ArticlePloS one2013
Increased tau phosphorylation and tau truncation, and decreased synaptophysin levels in mutant BRI2/tau transgenic mice.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 25 citations in OpenAlex.
- Pathological mechanisms of motor dysfunction in familial Danish dementia: insights from a knock-in rat model.Journal of neuroinflammation · 2025Article
- Phosphorylation at serine 214 correlates with tau seeding activity in an age-dependent manner in two mouse models for tauopathies and is required for tau transsynaptic propagation.Journal of Alzheimer's disease : JAD · 2025Article
- Resistance training boosts lactate transporters and synaptic proteins in insulin-resistance mice.Heliyon · 2024Article
- Genetic forms of tauopathies: inherited causes and implications of Alzheimer's disease-like TAU pathology in primary and secondary tauopathies.Journal of neurology · 2024Review
- Alzheimer's disease is an inherent, natural part of human brain aging: an integrated perspective.Free neuropathology · 2022Article
- The Amyloid-Tau-Neuroinflammation Axis in the Context of Cerebral Amyloid Angiopathy.International journal of molecular sciences · 2019Review
- Cornel iridoid glycoside induces autophagy to protect against tau oligomer neurotoxicity induced by the activation of glycogen synthase kinase-3β.Journal of natural medicines · 2019Article
- Tau as a mediator of neurotoxicity associated to cerebral amyloid angiopathy.Acta neuropathologica communications · 2019Article
- DA-JC1 improves learning and memory by antagonizing Aβ31-35-induced circadian rhythm disorder.Molecular brain · 2019Article
- Tracking Effects of SIL1 Increase: Taking a Closer Look Beyond the Consequences of Elevated Expression Level.Molecular neurobiology · 2018Article
- Article
- Amyloid and intracellular accumulation of BRINeurobiology of aging · 2017Article
- Co-immunoprecipitation with Tau Isoform-specific Antibodies Reveals Distinct Protein Interactions and Highlights a Putative Role for 2N Tau in Disease.The Journal of biological chemistry · 2016Article
- Lessons from a Rare Familial Dementia: Amyloid and Beyond.Journal of Parkinson's disease and Alzheimer's disease · 2015Article
- BRI2 ectodomain affects Aβ42 fibrillation and tau truncation in human neuroblastoma cells.Cellular and molecular life sciences : CMLS · 2015Article
- Amyloid peptides ABri and ADan show differential neurotoxicity in transgenic Drosophila models of familial British and Danish dementia.Molecular neurodegeneration · 2014Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Familial Danish dementia (FDD) is an autosomal dominant neurodegenerative disease caused by a 10-nucleotide duplication-insertion in the BRI(2) gene. FDD is clinically characterized by loss of vision, hearing impairment, cerebellar ataxia and dementia. The main neuropathologic findings in FDD are the deposition of Danish amyloid (ADan) and the presence of neurofibrillary tangles (NFTs). Here we investigated tau accumulation and truncation in double transgenic (Tg-FDD-Tau) mice generated by crossing transgenic mice expressing human Danish mutant BRI(2) (Tg-FDD) with mice expressing human 4-repeat mutant Tau-P301S (Tg-Tau). Compared to Tg-Tau mice, we observed a significant enhancement of tau deposition in Tg-FDD-Tau mice. In addition, a significant increase in tau cleaved at aspartic acid (Asp) 421 was observed in Tg-FDD-Tau mice. Tg-FDD-Tau mice also showed a significant decrease in synaptophysin levels, occurring before widespread deposition of fibrillar ADan and tau can be observed. Thus, the presence of soluble ADan/mutant BRI(2) can lead to significant changes in tau metabolism and synaptic dysfunction. Our data provide new in vivo insights into the pathogenesis of FDD and the pathogenic pathway(s) by which amyloidogenic peptides, regardless of their primary amino acid sequence, can cause neurodegeneration.
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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.