ArticleBrain : a journal of neurology2018
Tau reduction in the presence of amyloid-β prevents tau pathology and neuronal death in vivo.
Article in Brain : a journal of neurology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 104 citations in OpenAlex.
- Prospect in Alzheimer's disease integrative therapy targeting both amyloid-beta and tau.Neural regeneration research · 2026Article
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- tRNA-derived fragments elevated in Alzheimer's disease promote Tau aggregation.bioRxiv : the preprint server for biology · 2026Article
- Beyond microtubule regulation: the multifaceted roles of tau in neuronal function and dysfunction.Translational psychiatry · 2026Review
- Presenilin-dependent regulation of neuronal tau pathology via the autophagy and proteasome pathways.Acta neuropathologica communications · 2026Article
- Promoter mutagenesis and a massively parallel reporter screen of thebioRxiv : the preprint server for biology · 2026Article
- Neuronal PARIS-STAT3 axis drives tau pathology and glial activation in Alzheimer's disease.bioRxiv : the preprint server for biology · 2025Article
- AAV delivery of artificial miRNA targeting MAPT for the reduction of tau pathology in Alzheimer's disease.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- miR-132 and Its Exosomal Form in Alzheimer's Disease: Linking Epigenetic Regulation to Neurodegeneration.Molecular neurobiology · 2025Review
- Article
- Patterns of tau, amyloid and synuclein pathology in ageing, Alzheimer's disease and synucleinopathies.Brain : a journal of neurology · 2025Article
- Cyclophilin D (CypD) ablation prevents neurodegeneration and cognitive damage induced by caspase-3 cleaved tau.Free radical biology & medicine · 2025Article
- Insights into pathophysiology, biomarkers, and therapeutics in tauopathies: Proceedings of the Tau2024 Global Conference.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Tau, synapse loss and gliosis progress in an Alzheimer's mouse model after amyloid-β immunotherapy.Brain : a journal of neurology · 2025Article
- Ketone body metabolism and the NLRP3 inflammasome in Alzheimer's disease.Immunological reviews · 2025Review
- Article
- Recent Advances in Targeting Transition Metals (Copper, Iron, and Zinc) in Alzheimer's Disease.Molecular neurobiology · 2024Review
- FGFR3 drives Aβ-induced tau uptake.Experimental & molecular medicine · 2024Article
- Neuronal MAPT expression is mediated by long-range interactions with cis-regulatory elements.American journal of human genetics · 2024Article
- DnaJs are enriched in tau regulators.International journal of biological macromolecules · 2023Article
Corrections and comments
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Authors and funding
17 authors at 4 institutions in 1 country.
Funding
Abstract
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.