Altered DNA base excision repair profile in brain tissue and blood in Alzheimer’s disease
Open accessAbstract
BACKGROUND: Alzheimer's disease (AD) is a progressive, multifactorial neurodegenerative disorder that is the main cause of dementia globally. AD is associated with increased oxidative stress, resulting from imbalance in production and clearance of reactive oxygen species (ROS). ROS can damage DNA and other macromolecules, leading to genome instability and disrupted cellular functions. Base excision repair (BER) plays a major role in repairing oxidative DNA lesions. Here, we compared the expression of BER components APE1, OGG1, PARP1 and Polβ in blood and postmortem brain tissue from patients with AD, mild cognitive impairment (MCI) and healthy controls (HC). RESULTS: BER mRNA levels were correlated to clinical signs and cerebrospinal fluid biomarkers for AD. Notably, the expression of BER genes was higher in brain tissue than in blood samples. Polβ mRNA and protein levels were significantly higher in the cerebellum than in the other brain regions, more so in AD patients than in HC. Blood mRNA levels of OGG1 was low and PARP1 high in MCI and AD. CONCLUSIONS: These findings reflect the oxidative stress-generating energy-consumption in the brain and the importance of BER in repairing these damage events. The data suggest that alteration in BER gene expression is an event preceding AD. The results link DNA repair in brain and blood to the etiology of AD at the molecular level and can potentially serve in establishing novel biomarkers, particularly in the AD prodromal phase.
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AD brains have decreased base-excision repair (BER) pathway activity.
“AD brains have been reported as having decreased base-excision repair (BER) pathway activity [87].”
From DNA repair deficiency and senescence in concussed professional athletes involved in contact sports (2019) · cites this paper as [87]
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- Authors
- Lillenes, M. S., Rabano, A., Støen, M., Riaz, T., Misaghian, D., Møllersen, L., Esbensen, Y., Günther, C.-C., Selnes, P., Stenset, V. T. V., Fladby, T., & Tønjum, T.
- Affiliations
- Oslo University Hospital (NO)
- University of Oslo (NO)
- Norwegian Computing Center (NO)
- Corresponding author
- Tønjum, Tone
- Venue
- Molecular Brain
- Published
- 2016-05-28
- Volume
- 9
- Issue
- 1
- Pages
- 61-61
- ISSN
- 1756-6606 (ISSN-L)
- PMC
- PMC4884418
- OpenAlex
- W2406870746
- Cited by
- 46
- References
- 71
- Citations by year
- 2026: 2 · 2025: 2 · 2024: 2 · 2023: 7 · 2022: 7 · 2021: 7 · 2020: 3 · 2019: 9 · 2018: 2 · 2017: 5
- FWCI
- 4.29
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Molecular Brain (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- NORA - Norwegian Open Research Archives (submittedVersion, cc-by)
- Funders
- Norges Forskningsråd (191459, 220901)
- Helse Sør-Øst RHF (2014050, 2014020)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, mild cognitive impairment, DNA base excision repair, oxidative stress, reactive oxygen species, APE1, OGG1, PARP1, DNA polymerase beta, cerebellum, blood biomarkers, cerebrospinal fluid biomarkers, genomic instability, DNA repair gene expression, prodromal Alzheimer's disease
- MeSH terms
- Poly (ADP-Ribose) Polymerase-1, Aged, Aged, 80 and over, Alzheimer Disease, Brain, DNA Repair, Female, Gene Expression Regulation, Humans, Male, Middle Aged, RNA, Messenger, Biomarkers, Case-Control Studies, Sequence Analysis, RNA, DNA Polymerase beta, DNA-(Apurinic or Apyrimidinic Site) Lyase, DNA Glycosylases, High-Throughput Nucleotide Sequencing, Real-Time Polymerase Chain Reaction, Prodromal Symptoms
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