ArticleNeurobiology of aging2017
Candidate gene analysis for Alzheimer's disease in adults with Down syndrome.
Article in Neurobiology of aging, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 34 citations in OpenAlex.
- Genome-wide association analyses identify candidate loci for amyloid imaging and plasma biomarkers in adults with Down syndrome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Pooled it
- MARK4 enhances stress granule formation under oxidative stress and increases tau accumulation.FEBS open bio · 2026Article
- The Wnt/β-catenin pathway maintains homeostasis of amniocytes in Down syndrome.BMC molecular and cell biology · 2026Article
- Genome-wide association of tau neuroimaging and plasma biomarkers in adults with Down syndrome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- What Can We Learn About Alzheimer's Disease from People with Down Syndrome?Current topics in behavioral neurosciences · 2025Review
- Spatial and single-nucleus transcriptomic analysis of genetic and sporadic forms of Alzheimer's disease.Nature genetics · 2024Article
- Whole genome-wide sequence analysis of long-lived families (Long-Life Family Study) identifies MTUS2 gene associated with late-onset Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Endosomal structure and APP biology are not altered in a preclinical mouse cellular model of Down syndrome.PloS one · 2022Article
- The Clinical and Neuropathological Features of Sporadic (Late-Onset) and Genetic Forms of Alzheimer's Disease.Journal of clinical medicine · 2021Review
- Genetic dissection of down syndrome-associated alterations in APP/amyloid-β biology using mouse models.Scientific reports · 2021Article
- Alzheimer's risk and quality of life: History of Down syndrome as a case in point.Alzheimer's & dementia (Amsterdam, Netherlands) · 2021Article
- The Alzheimer's Biomarker Consortium-Down Syndrome: Rationale and methodology.Alzheimer's & dementia (Amsterdam, Netherlands) · 2020Review
- Proteomic profiles of incident mild cognitive impairment and Alzheimer's disease among adults with Down syndrome.Alzheimer's & dementia (Amsterdam, Netherlands) · 2020Article
- Proteomic profiles of prevalent mild cognitive impairment and Alzheimer's disease among adults with Down syndrome.Alzheimer's & dementia (Amsterdam, Netherlands) · 2020Article
- Genetic and epigenetic pathways in Down syndrome: Insights to the brain and immune system from humans and mouse models.Progress in brain research · 2020Review
- Dementia in Down syndrome: unique insights for Alzheimer disease research.Nature reviews. Neurology · 2019Review
- Exosomal biomarkers in Down syndrome and Alzheimer's disease.Free radical biology & medicine · 2018Review
- Individualized estimated years from onset of Alzheimer's disease- related decline for adults with Down syndrome.Alzheimer's & dementia (Amsterdam, Netherlands)Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 3 institutions in 1 country.
Funding
Abstract
Individuals with Down syndrome (DS) overexpress many genes on chromosome 21 due to trisomy and have high risk of dementia due to the Alzheimer's disease (AD) neuropathology. However, there is a wide range of phenotypic differences (e.g., age at onset of AD, amyloid β levels) among adults with DS, suggesting the importance of factors that modify risk within this particularly vulnerable population, including genotypic variability. Previous genetic studies in the general population have identified multiple genes that are associated with AD. This study examined the contribution of polymorphisms in these genes to the risk of AD in adults with DS ranging from 30 to 78 years of age at study entry (N = 320). We used multiple logistic regressions to estimate the likelihood of AD using single-nucleotide polymorphisms (SNPs) in candidate genes, adjusting for age, sex, race/ethnicity, level of intellectual disability and APOE genotype. This study identified multiple SNPs in APP and CST3 that were associated with AD at a gene-wise level empirical p-value of 0.05, with odds ratios in the range of 1.5-2. SNPs in MARK4 were marginally associated with AD. CST3 and MARK4 may contribute to our understanding of potential mechanisms where CST3 may contribute to the amyloid pathway by inhibiting plaque formation, and MARK4 may contribute to the regulation of the transition between stable and dynamic microtubules.
Indexed as
Identifiers
What Socratic 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 Socratic graph.