ArticlePloS one2009
Generation and initial characterization of FDD knock in mice.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 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
27 citing papers in PubMed, 34 citations in OpenAlex.
- Pathological mechanisms of motor dysfunction in familial Danish dementia: insights from a knock-in rat model.Journal of neuroinflammation · 2025Article
- Article
- Facilitation of glutamate, but not GABA, release in Familial Alzheimer's APP mutant Knock-in rats with increased β-cleavage of APP.Aging cell · 2019Article
- Tuning of Glutamate, But Not GABA, Release by an Intrasynaptic Vesicle APP Domain Whose Function Can Be Modulated by β- or α-Secretase Cleavage.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- BRI2 as an anti-Alzheimer gene.Medical molecular morphology · 2019Review
- Abolishing Tau cleavage by caspases at AspartateTranslational psychiatry · 2017Article
- Article
- Interaction of ApoE3 and ApoE4 isoforms with an ITM2b/BRI2 mutation linked to the Alzheimer disease-like Danish dementia: Effects on learning and memory.Neurobiology of learning and memory · 2015Article
- Lessons from a Rare Familial Dementia: Amyloid and Beyond.Journal of Parkinson's disease and Alzheimer's disease · 2015Article
- The Familial British Dementia Mutation Promotes Formation of Neurotoxic Cystine Cross-linked Amyloid Bri (ABri) Oligomers.The Journal of biological chemistry · 2015Article
- Amyloid peptides ABri and ADan show differential neurotoxicity in transgenic Drosophila models of familial British and Danish dementia.Molecular neurodegeneration · 2014Article
- BRI2 interacts with BACE1 and regulates its cellular levels by promoting its degradation and reducing its mRNA levels.Current Alzheimer research · 2013Article
- An intracellular threonine of amyloid-β precursor protein mediates synaptic plasticity deficits and memory loss.PloS one · 2013Article
- Increased tau phosphorylation and tau truncation, and decreased synaptophysin levels in mutant BRI2/tau transgenic mice.PloS one · 2013Article
- Caspase-9 mediates synaptic plasticity and memory deficits of Danish dementia knock-in mice: caspase-9 inhibition provides therapeutic protection.Molecular neurodegeneration · 2012Article
- Inhibition of γ-secretase worsens memory deficits in a genetically congruous mouse model of Danish dementia.Molecular neurodegeneration · 2012Article
- Memory deficits of British dementia knock-in mice are prevented by Aβ-precursor protein haploinsufficiency.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- β- but not γ-secretase proteolysis of APP causes synaptic and memory deficits in a mouse model of dementia.EMBO molecular medicine · 2012Article
- Proteomic characterization of a mouse model of familial Danish dementia.Journal of biomedicine & biotechnology · 2012Article
- APP heterozygosity averts memory deficit in knockin mice expressing the Danish dementia BRI2 mutant.The EMBO journal · 2011Article
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 1 country.
Funding
Abstract
backgroundMutations in the integral membrane protein 2B, also known as BRI(2), a type II trans-membrane domain protein cause two autosomal dominant neurodegenerative diseases, Familial British and Danish Dementia. In these conditions, accumulation of a C-terminal peptide (ABri and ADan) cleaved off from the mutated precursor protein by the pro-protein convertase furin, leads to amyloid deposition in the walls of blood vessels and parenchyma of the brain. Recent advances in the understanding of the generation of amyloid in Alzheimer's disease has lead to the finding that BRI(2) interacts with the Amyloid Precursor Protein (APP), decreasing the efficiency of APP processing to generate Abeta. The interaction between the two precursors, APP and BRI(2), and possibly between Abeta and ABri or ADan, could be important in influencing the rate of amyloid production or the tendency of these peptides to aggregate. METHODOLOGY/PRINCIPAL
findingsWe have generated the first BRI(2) Danish Knock-In (FDD(KI)) murine model of FDD, expressing the pathogenic decamer duplication in exon 6 of the BRI(2) gene. FDD(KI) mice do not show any evident abnormal phenotype, with normal brain histology and no detectable amyloid deposition in blood vessel walls or parenchyma. CONCLUSIONS/SIGNIFICANCE: This new murine mouse model will be important to further understand the interaction between APP and BRI(2), and to provide insights into the molecular basis of FDD.
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.