ArticleNature communications2016
The neuritic plaque facilitates pathological conversion of tau in an Alzheimer's disease mouse model.
Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 61 papers.
What it found
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Who cites it
61 citing papers in PubMed, 128 citations in OpenAlex.
- Corpora amylacea profiling reveals disease stage and brain region-specific alterations in glycogen metabolism in Alzheimer's disease patient brains.Cell reports. Medicine · 2026Article
- Phytochemicals in Alzheimer's Disease Prevention and Management: Molecular Mechanisms, Therapeutic Potential, Translational Challenges, and Emerging Research Directions.International journal of molecular sciences · 2026Review
- TDP-43 dysfunction facilitates the pathological conversion of tau.Molecular neurodegeneration · 2026Article
- Thermodynamic Frontiers in Hemoglobin-Inspired Polymer Science for Diagnosis and Modulation of Neurodegenerative Diseases.Cell biochemistry and function · 2026Review
- Neuronal overexpression of Nrf2 reduces dystrophic neurites in 5XFAD Alzheimer's disease model mice.Alzheimer's research & therapy · 2026Article
- Neuronal microscale biophysical instability mediates macroscale network dynamics shaping pathological manifestations.bioRxiv : the preprint server for biology · 2026Article
- Neuronal overexpression of Nrf2 reduces dystrophic neurites in 5XFAD Alzheimer's disease model mice.bioRxiv : the preprint server for biology · 2026Article
- Metabolic Regulatory Networks in Ferroptosis During Alzheimer's Disease, Mechanisms of Glial Cell Action, and Pathological Correlations with Neuritic Plaques.International journal of general medicine · 2026Review
- Long-term Locus Coeruleus Stimulation Exacerbates Tau Pathology in PS19 Mice.bioRxiv : the preprint server for biology · 2025Article
- Interactions with tau's microtubule-binding repeats modulate amyloid-β aggregation and toxicity.Nature chemical biology · 2025Article
- ITCH regulates Golgi integrity and proteotoxicity in neurodegeneration.Science advances · 2025Article
- APOE deficiency inhibits amyloid-facilitated (A) tau pathology (T) and neurodegeneration (N), halting progressive ATN pathology in a preclinical model.Molecular psychiatry · 2025Article
- Article
- Exploring Iron Deposition Patterns Using Light and Electron Microscopy in the Mouse Brain Across Aging and Alzheimer's Disease Pathology Conditions.Journal of neurochemistry · 2025Article
- Investigating the neural network correlates of apathy, disinhibition, and executive dysfunction in active-duty United States Special Operations Forces.Brain imaging and behavior · 2025Article
- Annexin A6 membrane repair protein protects against amyloid-induced dystrophic neurites and tau phosphorylation in Alzheimer's disease model mice.Acta neuropathologica · 2025Article
- Seeding-competent early tau multimers are associated with cell type-specific transcriptional signatures.Acta neuropathologica · 2025Article
- Transcriptional signatures of hippocampal tau pathology in primary age-related tauopathy and Alzheimer's disease.Cell reports · 2025Article
- Review
- Exploring temporal and sex-linked dysregulation in Alzheimer disease phosphoproteome.iScience · 2024Article
1 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
A central question in Alzheimer's Disease (AD) is whether the neuritic plaque is necessary and sufficient for the development of tau pathology. Hyperphosphorylation of tau is found within dystrophic neurites surrounding β-amyloid deposits in AD mouse models but the pathological conversion of tau is absent. Likewise, expression of a human tau repeat domain in mice is insufficient to drive the pathological conversion of tau. Here we developed an Aβ-amyloidosis mouse model that expresses the human tau repeat domain and show that in these mice, the neuritic plaque facilitates the pathological conversion of wild-type tau. We show that this tau fragment seeds the neuritic plaque-dependent pathological conversion of wild-type tau that spreads from the cortex and hippocampus to the brain stem. These results establish that in addition to the neuritic plaque, a second determinant is required to drive the conversion of wild-type tau.
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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.