Activation of p53 in Down Syndrome and in the Ts65Dn mouse brain is associated with a pro-apoptotic phenotype
Open accessAbstract
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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Oxidative damage to MnSOD and p53 in MCI and AD brain may affect their interplay, contributing to apoptosis and to the spread of ROS and subsequent oxidative damage beyond the subcellular localization of the mitochondria.
“but oxidative damage to MnSOD and p53 in MCI and AD brain may affect this interplay, which contributes to apoptosis [93] and to the spread of ROS and subsequent oxidative damage beyond the subcellular localization of the mitochondria.”
From Mitochondrial Oxidative and Nitrosative Stress and Alzheimer Disease (2020) · cites this paper as [93]
The Discussion (page not provided) links oxidative stress and p53 activity to a pro-apoptotic phenotype in Down syndrome brains with AD pathology, supporting the apoptosis portion of the citation. It does not establish oxidative damage to both MnSOD and p53, or their interplay, in MCI and AD brains. The claim about ROS spreading beyond mitochondria is also not addressed, though it appears after the citation in the printed sentence. (LLM, conf=0.84)
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- Authors
- Tramutola, A., Pupo, G., Di Domenico, F., Barone, E., Arena, A., Lanzillotta, C., Broekaart, D., Blarzino, C., Head, E., Butterfield, D. A., & Perluigi, M.
- Affiliations
- Sapienza University of Rome (IT)
- Department of Biochemical Sciences, Sapienza University of Rome, Italy
- Universidad Autónoma de Chile (CL)
- University of Amsterdam (NL)
- University of Kentucky (US)
- ORCID
- Venue
- Journal of Alzheimer s Disease
- Publisher
- SAGE Publications
- Published
- 2016-04-26
- Volume
- 52
- Issue
- 1
- Pages
- 359-371
- ISSN
- 1387-2877 (ISSN-L)
- 1875-8908
- PMC
- PMC4968087
- OpenAlex
- W2296991500
- Cited by
- 40
- References
- 70
- Citations by year
- 2026: 2 · 2025: 1 · 2024: 4 · 2022: 3 · 2021: 7 · 2020: 6 · 2019: 5 · 2018: 6 · 2017: 2 · 2016: 4
- FWCI
- 5.62
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Journal of Alzheimer s Disease (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- IRIS Research product catalog (Sapienza University of Rome) (submittedVersion, cc-by-nc-nd)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- European Commission (2007–2013, FP7 2007-2013, 624341, FP7/2007)
- National Institutes of Health (FP7/2007-2013)
- National Institute on Aging (P30AG028383, P50AG016573)
- National Institute of Child Health and Human Development
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD064993)
- Topics
- Health Sciences › Medicine › Public Health, Environmental and Occupational Health › Down syndrome and intellectual disability research
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Keywords
- Down syndrome, p53 activation
- MeSH terms
- Acetylation, Alzheimer Disease, Animals, Disease Models, Animal, Down Syndrome, Female, Frontal Lobe, Humans, Male, Mice, Inbred C3H, Mice, Inbred C57BL, Mice, Transgenic, Middle Aged, Phenotype, Phosphorylation, Blotting, Western, Tumor Suppressor Protein p53, Apoptosis, Immunoprecipitation, Young Adult
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