ReviewBrain pathology (Zurich, Switzerland)2006
Modeling familial British dementia in transgenic mice.
Review in Brain pathology (Zurich, Switzerland), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
What it found
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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.
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Who cites it
12 citing papers in PubMed, 22 citations in OpenAlex.
- Parallel in-register contact propensity predicts the Amyloidogenicity of ADan and ABri in familial dementias.International journal of biological macromolecules · 2026Article
- Massive mutagenesis reveals an incomplete amyloid motif in Bri2 that turns amyloidogenic upon C-terminal extension.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Aß40 displays amyloidogenic properties in the non-transgenic mouse brain but does not exacerbate Aß42 toxicity in Drosophila.Alzheimer's research & therapy · 2020Article
- Lessons from a Rare Familial Dementia: Amyloid and Beyond.Journal of Parkinson's disease and Alzheimer's disease · 2015Article
- Amyloid peptides ABri and ADan show differential neurotoxicity in transgenic Drosophila models of familial British and Danish dementia.Molecular neurodegeneration · 2014Article
- Proteomic characterization of a mouse model of familial Danish dementia.Journal of biomedicine & biotechnology · 2012Article
- Modeling familial Danish dementia in mice supports the concept of the amyloid hypothesis of Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
- Modeling familial British and Danish dementia.Brain structure & function · 2010Review
- Article
- Animal models of human amyloidoses: are transgenic mice worth the time and trouble?FEBS letters · 2009Review
- BRI2 inhibits amyloid beta-peptide precursor protein processing by interfering with the docking of secretases to the substrate.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2008Article
- Human herpesvirus 6 and multiple sclerosis: a one-year follow-up study.Brain pathology (Zurich, Switzerland) · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
The chromosome 13 linked amyloidopathies familial British dementia (FBD) and familial Danish dementia (FDD) are caused by mutations in the C-terminus of the BRI2 gene. In both diseases, novel peptides are deposited in amyloid plaques in the brain. Several laboratories have attempted to model these diseases in BRI2 transgenic mice with limited success. While high expression levels of BRI protein were achieved in transgenic lines, no ABri-amyloidosis was observed in aged mice. This review discusses the strategies chosen and problems experienced with the development of FBD/FDD models and suggests novel approaches to model the diseases in murine models.
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.