ReviewHuman molecular genetics2009
Down syndrome--recent progress and future prospects.
Review in Human molecular genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
95 citing papers in PubMed, 1 synthesis or guideline pooled it, 243 citations in OpenAlex.
- Meta-analysis of heterogeneous Down Syndrome data reveals consistent genome-wide dosage effects related to neurological processes.BMC genomics · 2011Pooled it
- Parental and grandparental age in relation to Down syndrome risk and congenital heart disease in affected children: a case-control study in Peru.European journal of pediatrics · 2026Article
- Metabolomic Profiles in Down Syndrome: A Scoping Review of Convergent and Context-Dependent Patterns.Journal of intellectual disability research : JIDR · 2026Article
- The forgotten population: Early-onset Alzheimer's in people with Down syndrome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- The role of Goldilocks protein kinase DYRK1A in embryonic development.Developmental biology · 2025Review
- Exploratory analysis of the proteomic profile in plasma in adults with Down syndrome in the context of Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Reduction of Cystatin B results in increased cathepsin B activity in disomic but not Trisomy 21 human cellular and mouse models.PloS one · 2025Article
- What Can We Learn About Alzheimer's Disease from People with Down Syndrome?Current topics in behavioral neurosciences · 2025Review
- FastGrow: on-the-fly growing and its application to DYRK1A.Journal of computer-aided molecular design · 2022Article
- Rodent Modeling of Alzheimer's Disease in Down Syndrome:Frontiers in neuroscience · 2022Review
- MultimodalFrontiers in medicine · 2022Article
- Novel Approaches to an Integrated Route for Trisomy 21 Evaluation.Biomolecules · 2021Review
- Diabetic Kinome Inhibitors-A New Opportunity for β-Cells Restoration.International journal of molecular sciences · 2021Review
- Current Analysis of Skeletal Phenotypes in Down Syndrome.Current osteoporosis reports · 2021Review
- Metabolic Diseases and Down Syndrome: How Are They Linked Together?Biomedicines · 2021Review
- Intellectual disability: dendritic anomalies and emerging genetic perspectives.Acta neuropathologica · 2021Review
- Impact of the Olig Family on Neurodevelopmental Disorders.Frontiers in neuroscience · 2021Review
- Ten Reasons Why People With Down Syndrome are Protected From the Development of Most Solid Tumors -A Review.Frontiers in genetics · 2021Review
- Article
- ViceCT and whiceCT for simultaneous high-resolution visualization of craniofacial, brain and ventricular anatomy from micro-computed tomography.Scientific reports · 2020Article
35 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Down syndrome (DS) is caused by trisomy of chromosome 21 (Hsa21) and is associated with a number of deleterious phenotypes, including learning disability, heart defects, early-onset Alzheimer's disease and childhood leukaemia. Individuals with DS are affected by these phenotypes to a variable extent; understanding the cause of this variation is a key challenge. Here, we review recent research progress in DS, both in patients and relevant animal models. In particular, we highlight exciting advances in therapy to improve cognitive function in people with DS and the significant developments in understanding the gene content of Hsa21. Moreover, we discuss future research directions in light of new technologies. In particular, the use of chromosome engineering to generate new trisomic mouse models and large-scale studies of genotype-phenotype relationships in patients are likely to significantly contribute to the future understanding of DS.
Indexed as
Identifiers
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.