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p53-dependent SIRT6 expression protects Aβ42-induced DNA damage
Eun Sun Jung1, Hyunjung Choi1, Hyundong Song1
1Department of Biochemistry &Biomedical Science, Seoul National University College of Medicine, Seoul 03080, Republic of Korea.
Scientific Reports
|May 10, 2016
Summary
Alzheimer's disease involves reduced SIRT6 protein. This study shows p53-dependent SIRT6 protects against amyloid-beta 42 induced DNA damage, suggesting SIRT6 as a therapeutic target for Alzheimer's disease.
Area of Science:
- Neuroscience
- Genetics
- Molecular Biology
Background:
- Alzheimer's disease (AD) is a leading cause of dementia linked to aging.
- Understanding cellular changes in aging is crucial for neurodegenerative disease research.
- SIRT6, an anti-aging gene, has an unknown role in AD pathogenesis.
Purpose of the Study:
- To investigate the relationship between SIRT6 and Alzheimer's disease.
- To determine the role of SIRT6 in cellular response to amyloid-beta 42.
Main Methods:
- Compared SIRT6 protein levels in AD mouse models and human patients.
- Examined the effect of amyloid-beta 42 on SIRT6 expression and DNA damage in neuronal cells.
- Investigated the role of p53 in regulating SIRT6 and protecting against amyloid-beta 42 toxicity.
Main Results:
- SIRT6 protein levels were decreased in AD brains and mouse models.
- Amyloid-beta 42 reduced SIRT6 expression and caused DNA damage.
- Overexpressing SIRT6 protected neurons from amyloid-beta 42-induced DNA damage.
- p53 upregulation prevented SIRT6 reduction and DNA damage caused by amyloid-beta 42.
Conclusions:
- p53-dependent SIRT6 expression safeguards cells against amyloid-beta 42-induced DNA damage.
- SIRT6 emerges as a potential therapeutic target for Alzheimer's disease treatment.
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