ArticleJournal of Alzheimer's disease : JAD2016
Activation of p53 in Down Syndrome and in the Ts65Dn Mouse Brain is Associated with a Pro-Apoptotic Phenotype.
Article in Journal of Alzheimer's disease : JAD, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 38 citations in OpenAlex.
- Necroptosis in Down Syndrome.Cell death & disease · 2026Article
- Aneuploidy generates enhanced nucleotide dependency and sensitivity to metabolic perturbation.Genes & development · 2025Article
- Analysis of genotype effects and inter-individual variability in iPSC-derived trisomy 21 neural progenitor cells.Human molecular genetics · 2025Article
- Altered Brain Cholesterol Machinery in a Down Syndrome Mouse Model: A Possible Common Feature with Alzheimer's Disease.Antioxidants (Basel, Switzerland) · 2024Article
- 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
- MicroRNA-668-3p regulates oxidative stress and cell damage induced by Aβ1-42 by targeting theAnnals of translational medicine · 2022Article
- Aberrant crosstalk between insulin signaling and mTOR in young Down syndrome individuals revealed by neuronal-derived extracellular vesicles.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2022Article
- 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
- A Novel Inhibitor Targeting NLRP3 Inflammasome Reduces Neuropathology and Improves Cognitive Function in Alzheimer's Disease Transgenic Mice.Journal of Alzheimer's disease : JAD · 2021Article
- Signalling Pathways Implicated in Alzheimer's Disease Neurodegeneration in Individuals with and without Down Syndrome.International journal of molecular sciences · 2020Review
- Mitochondrial Oxidative and Nitrosative Stress and Alzheimer Disease.Antioxidants (Basel, Switzerland) · 2020Review
- Antioxidants in Down Syndrome: From Preclinical Studies to Clinical Trials.Antioxidants (Basel, Switzerland) · 2020Review
- Cellular Senescence in Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2020Review
- A novel small molecular NLRP3 inflammasome inhibitor alleviates neuroinflammatory response following traumatic brain injury.Journal of neuroinflammation · 2019Article
- Down Syndrome, Obesity, Alzheimer's Disease, and Cancer: A Brief Review and Hypothesis.Brain sciences · 2018Review
- Early and Selective Activation and Subsequent Alterations to the Unfolded Protein Response in Down Syndrome Mouse Models.Journal of Alzheimer's disease : JAD · 2018Article
- Oxidative Stress, Amyloid-β Peptide, and Altered Key Molecular Pathways in the Pathogenesis and Progression of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2018Review
- Chronic MK-801 Application in Adolescence and Early Adulthood: A Spatial Working Memory Deficit in Adult Long-Evans Rats But No Changes in the Hippocampal NMDA Receptor Subunits.Frontiers in pharmacology · 2018Article
- mTOR in Down syndrome: Role in Aß and tau neuropathology and transition to Alzheimer disease-like dementia.Free radical biology & medicine · 2018Review
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 4 countries.
Funding
Abstract
Down syndrome (DS) is the most common genetic cause of intellectual disability, resulting from trisomy of chromosome 21. The main feature of DS neuropathology includes early onset of Alzheimer's disease (AD), with deposition of senile plaques and tangles. We hypothesized that apoptosis may be activated in the presence of AD neuropathology in DS, thus we measured proteins associated with upstream and downstream pathways of p53 in the frontal cortex from DS cases with and without AD pathology and from Ts65Dn mice, at different ages. We observed increased acetylation and phosphorylation of p53, coupled to reduced MDM2/p53 complex level and lower levels of SIRT1. Activation of p53 was associated with a number of targets (BAX, PARP1, caspase-3, p21, heat shock proteins, and PGC1α) that were modulated in both DS and DS/AD compared with age-matched controls. In particular, the most relevant changes (increased p-p53 and acetyl-p53 and reduced formation of MDM2/p53 complex) were found to be modified only in the presence of AD pathology in DS. In addition, a similar pattern of alterations in the p53 pathway was found in Ts65Dn mice. These results suggest that p53 may integrate different signals, which can result in a pro-apoptotic-phenotype contributing to AD neuropathology in people with DS.
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