ArticleNeurobiology of aging2012
Altered regulation of tau phosphorylation in a mouse model of down syndrome aging.
Article in Neurobiology of aging, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 54 citations in OpenAlex.
- Leucettinib-21 decreases dosage effects of DYRK1A in human trisomy 21 induced pluripotent stem cell-derived neural cells.Disease models & mechanisms · 2026Article
- Age-related behavioral and molecular landmarks in new mouse models for studying Alzheimer's disease in Down syndrome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Loss of Proteostasis and Early-Onset Neurodegeneration in Down Syndrome: From Mechanisms to Interventions.Antioxidants (Basel, Switzerland) · 2026Review
- Leucettinib-21 decreases dosage effects of DYRK1A in human trisomy 21 iPSC-derived neural cells.bioRxiv : the preprint server for biology · 2026Article
- Amyloid-β peptide signature associated with cerebral amyloid angiopathy in familial Alzheimer's disease with APPdup and Down syndrome.Acta neuropathologica · 2024Article
- Targeted Dephosphorylation of Tau by Phosphorylation Targeting Chimeras (PhosTACs) as a Therapeutic Modality.Journal of the American Chemical Society · 2023Article
- Modeling Alzheimer's disease related phenotypes in the Ts65Dn mouse: impact of age on Aβ, Tau, pTau, NfL, and behavior.Frontiers in neuroscience · 2023Article
- Genetic Mapping of APP and Amyloid-β Biology Modulation by Trisomy 21.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- The accumulation of copper in the brain of Down syndrome promotes oxidative stress: possible mechanism underlying cognitive impairment.Journal of clinical biochemistry and nutrition · 2022Article
- Cell models for Down syndrome-Alzheimer's disease research.Neuronal signaling · 2022Review
- Rodent Modeling of Alzheimer's Disease in Down Syndrome:Frontiers in neuroscience · 2022Review
- Phosphorylated tau targeted small-molecule PROTACs for the treatment of Alzheimer's disease and tauopathies.Biochimica et biophysica acta. Molecular basis of disease · 2021Review
- The effects of Cstb duplication on APP/amyloid-β pathology and cathepsin B activity in a mouse model.PloS one · 2021Article
- Article
- Cellular polyamines condense hyperphosphorylated Tau, triggering Alzheimer's disease.Scientific reports · 2020Article
- Downregulated Wnt/β-catenin signalling in the Down syndrome hippocampus.Scientific reports · 2019Article
- DYRK1A Overexpression Alters Cognition and Neural-Related Proteomic Pathways in the Hippocampus That Are Rescued by Green Tea Extract and/or Environmental Enrichment.Frontiers in molecular neuroscience · 2019Article
- Trisomy of human chromosome 21 enhances amyloid-β deposition independently of an extra copy of APP.Brain : a journal of neurology · 2018Article
- DYRK1A inhibition and cognitive rescue in a Down syndrome mouse model are induced by new fluoro-DANDY derivatives.Scientific reports · 2018Article
- In vivo and ex vivo analyses of amyloid toxicity in the Tc1 mouse model of Down syndrome.Journal of psychopharmacology (Oxford, England) · 2018Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Down syndrome (DS) results from trisomy of human chromosome 21 (Hsa21) and is associated with an increased risk of Alzheimer's disease (AD). Here, using the unique transchromosomic Tc1 mouse model of DS we investigate the influence of trisomy of Hsa21 on the protein tau, which is hyperphosphorylated in Alzheimer's disease. We show that in old, but not young, Tc1 mice increased phosphorylation of tau occurs at a site suggested to be targeted by the Hsa21 encoded kinase, dual-specificity tyrosine-(Y)-phosphorylation regulated kinase 1A (DYRK1A). We show that DYRK1A is upregulated in young and old Tc1 mice, but that young trisomic mice may be protected from accumulating aberrantly phosphorylated tau. We observe that the key tau kinase, glycogen synthase kinase3-β (GSK-3β) is aberrantly phosphorylated at an inhibitory site in the aged Tc1 brain which may reduce total glycogen synthase kinase3-β activity. It is possible that a similar mechanism may also occur in people with DS.
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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.