Tau Immunotherapy Modulates Both Pathological Tau and Upstream Amyloid Pathology in an Alzheimer's Disease Mouse Model
Open accessAbstract
In Alzheimer's disease (AD), the pathological accumulation of tau appears to be a downstream effect of amyloid β protein (Aβ). However, the relationship between these two proteins and memory loss is unclear. In this study, we evaluated the specific removal of pathological tau oligomers in aged Tg2576 mice by passive immunotherapy using tau oligomer-specific monoclonal antibody. Removal of tau oligomers reversed memory deficits and accelerated plaque deposition in the brain. Surprisingly, Aβ*56 levels decreased, suggesting a link between tau and Aβ oligomers in the promotion of cognitive decline. The results suggest that tau oligomerization is not only a consequence of Aβ pathology but also a critical mediator of the toxic effects observed afterward in AD. Overall, these findings support the potential of tau oligomers as a therapeutic target for AD.
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TauO, senescence, and inflammaging are crucial elements in Alzheimer's disease and may cooperatively trigger complex pathomechanisms involved in Alzheimer's disease progression and cognitive decline.
“These findings suggest that TauO, senescence, and inflammaging are crucial elements in AD and may cooperatively trigger the underlying complex pathomechanisms involved in AD progression and cognitive decline. 9 , 29 , 30 , 31 , 32 , 33”
From Senescence, brain inflammation, and oligomeric tau drive cognitive decline in Alzheimer's disease: Evidence from clinical and preclinical studies (2024) · cites this paper as [30]
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RETRACTED ARTICLE: A specific amyloid-β protein assembly in the brain impairs memory
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Self-citation
- Authors
- Castillo-Carranza, D. L., Guerrero-Muñoz, M. J., Sengupta, U., Hernandez, C., Barrett, A. D. T., Dineley, K., & Kayed, R.
- Affiliations
- The University of Texas Medical Branch at Galveston (US)
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2015-03-25
- Volume
- 35
- Issue
- 12
- Pages
- 4857-4868
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6705372
- OpenAlex
- W2065413916
- Cited by
- 149
- References
- 82
- Citations by year
- 2026: 7 · 2025: 10 · 2024: 7 · 2023: 13 · 2022: 8 · 2021: 8 · 2020: 13 · 2019: 18 · 2018: 15 · 2017: 24 · 2016: 15 · 2015: 11
- FWCI
- 15.96
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Alzheimer's Drug Discovery Foundation
- 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
- Alzheimer's disease, tau oligomers, passive immunotherapy, amyloid-beta, Tg2576 mice, memory impairment, amyloid plaques, tau oligomerization, therapeutic target
- MeSH terms
- Aging, Alzheimer Disease, Animals, Antibodies, Monoclonal, Brain, Disease Models, Animal, Male, Memory Disorders, Mice, Transgenic, Peptide Fragments, Amyloid beta-Peptides, tau Proteins, 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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