The DOI matches its Crossref record; 240 of the 241 references it cites were found in a registry or an index.
Contributions of DNA Damage to Alzheimer’s Disease
Open accessAbstract
Alzheimer’s disease (AD) is the most common type of neurodegenerative disease. Its typical pathology consists of extracellular amyloid-β (Aβ) plaques and intracellular tau neurofibrillary tangles. Mutations in the APP, PSEN1, and PSEN2 genes increase Aβ production and aggregation, and thus cause early onset or familial AD. Even with this strong genetic evidence, recent studies support AD to result from complex etiological alterations. Among them, aging is the strongest risk factor for the vast majority of AD cases: Sporadic late onset AD (LOAD). Accumulation of DNA damage is a well-established aging factor. In this regard, a large amount of evidence reveals DNA damage as a critical pathological cause of AD. Clinically, DNA damage is accumulated in brains of AD patients. Genetically, defects in DNA damage repair resulted from mutations in the BRAC1 and other DNA damage repair genes occur in AD brain and facilitate the pathogenesis. Abnormalities in DNA damage repair can be used as diagnostic biomarkers for AD. In this review, we discuss the association, the causative potential, and the biomarker values of DNA damage in AD pathogenesis.
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“Conversely, 5xFAD-Dp16 also exhibited greatly decreased NES for several gene sets, including DNA repair, Myc targets V1, and oxidative phosphorylation, all of which are linked to cellular damage or stress facilitating the progression of the pathogenesis and contributing to neurodegeneration in AD48,49,50 (Figures 3A and S3A).”
From Interferon signaling modulates Down syndrome-associated Alzheimer’s disease pathology in a mouse model (2025) · cites this paper as [49]
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Conversely, 5xFAD-Dp16 also exhibited greatly decreased NES for several gene sets, including DNA repair, Myc targets V1, and oxidative phosphorylation, all of which are linked to cellular damage or stress facilitating the progression of the pathogenesis and contributing to neurodegeneration in AD48,49,50 (Figures 3A and S3A).”
From Interferon signaling modulates Down syndrome-associated Alzheimer’s disease pathology in a mouse model (2025) · cites this paper as [49]
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“Oxidative DNA damage and mitochondrial dysfunction are thought to contribute to the neurodegeneration of AD [75,76], vascular dementia [77], HD [78], PD [79] and epilepsy [80].”
From Rlip76: An Unexplored Player in Neurodegeneration and Alzheimer’s Disease? (2022) · cites this paper as [75]
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2 retracted
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1 of the 241 references couldn’t be matched to a known paper.
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Items 101–117 of 117
How Banf1 Functions to Inhibit the Activity of PARP1
Bai, B. (2024) · Queensland University of Technology · doi:10.5204/thesis.eprints.254811
Honda, K., & Awazu, A. (2025) · PLoS ONE · doi:10.1371/journal.pone.0313733
“Here, the downregulation of genes that suppress apoptosis in response to DNA damage would also promote AD progression through the enhancement of cell death in the central nervous system [74,75].”
Brenner, E., Gutta, G., Stauffer, F., Mehta, J., Kingston, R., Bagnell, M., Welty, S., Dixon, N., Zinzell, E., Herrup, K., et al. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.09.07.674780
“There is ample evidence that DNA damage increases in AD compared to age-matched controls (Suberbielle et al., 2013; Suberbielle et al., 2015; Lin et al., 2020; Gutta et al., 2024; Sharma et al., 2025), and that the damage appears early in the progression of the disease (Shanbhag et al., 2019).”
Bartman, S., Hunter, D., Gaspar, L., Tobias-Wallingford, H., Zamor, D., Sinclair, D. A., Coppotelli, G., & Ross, J. M. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.10.21.683739
“These findings complement and extend prior reports that DNA damage and epigenetic dysregulation are pervasive in AD brains and models, but causality and directionality have remained difficult to disentangle (Lin et al., 2020).”
