ArticleProceedings of the National Academy of Sciences of the United States of America2010
Modeling familial Danish dementia in mice supports the concept of the amyloid hypothesis of Alzheimer's disease.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 75 citations in OpenAlex.
- Nanomaterial strategies for mitigating protein misfolding and neuroinflammation in neurodegenerative diseases.Zoological research · 2026Review
- Parallel in-register contact propensity predicts the Amyloidogenicity of ADan and ABri in familial dementias.International journal of biological macromolecules · 2026Article
- Functions of the basal lamina and ApoE in cerebral amyloid angiopathy.Fluids and barriers of the CNS · 2025Review
- Pathological mechanisms of motor dysfunction in familial Danish dementia: insights from a knock-in rat model.Journal of neuroinflammation · 2025Article
- Xenografted human microglia display diverse transcriptomic states in response to Alzheimer's disease-related amyloid-β pathology.Nature neuroscience · 2024Article
- Transfixed by transgenics: how pathology assumptions are slowing progress in Alzheimer's disease and related dementia research.EMBO molecular medicine · 2023Article
- The Commonly Used Stabilizers for Phytochemical-Based Nanoparticles: Stabilization Effects, Mechanisms, and Applications.Nutrients · 2023Review
- CSF p-tau increase in response to Aβ-type and Danish-type cerebral amyloidosis and in the absence of neurofibrillary tangles.Acta neuropathologica · 2022Article
- Mice Treated Subcutaneously with Mouse LPS-Converted PrPVeterinary sciences · 2021Article
- Medin aggregation causes cerebrovascular dysfunction in aging wild-type mice.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Article
- JBPOS0101 regulates amyloid beta, tau, and glial cells in an Alzheimer's disease model.PloS one · 2020Article
- BRI2 as an anti-Alzheimer gene.Medical molecular morphology · 2019Review
- Anthocyanins encapsulated by PLGA@PEG nanoparticles potentially improved its free radical scavenging capabilities via p38/JNK pathway against AβJournal of nanobiotechnology · 2017Article
- Vanillic acid attenuates AβScientific reports · 2017Article
- Humanized Tau Mice with Regionalized Amyloid Exhibit Behavioral Deficits but No Pathological Interaction.PloS one · 2016Article
- 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
- A molecular chaperone breaks the catalytic cycle that generates toxic Aβ oligomers.Nature structural & molecular biology · 2015Article
- Amyloid peptides ABri and ADan show differential neurotoxicity in transgenic Drosophila models of familial British and Danish dementia.Molecular neurodegeneration · 2014Article
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Authors and funding
16 authors at 9 institutions in 6 countries.
Funding
Abstract
Familial Danish dementia (FDD) is a progressive neurodegenerative disease with cerebral deposition of Dan-amyloid (ADan), neuroinflammation, and neurofibrillary tangles, hallmark characteristics remarkably similar to those in Alzheimer's disease (AD). We have generated transgenic (tg) mouse models of familial Danish dementia that exhibit the age-dependent deposition of ADan throughout the brain with associated amyloid angiopathy, microhemorrhage, neuritic dystrophy, and neuroinflammation. Tg mice are impaired in the Morris water maze and exhibit increased anxiety in the open field. When crossed with TauP301S tg mice, ADan accumulation promotes neurofibrillary lesions, in all aspects similar to the Tau lesions observed in crosses between beta-amyloid (Abeta)-depositing tg mice and TauP301S tg mice. Although these observations argue for shared mechanisms of downstream pathophysiology for the sequence-unrelated ADan and Abeta peptides, the lack of codeposition of the two peptides in crosses between ADan- and Abeta-depositing mice points also to distinguishing properties of the peptides. Our results support the concept of the amyloid hypothesis for AD and related dementias, and suggest that different proteins prone to amyloid formation can drive strikingly similar pathogenic pathways in the brain.
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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.