ReviewProteomics. Clinical applications2014
Unraveling the complexity of neurodegeneration in brains of subjects with Down syndrome: insights from proteomics.
Review in Proteomics. Clinical applications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 59 citations in OpenAlex.
- Growth Assessment and Nutritional Status in Children with Congenital Adrenal Hyperplasia-A Cross-Sectional Study from a Vietnamese Tertiary Pediatric Center.Diagnostics (Basel, Switzerland) · 2025Article
- Mitochondrial Imbalance in Down Syndrome: A Driver of Accelerated Brain Aging?Aging and disease · 2025Review
- Risk of Alzheimer's disease in Down syndrome: Insights gained by multi-omics.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Review
- Oxidative damage in neurodegeneration: roles in the pathogenesis and progression of Alzheimer disease.Physiological reviews · 2024Review
- Clinical Management and Therapy of Precocious Puberty in the Sapienza University Pediatrics Hospital of Rome, Italy.Children (Basel, Switzerland) · 2023Review
- Review
- Oxidative-Stress-Associated Proteostasis Disturbances and Increased DNA Damage in the Hippocampal Granule Cells of the Ts65Dn Model of Down Syndrome.Antioxidants (Basel, Switzerland) · 2022Article
- The Impact of Oxidative Stress on Pediatrics Syndromes.Antioxidants (Basel, Switzerland) · 2022Review
- Neurogenesis and neuronal differentiation in the postnatal frontal cortex in Down syndrome.Acta neuropathologica communications · 2022Article
- An Autoantigen Atlas From Human Lung HFL1 Cells Offers Clues to Neurological and Diverse Autoimmune Manifestations of COVID-19.Frontiers in immunology · 2022Article
- MultimodalFrontiers in medicine · 2022Article
- An Autoantigen Atlas from Human Lung HFL1 Cells Offers Clues to Neurological and Diverse Autoimmune Manifestations of COVID-19.bioRxiv : the preprint server for biology · 2021Article
- Astrocytes in Down Syndrome Across the Lifespan.Frontiers in cellular neuroscience · 2021Review
- The Dysregulation of OGT/OGA Cycle Mediates Tau and APP Neuropathology in Down Syndrome.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Article
- Proteomics Study of Peripheral Blood Mononuclear Cells in Down Syndrome Children.Antioxidants (Basel, Switzerland) · 2020Article
- The BACH1/Nrf2 Axis in Brain in Down Syndrome and Transition to Alzheimer Disease-Like Neuropathology and Dementia.Antioxidants (Basel, Switzerland) · 2020Review
- Antioxidants in Down Syndrome: From Preclinical Studies to Clinical Trials.Antioxidants (Basel, Switzerland) · 2020Review
- Prenatal Hypoxia and Placental Oxidative Stress: Insights from Animal Models to Clinical Evidences.Antioxidants (Basel, Switzerland) · 2020Review
- Immune Dysregulation in Children With Down Syndrome.Frontiers in pediatrics · 2020Review
- Proteomic profiles of incident mild cognitive impairment and Alzheimer's disease among adults with Down syndrome.Alzheimer's & dementia (Amsterdam, Netherlands) · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
Abstract
Down syndrome (DS) is one of the most common genetic causes of intellectual disability characterized by multiple pathological phenotypes, among which neurodegeneration is a key feature. The neuropathology of DS is complex and likely results from impaired mitochondrial function, increased oxidative stress, and altered proteostasis. After the age of 40 years, many (most) DS individuals develop a type of dementia that closely resembles that of Alzheimer's disease with deposition of senile plaques and neurofibrillary tangles. A number of studies demonstrated that increased oxidative damage, accumulation of damaged/misfolded protein aggregates, and dysfunction of intracellular degradative systems are critical events in the neurodegenerative processes. This review summarizes the current knowledge that demonstrates a “chronic” condition of oxidative stress in DS pointing to the putative molecular pathways that could contribute to accelerate cognition and memory decline. Proteomics and redox proteomics studies are powerful tools to unravel the complexity of DS phenotypes, by allowing to identifying protein expression changes and oxidative PTMs that are proved to be detrimental for protein function. It is reasonable to suggest that changes in the cellular redox status in DS neurons, early from the fetal period, could provide a fertile environment upon which increased aging favors neurodegeneration. Thus, after a critical age, DS neuropathology can be considered a human model of early Alzheimer's disease and could contribute to understanding the overlapping mechanisms that lead from normal aging to development of 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.