and animal experiments have verified that Aβ may induce pathologically relevant alterations in neuronal tau, including increased phosphorylation and release of tau (4, 5).”
From Aβ deposition is associated with increases in soluble and phosphorylated tau that precede a positive tau PET in Alzheimer's disease (2020) · cites this paper as [5]
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References 30 · Cited by 204
- Authors
- Maia, L. F., Kaeser, S. A., Reichwald, J., Hruscha, M., Martus, P., Staufenbiel, M., & Jucker, M.
- Affiliations
- Department of Cellular Neurology, Hertie Institute for Clinical Brain Research, University of Tübingen, D-72076 Tübingen, Germany.
- German Center for Neurodegenerative Diseases (DE)
- Novartis (Switzerland) (CH)
- University of Tübingen (DE)
- Corresponding author
- Kaeser, Stephan A.
- Jucker, Mathias
- Venue
- Science Translational Medicine
- Published
- 2013-07-17
- Volume
- 5
- Issue
- 194
- Pages
- 194re2-194re2
- ISSN
- 1946-6234 (ISSN-L)
- 1946-6242
- OpenAlex
- W2159462479
- Cited by
- 204
- References
- 30
- Citations by year
- 2026: 7 · 2025: 11 · 2024: 14 · 2023: 18 · 2022: 26 · 2021: 17 · 2020: 26 · 2019: 14 · 2018: 13 · 2017: 14 · 2016: 12 · 2015: 17 · 2014: 14 · 2013: 1
- FWCI
- 10.19
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science Translational Medicine (publishedVersion)
- PubMed (publishedVersion)
- DZNE Pub (submittedVersion)
- Topics
- Health Sciences › Medicine › Physiology › 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
- amyloid-beta, tau protein, cerebrospinal fluid biomarkers, Alzheimer's disease, amyloid precursor protein, APP23 transgenic mice, presenilin 1, amyloid-beta 42, Aβ40, disease markers, transgenic mouse model
- MeSH terms
- Aging, Alzheimer Disease, Animals, Female, Humans, Male, Mice, Transgenic, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, tau Proteins, Disease Progression, Mice, alpha-Synuclein
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