Tau reduction in the presence of amyloid-β prevents tau pathology and neuronal death in vivo
Open accessAbstract
Several studies have now supported the use of a tau lowering agent as a possible therapy in the treatment of tauopathy disorders, including Alzheimer's disease. In human Alzheimer's disease, however, concurrent amyloid-β deposition appears to synergize and accelerate tau pathological changes. Thus far, tau reduction strategies that have been tested in vivo have been examined in the setting of tau pathology without confounding amyloid-β deposition. To determine whether reducing total human tau expression in a transgenic model where there is concurrent amyloid-β plaque formation can still reduce tau pathology and protect against neuronal loss, we have taken advantage of the regulatable tau transgene in APP/PS1 × rTg4510 mice. These mice develop both neurofibrillary tangles as well as amyloid-β plaques throughout the cortex and hippocampus. By suppressing human tau expression for 6 months in the APP/PS1 × rTg4510 mice using doxycycline, AT8 tau pathology, bioactivity, and astrogliosis were reduced, though importantly to a lesser extent than lowering tau in the rTg4510 alone mice. Based on non-denaturing gels and proteinase K digestions, the remaining tau aggregates in the presence of amyloid-β exhibit a longer-lived aggregate conformation. Nonetheless, lowering the expression of the human tau transgene was sufficient to equally ameliorate thioflavin-S positive tangles and prevent neuronal loss equally well in both the APP/PS1 × rTg4510 mice and the rTg4510 cohort. Together, these results suggest that, although amyloid-β stabilizes tau aggregates, lowering total tau levels is still an effective strategy for the treatment of tau pathology and neuronal loss even in the presence of amyloid-β deposition.
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Aggregated Aβ peptides stabilize tau aggregates.
“stabilize tau aggregates (27)”
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 [27]
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Self-citationAmyloid-β-independent regulators of tau pathology in Alzheimer disease
van der Kant, R., Goldstein, L. S. B., & Ossenkoppele, R. (2020) · Nature reviews. Neuroscience · doi:10.1038/s41583-019-0240-3 · Cited by 580 · see citing works
Tau molecular diversity contributes to clinical heterogeneity in Alzheimer’s disease
Dujardin, S., Commins, C., Lathuiliere, A., Beerepoot, P., Fernandes, A. R., Kamath, T. V., De Los Santos, M. B., Klickstein, N., Corjuc, D. L., Corjuc, B. T., et al. (2020) · Nature Medicine · doi:10.1038/s41591-020-0938-9 · Cited by 438 · see citing works
Self-citationTau Protein Disrupts Nucleocytoplasmic Transport in Alzheimer’s Disease
Eftekharzadeh, B., Daigle, J. G., Kapinos, L. E., Coyne, A., Schiantarelli, J., Carlomagno, Y., Cook, C., Miller, S. J., Dujardin, S., Amaral, A. S., et al. (2018) · Neuron · doi:10.1016/j.neuron.2018.07.039 · Cited by 460 · see citing works
Self-citationMattsson-Carlgren, N., Andersson, E., Janelidze, S., Ossenkoppele, R., Insel, P., Strandberg, O., Zetterberg, H., Rosen, H. J., Rabinovici, G., Chai, X., et al. (2020) · Science Advances · doi:10.1126/sciadv.aaz2387 · Cited by 359 · see citing works
“Our findings are in agreement with previous results from many different experimental systems using both cell and animal models (4), which have shown that aggregated A peptides may induce tau hyperphosphorylation both in vitro and in vivo (6, 26), stabilize tau aggregates (27), and promote the propagation of new tau a…”
Immune Signaling in Neurodegeneration
Hammond, T. R., Marsh, S. E., & Stevens, B. (2019) · Immunity · doi:10.1016/j.immuni.2019.03.016 · Cited by 336 · see citing works
Role of tau protein in Alzheimer’s disease: The prime pathological player
Muralidar, S., Ambi, S. V., Sekaran, S., Thirumalai, D., & Palaniappan, B. (2020) · International Journal of Biological Macromolecules · doi:10.1016/j.ijbiomac.2020.07.327 · Cited by 278 · see citing works
Tau: Enabler of diverse brain disorders and target of rapidly evolving therapeutic strategies
Chang, C.-W., Shao, E., & Mucke, L. (2021) · Science · doi:10.1126/science.abb8255 · Cited by 263 · see citing works
Li, H., Liu, C.-C., Zheng, H., & Huang, T. Y. (2018) · Translational Neurodegeneration · doi:10.1186/s40035-018-0139-3 · Cited by 103 · see citing works
Microglia: Friend and foe in tauopathy
Odfalk, K. F., Bieniek, K. F., & Hopp, S. C. (2022) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2022.102306 · Cited by 60 · see citing works
Retromer dysfunction at the nexus of tauopathies
Carosi, J. M., Denton, D., Kumar, S., & Sargeant, T. J. (2021) · Cell Death & Differentiation · doi:10.1038/s41418-020-00727-2 · Cited by 16 · see citing works
- Authors
- DeVos, S. L., Corjuc, B. T., Commins, C., Dujardin, S., Bannon, R. N., Corjuc, D., Moore, B. D., Bennett, R. E., Jorfi, M., Gonzales, J. A., Dooley, P. M., Roe, A. D., Pitstick, R., Irimia, D., Frosch, M. P., Carlson, G. A., & Hyman, B. T.
- Affiliations
- Harvard University (US)
- McLaughlin Research Institute (US)
- Corresponding author
- Hyman, Bradley T
- ORCID
- Venue
- Brain
- Publisher
- Oxford University Press (OUP)
- Published
- 2018-05-03
- Volume
- 141
- Issue
- 7
- Pages
- 2194-2212
- ISSN
- 0006-8950 (ISSN-L)
- 1460-2156
- PMC
- PMC6022692
- OpenAlex
- W2802649373
- Cited by
- 106
- References
- 76
- Citations by year
- 2026: 7 · 2025: 7 · 2024: 13 · 2023: 15 · 2022: 9 · 2021: 22 · 2020: 16 · 2019: 12 · 2018: 5
- FWCI
- 9.45
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Brain (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Division of Medical Sciences at Harvard University (T32 AG000222)
- Brightfocus Foundation
- Massachusetts Alzheimer’s Disease Center (P50AG05134)
- JPB Foundation
- NIH (P30 NS045776, AG026249)
- 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, tauopathy, Alzheimer's disease, neurofibrillary tangles, tau aggregation, neuronal cell death, rTg4510 mice, astrocyte activation
- MeSH terms
- Alzheimer Disease, Animals, Disease Models, Animal, Hippocampus, Humans, Mice, Transgenic, Neurons, Phosphorylation, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, Neurofibrillary Tangles, tau Proteins, Tauopathies, Mice, Presenilin-1, Plaque, Amyloid
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