ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
Memory deficits of British dementia knock-in mice are prevented by Aβ-precursor protein haploinsufficiency.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 26 citations in OpenAlex.
- Pathological mechanisms of motor dysfunction in familial Danish dementia: insights from a knock-in rat model.Journal of neuroinflammation · 2025Article
- Functional BRI2-TREM2 interactions in microglia: implications for Alzheimer's and related dementias.EMBO reports · 2024Article
- Comorbidity Genes of Alzheimer's Disease and Type 2 Diabetes Associated with Memory and Cognitive Function.International journal of molecular sciences · 2024Review
- Article
- The role of the integral type II transmembrane protein BRI2 in health and disease.Cellular and molecular life sciences : CMLS · 2021Review
- Cross-species genetic screens to identify kinase targets for APP reduction in Alzheimer's disease.Human molecular genetics · 2019Article
- The Familial dementia gene ITM2b/BRI2 facilitates glutamate transmission via both presynaptic and postsynaptic mechanisms.Scientific reports · 2019Article
- Abolishing Tau cleavage by caspases at AspartateTranslational psychiatry · 2017Article
- Amyloid and intracellular accumulation of BRINeurobiology of aging · 2017Article
- Article
- 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
- The ITM2B (BRI2) gene is a target of BCL6 repression: Implications for lymphomas and neurodegenerative diseases.Biochimica et biophysica acta · 2015Article
- BRI2 ectodomain affects Aβ42 fibrillation and tau truncation in human neuroblastoma cells.Cellular and molecular life sciences : CMLS · 2015Article
- Article
- Amyloid beta precursor protein and prion protein have a conserved interaction affecting cell adhesion and CNS development.PloS one · 2012Article
- Danish and British dementia ITM2b/BRI2 mutations reduce BRI2 protein stability and impair glutamatergic synaptic transmission.The Journal of biological chemistryArticle
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 3 countries.
Funding
Abstract
Familial British Dementia (FBD) is caused by an autosomal dominant mutation in the BRI2/ITM2B gene (Vidal et al., 1999). FBD(KI) mice are a model of FBD that is genetically congruous to the human disease, because they carry one mutant and one wild-type Bri2/Itm2b allele. Analysis of these mice has shown that the British mutation causes memory impairments due to loss of Bri2 function (Tamayev et al., 2010b). BRI2 is a physiologic inhibitor of processing of the Aβ-precursor protein (APP; Matsuda et al., 2008), a gene associated with Alzheimer's disease (Bertram et al., 2010). Here we show that APP haploinsufficiency prevents memory dysfunctions seen in FBD(KI) mice. This genetic suppression is consistent with a role for APP in the pathogenesis of memory deficits. Moreover, it provides compelling evidence that the memory dysfunctions caused by the British BRI2 mutant are dependent on endogenous APP and that BRI2 and APP functionally interact. This evidence establishes a mechanistic connection between Familial British and Alzheimer's dementias.
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.