ReviewFree radical biology & medicine2018
Disturbance of redox homeostasis in Down Syndrome: Role of iron dysmetabolism.
Review in Free radical biology & medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
What it found
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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
34 citing papers in PubMed, 54 citations in OpenAlex.
- Metabolic breakdown: Linking insulin resistance and mitochondrial dysfunction to neurodegeneration in Alzheimer's disease.Neural regeneration research · 2026Article
- The placental effects of trisomy for human chromosome 21 orthologs in four mouse models of Down syndrome.Biology open · 2025Article
- Insulin resistance: fueling oxidative stress and neurodegeneration.Journal of neural transmission (Vienna, Austria : 1996) · 2025Review
- Salivary lactoferrin levels in Down Syndrome: a case-control study.Brain, behavior, & immunity - health · 2025Article
- Oxidative stress biomarkers as novel screening tools for trisomy 21: a case-control study.BMC pregnancy and childbirth · 2025Article
- Metformin modulates oxidative stress via activation of AMPK/NF-κB signaling in Trisomy 21 fibroblasts: anFrontiers in molecular biosciences · 2025Article
- Superoxide dismutase and neurological disorders.IBRO neuroscience reports · 2024Review
- Down Syndrome Biobank Consortium: A perspective.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- The Role of Tau Pathology in Alzheimer's Disease and Down Syndrome.Journal of clinical medicine · 2024Review
- Autophagy is a promising process for linking inflammation and redox homeostasis in Down syndrome.Frontiers in pharmacology · 2024Review
- Zinc metabolism and its role in immunity status in subjects with trisomy 21: chromosomal dosage effect.Frontiers in immunology · 2024Article
- The Role of Oxidative Stress in Trisomy 21 Phenotype.Cellular and molecular neurobiology · 2023Review
- The Impact of Oxidative Stress on Pediatrics Syndromes.Antioxidants (Basel, Switzerland) · 2022Review
- Biochemical Discrimination of the Down Syndrome-Related Metabolic and Oxidative/Nitrosative Stress Alterations from the Physiologic Age-Related Changes through the Targeted Metabolomic Analysis of Serum.Antioxidants (Basel, Switzerland) · 2022Article
- Catechins as a Potential Dietary Supplementation in Prevention of Comorbidities Linked with Down Syndrome.Nutrients · 2022Review
- Association between the Concentrations of Essential and Toxic Elements in Mid-Trimester Amniotic Fluid and Fetal Chromosomal Abnormalities in Pregnant Polish Women.Diagnostics (Basel, Switzerland) · 2022Article
- Future Perspectives in Oxidative Stress in Trisomy 13 and 18 Evaluation.Journal of clinical medicine · 2022Review
- Efficacy and Safety of Q10 Ubiquinol With Vitamins B and E in Neurodevelopmental Disorders: A Retrospective Chart Review.Frontiers in psychiatry · 2022Article
- Novel Approaches to an Integrated Route for Trisomy 21 Evaluation.Biomolecules · 2021Review
- N-Acetylcysteine prevents amyloid-β secretion in neurons derived from human pluripotent stem cells with trisomy 21.Scientific reports · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 3 countries.
Funding
Abstract
Down Syndrome (DS) is the most common genetic form of intellectual disability that leads in the majority of cases to development of early-onset Alzheimer-like dementia (AD). The neuropathology of DS has several common features with AD including alteration of redox homeostasis, mitochondrial deficits, and inflammation among others. Interestingly, some of the genes encoded by chromosome 21 are responsible of increased oxidative stress (OS) conditions that are further exacerbated by decreased antioxidant defense. Previous studies from our groups showed that accumulation of oxidative damage is an early event in DS neurodegeneration and that oxidative modifications of selected proteins affects the integrity of the protein degradative systems, antioxidant response, neuronal integrity and energy metabolism. In particular, the current review elaborates recent findings demonstrating the accumulation of oxidative damage in DS and we focus attention on specific deregulation of iron metabolism, which affects both the central nervous system and the periphery. Iron dysmetabolism is a well-recognized factor that contributes to neurodegeneration; thus we opine that better understanding how and to what extent the concerted loss of iron dyshomeostasis and increased OS occur in DS could provide novel insights for the development of therapeutic strategies for the treatment of Alzheimer-like dementia.
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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.