ArticleThe American journal of pathology2005
Accumulation of filamentous tau in the cerebral cortex of human tau R406W transgenic mice.
Article in The American journal of pathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
54 citing papers in PubMed, 117 citations in OpenAlex.
- Tau-induced increase in promoter-proximal RNA polymerase II pausing is linked to suppressed expression of long neuronal genes in aFrontiers in aging neuroscience · 2026Article
- Osteopontin drives neuroinflammation and cell loss in MAPT-N279K frontotemporal dementia patient neurons.Cell stem cell · 2024Article
- Methods for Biochemical Isolation of Insoluble Tau in Rodent Models of Tauopathies.Methods in molecular biology (Clifton, N.J.) · 2024Review
- An Insight into Cellular and Molecular Mechanisms Underlying the Pathogenesis of Neurodegeneration in Alzheimer's Disease.Biomedicines · 2023Review
- Article
- Astrocytes in Neurodegenerative Diseases: A Perspective from Tauopathy and α-Synucleinopathy.Life (Basel, Switzerland) · 2021Review
- Astrocytic Propagation of Tau in the Context of Alzheimer's Disease.Frontiers in cellular neuroscience · 2021Review
- An Overview of Astrocyte Responses in Genetically Induced Alzheimer's Disease Mouse Models.Cells · 2020Review
- Article
- Tau is not necessary for amyloid-β-induced synaptic and memory impairments.The Journal of clinical investigation · 2020Article
- Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer's disease.Molecular neurodegeneration · 2020Review
- Knock-in of Mutated hTAU Causes Insulin Resistance, Inflammation and Proteostasis Disturbance in a Mouse Model of Frontotemporal Dementia.Molecular neurobiology · 2020Article
- Cellular Biology of Tau Diversity and Pathogenic Conformers.Frontiers in neurology · 2020Review
- Pathological Progression Induced by the Frontotemporal Dementia-Associated R406W Tau Mutation in Patient-Derived iPSCs.Stem cell reports · 2019Article
- Intersection of pathological tau and microglia at the synapse.Acta neuropathologica communications · 2019Review
- A single systemic inflammatory insult causes acute motor deficits and accelerates disease progression in a mouse model of human tauopathy.Alzheimer's & dementia (New York, N. Y.) · 2019Article
- Early intervention of tau pathology prevents behavioral changes in the rTg4510 mouse model of tauopathy.PloS one · 2018Article
- Microglia in Alzheimer's Disease: A Role for Ion Channels.Frontiers in neuroscience · 2018Review
- Glial contributions to neurodegeneration in tauopathies.Molecular neurodegeneration · 2017Review
- Recent Advances in the Study of Bipolar/Rod-Shaped Microglia and their Roles in Neurodegeneration.Frontiers in aging neuroscience · 2017Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors at 10 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Missense mutations of the tau gene cause autosomal dominant frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17), an illness characterized by progressive personality changes, dementia, and parkinsonism. There is prominent frontotemporal lobe atrophy of the brain accompanied by abundant tau accumulation with neurofibrillary tangles and neuronal cell loss. Using a hamster prion protein gene expression vector, we generated several independent lines of transgenic (Tg) mice expressing the longest form of the human four-repeat tau with the R406W mutation associated with FTDP-17. The TgTauR406W 21807 line showed tau accumulation beginning in the hippocampus and amygdala at 6 months of age, which subsequently spread to the cortices and subcortical areas. The accumulated tau was phosphorylated, ubiquitinated, conformationally changed, argyrophilic, and sarcosyl-insoluble. Activation of GSK-3beta and astrocytic induction of mouse tau were observed. Astrogliosis and microgliosis correlated with prominent tau accumulation. Electron microscopic examination revealed the presence of straight filaments. Behavioral tests showed motor disturbances and progressive acquired memory loss between 10 to 12 months of age. These findings suggested that TgTauR406W mice would be a useful model in the study of frontotemporal dementia and other tauopathies such as Alzheimer's disease (AD).
Indexed as
Identifiers
What OpenQuestion holds
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.