ArticleScientific reports2021
Genetic dissection of down syndrome-associated alterations in APP/amyloid-β biology using mouse models.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 20 papers.
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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
20 citing papers in PubMed, 25 citations in OpenAlex.
- APOE and genetic risk variants influence Alzheimer's disease onset in carriers of an extra copy of APP, with and without Down syndrome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Necroptosis in Down Syndrome.Cell death & disease · 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
- Use of anti-amyloid-β monoclonal antibodies in persons with Down syndrome Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Chromosome duplication causes premature aging via defects in ribosome quality control.PLoS biology · 2025Article
- Interferon signaling modulates Down syndrome-associated Alzheimer's disease pathology in a mouse model.iScience · 2025Article
- Advancements in machine learning and biomarker integration for prenatal Down syndrome screening.Turkish journal of obstetrics and gynecology · 2025Article
- What Can We Learn About Alzheimer's Disease from People with Down Syndrome?Current topics in behavioral neurosciences · 2025Review
- Reduction of Cystatin B results in increased cathepsin B activity in disomic but not Trisomy 21 human cellular and mouse models.PloS one · 2025Article
- Genetic forms of tauopathies: inherited causes and implications of Alzheimer's disease-like TAU pathology in primary and secondary tauopathies.Journal of neurology · 2024Review
- Lamivudine modulates the expression of neurological impairment-related genes and LINE-1 retrotransposons in brain tissues of a Down syndrome mouse model.Frontiers in aging neuroscience · 2024Article
- Dissecting the contribution of human chromosome 21 syntenic regions to recognition memory processes in adult and aged mouse models of Down syndrome.Frontiers in behavioral neuroscience · 2024Article
- Cathepsin B abundance, activity and microglial localisation in Alzheimer's disease-Down syndrome and early onset Alzheimer's disease; the role of elevated cystatin B.Acta neuropathologica communications · 2023Article
- Unraveling Molecular and Genetic Insights into Neurodegenerative Diseases: Advances in Understanding Alzheimer's, Parkinson's, and Huntington's Diseases and Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2023Review
- The Global Deterioration Scale for Down Syndrome Population (GDS-DS): A Rating Scale to Assess the Progression of Alzheimer's Disease.International journal of environmental research and public health · 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
- 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
- Oxidative Stress in Down and Williams-Beuren Syndromes: An Overview.Molecules (Basel, Switzerland) · 2021Review
- From Neurodevelopmental to Neurodegenerative Disorders: The Vascular Continuum.Frontiers in aging neuroscience · 2021Review
Corrections and comments
- Erratum issued
Authors and funding
13 authors at 7 institutions in 2 countries.
Funding
Abstract
Individuals who have Down syndrome (caused by trisomy of chromosome 21), have a greatly elevated risk of early-onset Alzheimer's disease, in which amyloid-β accumulates in the brain. Amyloid-β is a product of the chromosome 21 gene APP (amyloid precursor protein) and the extra copy or 'dose' of APP is thought to be the cause of this early-onset Alzheimer's disease. However, other chromosome 21 genes likely modulate disease when in three-copies in people with Down syndrome. Here we show that an extra copy of chromosome 21 genes, other than APP, influences APP/Aβ biology. We crossed Down syndrome mouse models with partial trisomies, to an APP transgenic model and found that extra copies of subgroups of chromosome 21 gene(s) modulate amyloid-β aggregation and APP transgene-associated mortality, independently of changing amyloid precursor protein abundance. Thus, genes on chromosome 21, other than APP, likely modulate Alzheimer's disease in people who have Down syndrome.
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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 Socratic graph.