Bazan, C. B., Laville-Dupuy, S. R., Klepfish, M., Cousineau, J., Maiuri, T., Peng, C. Y., Osterlund, E. J., Alpaugh, M., & Truant, R. (2025) · bioRxiv (Cold Spring Harbor Laboratory) · doi:10.1101/2025.11.21.689804
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“Moreover, mutations in DNA repair genes such as BRCA1 , ATM or RAD51 have been reported in AD (Lin et al. 2020), as well as accumulation of the marker of DNA damage gamma-H2A histone X in astrocytes of hippocampus and cerebral cortex of patients (Myung et al. 2008).”
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“Alzheimer’s disease (AD) affects approximately 50 million people worldwide and represents the most common neurodegenerative disorder [103].”
Avanesyan, H., Parsadanyan, M. A., Shahinyan, M. A., Багдасарович, Л. А., Mikaelyan, M. S., Grigoryan, S. V., & Vardevanyan, P. O. (2025) · Neurophysiology · doi:10.1007/s11062-026-10001-9
“The accumulation of these compounds triggers an apoptosis of neurons in the aforementioned regions, which results in memory loss [186, 187].”
Nanocarriers mediated DNA repair mechanism against neurological disorders
Bora, S., Jadav, M., Kulhari, H., & Pooja, D. (2026) · Elsevier eBooks · doi:10.1016/b978-0-443-33623-2.00009-x
Xu, T., Zhang, C., Yang, Y., Shen, Z., & Zhong, Z. (2026) · Canadian Journal of Physiology and Pharmacology · doi:10.1139/cjpp-2025-0340
The emerging role of nanobiomaterials in the early detection and treatment of Alzheimer’s disease
Asuku, A. O., & Olaoluwa, P. A. (2026) · Exploration of neuroscience · doi:10.37349/en.2026.1006147
Enzyme−Targeted Therapeutics for Neurological Disorders
Massignan, L., Lokesh, K., Ziadat, S., Uehling, D., Weaver, D. F., & Reed, M. A. (2026) · Journal of Medicinal Chemistry · doi:10.1021/acs.jmedchem.6c01274
Specific enrichment of somatic single nucleotide variants in Alzheimer-associated tetraploid neurons
López‐Sánchez, N., Rábano, A., & Frade, J. M. (2026) · Frontiers in Molecular Neuroscience · doi:10.3389/fnmol.2026.1929505
Metadata
- Authors
- Lin, X., Kapoor, A., Gu, Y., Chow, M. J., Peng, J., Zhao, K., & Tang, D.
- Affiliations
- St. Joseph’s Healthcare Hamilton (CA)
- Corresponding author
- Tang, Damu
- Venue
- International Journal of Molecular Sciences
- Publisher
- MDPI AG
- Published
- 2020-02-28
- Volume
- 21
- Issue
- 5
- Pages
- 1666
- ISSN
- 1422-0067 (ISSN-L)
- PMC
- PMC7084447
- OpenAlex
- W3009111493
- Cited by
- 117
- References
- 241
- Citations by year
- 2026: 15 · 2025: 19 · 2024: 22 · 2023: 18 · 2022: 19 · 2021: 16 · 2020: 5
- FWCI
- 1.85
- Type
- journal article
- Language
- en
- Open access
- gold
- dx.doi.org
- Licence
- Locations
- International Journal of Molecular Sciences (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- Funders
- Cancer Research Society (NA)
- Canadian Cancer Society (319412)
- Canadian Institutes of Health Research (NA)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Keywords
- Alzheimer's disease, DNA damage, DNA repair, aging, amyloid plaques, neurofibrillary tangles, BRCA1, familial Alzheimer's disease, late-onset Alzheimer's disease, diagnostic biomarkers, neurodegeneration
- MeSH terms
- Alzheimer Disease, DNA Damage, DNA Repair, Humans, Models, Biological, Risk Factors, Neurogenesis
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