ArticleThe EMBO journal2011
APP heterozygosity averts memory deficit in knockin mice expressing the Danish dementia BRI2 mutant.
Article in The EMBO journal, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 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.
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Who cites it
40 citing papers in PubMed, 53 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
- Isolation, Identification, Activity Evaluation, and Mechanism of Action of Neuroprotective Peptides from Walnuts: A Review.Nutrients · 2023Review
- Arteriolar neuropathology in cerebral microvascular disease.Neuropathology and applied neurobiology · 2023Review
- Review
- Article
- The role of vascular dementia associated genes in patients with Alzheimer's disease: A large case-control study in the Chinese population.CNS neuroscience & therapeutics · 2021Article
- The role of the integral type II transmembrane protein BRI2 in health and disease.Cellular and molecular life sciences : CMLS · 2021Review
- Amyloid β and Amyloid Precursor Protein Synergistically Suppress Large-Conductance Calcium-Activated Potassium Channel in Cortical Neurons.Frontiers in aging neuroscience · 2021Article
- Analyses Mutations inFrontiers in aging neuroscience · 2020Article
- 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
- Lysosomal Dysfunction in Down Syndrome Is APP-Dependent and Mediated by APP-βCTF (C99).The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- The Familial dementia gene ITM2b/BRI2 facilitates glutamate transmission via both presynaptic and postsynaptic mechanisms.Scientific reports · 2019Article
- BRI2 as an anti-Alzheimer gene.Medical molecular morphology · 2019Review
- Abolishing Tau cleavage by caspases at AspartateTranslational psychiatry · 2017Article
- Amyloid precursor protein and endosomal-lysosomal dysfunction in Alzheimer's disease: inseparable partners in a multifactorial disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Review
- Amyloid and intracellular accumulation of BRINeurobiology of aging · 2017Article
- APP Receptor? To Be or Not To Be.Trends in pharmacological sciences · 2016Review
- Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
An autosomal dominant mutation in the BRI2/ITM2B gene causes familial Danish dementia (FDD). Analysis of FDD(KI) mice, a mouse model of FDD genetically congruous to the human disease since they carry one mutant and one wild-type Bri2/Itm2b allele, has shown that the Danish mutation causes loss of Bri2 protein, synaptic plasticity and memory impairments. BRI2 is a physiological interactor of Aβ-precursor protein (APP), a gene associated with Alzheimer disease, which inhibits processing of APP. Here, we show that APP/Bri2 complexes are reduced in synaptic membranes of FDD(KI) mice. Consequently, APP metabolites derived from processing of APP by β-, α- and γ-secretases are increased in Danish dementia mice. APP haplodeficiency prevents memory and synaptic dysfunctions, consistent with a role for APP metabolites in the pathogenesis of memory and synaptic deficits. This genetic suppression provides compelling evidence that APP and BRI2 functionally interact, and that the neurological effects of the Danish form of BRI2 only occur when sufficient levels of APP are supplied by two alleles. This evidence establishes a pathogenic sameness between familial Danish and Alzheimer's dementias.
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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.