ArticleBiochimica et biophysica acta2012
Association between frontal cortex oxidative damage and beta-amyloid as a function of age in Down syndrome.
Article in Biochimica et biophysica acta, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 1 of them a synthesis that pooled it.
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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.
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.
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Who cites it
73 citing papers in PubMed, 1 synthesis or guideline pooled it, 119 citations in OpenAlex.
- Attention skills, learning and academic abilities in children and adolescents with genetic disorders: a systematic review.Frontiers in psychology · 2025Pooled it
- Intraindividual cognitive variability predicts amyloid beta, tau PET, and dementia conversion in Down syndrome: a potential marker of cognitive resilience.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- The association between APOE 𝜀4 carrierships and the detection of amyloid positivity using an Alzheimer's disease proteomic blood test in asymptomatic Down syndrome.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Adaptation of the Direct Assessment of Functional Status (DAFS):a new tool to assess functional changes in people with Down syndrome.Dementia & neuropsychologia · 2026Article
- Telomere Biology, Erosion, and Age-Related Conditions: Insights from Down Syndrome and Other Telomere-Associated Disorders.Molecular neurobiology · 2025Review
- Proteome Signature of Alzheimer-Like Phenotypes in Frontal Cortices From Young and Old Individuals With Down Syndrome.Molecular neurobiology · 2025Article
- What Can We Learn About Alzheimer's Disease from People with Down Syndrome?Current topics in behavioral neurosciences · 2025Review
- Oxidative damage in neurodegeneration: roles in the pathogenesis and progression of Alzheimer disease.Physiological reviews · 2024Review
- The Role of Oxidative Stress in Trisomy 21 Phenotype.Cellular and molecular neurobiology · 2023Review
- Cellular Stress Response (Hormesis) in Response to Bioactive Nutraceuticals with Relevance to Alzheimer Disease.Antioxidants & redox signaling · 2023Review
- Intranasal Administration of KYCCSRK Peptide Rescues Brain Insulin Signaling Activation and Reduces Alzheimer's Disease-like Neuropathology in a Mouse Model for Down Syndrome.Antioxidants (Basel, Switzerland) · 2023Article
- Pyrazolines as potential anti-Alzheimer's agents: DFT, molecular docking, enzyme inhibition and pharmacokinetic studies.RSC medicinal chemistry · 2022Article
- Aβ and tau prions feature in the neuropathogenesis of Down syndrome.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Neurogenesis and neuronal differentiation in the postnatal frontal cortex in Down syndrome.Acta neuropathologica communications · 2022Article
- Impact of increased APP gene dose in Down syndrome and the Dp16 mouse model.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2022Article
- Developmental Neuropathology and Neurodegeneration of Down Syndrome: Current Knowledge in Humans.Frontiers in cell and developmental biology · 2022Review
- Alzheimer's disease associated with Down syndrome: a genetic form of dementia.The Lancet. Neurology · 2021Review
- N-Acetylcysteine prevents amyloid-β secretion in neurons derived from human pluripotent stem cells with trisomy 21.Scientific reports · 2021Article
- Stress Responses in Down Syndrome Neurodegeneration: State of the Art and Therapeutic Molecules.Biomolecules · 2021Review
- Astrocytes in Down Syndrome Across the Lifespan.Frontiers in cellular neuroscience · 2021Review
13 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 2 countries.
Funding
Abstract
Down syndrome (DS) is the most common genetic cause of intellectual disability in children, and the number of adults with DS reaching old age is increasing. By the age of 40 years, virtually all people with DS have sufficient neuropathology for a postmortem diagnosis of Alzheimer disease (AD). Trisomy 21 in DS leads to an overexpression of many proteins, of which at least two are involved in oxidative stress and AD: superoxide dismutase 1 (SOD1) and amyloid precursor protein (APP). In this study, we tested the hypothesis that DS brains with neuropathological hallmarks of AD have more oxidative and nitrosative stress than those with DS but without significant AD pathology, as compared with similarly aged-matched non-DS controls. The frontal cortex was examined in 70 autopsy cases (n=29 control and n=41 DS). By ELISA, we quantified soluble and insoluble Aβ40 and Aβ42, as well as oligomers. Oxidative and nitrosative stress levels (protein carbonyls, 4-hydroxy-2-trans-nonenal (HNE)-bound proteins, and 3-nitrotyrosine) were measured by slot-blot. We found that soluble and insoluble amyloid beta peptide (Aβ) and oligomers increase as a function of age in DS frontal cortex. Of the oxidative stress markers, HNE-bound proteins were increased overall in DS. Protein carbonyls were correlated with Aβ40 levels. These results suggest that oxidative damage, but not nitrosative stress, may contribute to the onset and progression of AD pathogenesis in DS. Conceivably, treatment with antioxidants may provide a point of intervention to slow pathological alterations in 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.