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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]
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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]
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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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Talbot, E., Joshi, L., Thornton, P., Dezfouli, M., Tsafou, K., Perkinton, M. S., & Khoronenkova, S. V. (2023) · Nucleic Acids Research · doi:10.1093/nar/gkad1184 · Cited by 38
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“If the damage remains unrepaired, genome instability, cellular senescence, and cell death can subsequently occur [84, 85] .”
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“Additionally, age-related DNA damage that occurs during the expression of learning-related genes may accelerate the progression of AD (Lin et al., 2020).”
The Potential Roles of Redox Enzymes in Alzheimer’s Disease: Focus on Thioredoxin
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Premature aging in genetic diseases: what conclusions can be drawn for physiological aging
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“Similarly, to age-dependent dementias and sporadic late onset Alzheimer ’ s disease (LOAD) (Bouhrara et al., 2018; Lin et al., 2020), CS is characterized by neuronal loss with severe demyelination, however with so far no detectable amyloid-beta accumulation and no hyperphosphorylated tau (Woody et…”
BackgroundXie, J., Cheng, J., Ko, H., & Tang, Y. (2024) · EMBO Molecular Medicine · doi:10.1038/s44321-024-00046-w · Cited by 17
“…(OGG1), Breast cancer gene 1(BRCA1), PARP1, and DNA-PKcs, as representatives for basic excision repair (BER), homologous repair (HR), and non-homologous end joining (NHEJ), respectively, are reported to decrease in AD due to aggravating oxidative stress (Lin et al, 2020; Pao et al, 2020).”
BackgroundSomatic mosaicism in the diseased brain
Iourov, I. Y., Vorsanova, S. G., Куринная, О. С., Kutsev, S. I., & Yurov, Y. B. (2022) · Molecular Cytogenetics · doi:10.1186/s13039-022-00624-y · Cited by 18
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BackgroundGlioblastoma and its treatment are associated with extensive accelerated brain aging
Ainslie, A. P., Klaver, M., Voshart, D. C., Gerrits, E., den Dunnen, W. F. A., Eggen, B. J. L., Bergink, S., & Barazzuol, L. (2024) · Aging Cell · doi:10.1111/acel.14066 · Cited by 17
“DNA damage and reduced expression of DNA damage response proteins have also been implicated in AD (Lin et al., 2020; Sykora et al., 2015 ).”
BackgroundRlip76: An Unexplored Player in Neurodegeneration and Alzheimer’s Disease?
Hindle, A., Singh, S. P., Pradeepkiran, J. A., Bose, C., Vijayan, M., Kshirsagar, S., Sawant, N. A., & Reddy, P. H. (2022) · International Journal of Molecular Sciences · doi:10.3390/ijms23116098 · Cited by 14
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“β-Amyloid precursor protein (APP) initiates the formation of extracellular amyloid-β (Aβ) in AD [61].”
BackgroundПричины и последствия геномной нестабильности при психических и нейродегенеративных заболеваниях
Yurov, Y. B., Vorsanova, S. G., Куринная, О. С., Zelenova, M. A., Vasin, K. S., & Yurov, Y. B. (2020) · Molecular Biology · doi:10.31857/s0026898421010158 · Cited by 14
Oxidative Stress in the Pathogenesis of Neurodegenerative Diseases
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“The hyperphosphorylated state of tau protein also interferes with the ability of tau to bind to chromatin and protect the genome from oxidative damage, thus enhancing the oxidative damage of DNA [105].”
Welty, S., Thathiah, A., & Levine, A. S. (2022) · Journal of Alzheimer s Disease · doi:10.3233/jad-220030 · Cited by 13
“Inefficient and unfaithful DNA repair can lead to cell cycle arrest, accumulation of detrimental mutations, innate immune system activation, and cell death (reviewed in [23]).”
Exercise May Affect Metabolism in Cancer-Related Cognitive Impairment
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“The association of DNA damage with aging is well-studied [33].”
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“Quercetin and hesperetin were discovered to upregulate the activity of Akt in preclinical research, resulting in neuronal survival (Khan et al., 2019; Lin et al., 2020).”
BackgroundA Review of PARP-1 Inhibitors: Assessing Emerging Prospects and Tailoring Therapeutic Strategies
Ramesh, S., Almeida, S. D., Hammigi, S., Radhakrishna, G. K., Sireesha, G., Theivendren, P., Vellingiri, S., Kunjiappan, S., Ammunje, D. N., & Pavadai, P. (2023) · Drug Research · doi:10.1055/a-2181-0813 · Cited by 12
“In AD, PARP-1 and SIRT1 contend with one another for a limited supply of NAD + [99–101].”
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“DNA damage accumulation is a risk factor for AD, and much evidence suggests that it may have a causative role in AD progression 36,37 .”
BackgroundBrain pathology and symptoms linked to concussion history: beyond chronic traumatic encephalopathy
Taskina, D., Zhu, C., Schwab, N., & Hazrati, L. (2024) · Brain Communications · doi:10.1093/braincomms/fcad314 · Cited by 10
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“Additionally, accumulation of damaged DNA has been directly linked to neuronal death in other syndromes, such as Alzheimer’s disease (57, 58).”
BackgroundCytogenomic landscape of the human brain
Iourov, I. Y., Vorsanova, S. G., & Yurov, Y. B. (2021) · Elsevier eBooks · doi:10.1016/b978-0-12-823579-9.00013-8 · Cited by 10
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“It is worth noting that growing evidence indicates that post-mitotic neurons are capable of becoming senescent and DNA damage that accumulates in aging neurons may be an important driving factor of senescence, contributing to both brain aging and possibly AD pathogenesis [42, 44].”
Lai, Y., Han, L., Chen, M., Lin, X., Wu, L., Zhao, Y., Lin, F., & Lin, C. (2023) · Frontiers in Immunology · doi:10.3389/fimmu.2023.1115202 · Cited by 9
“It was found that DDR deficiency caused by mutations in DDR regulators, including BRAC1 occurs in the brain regions of AD and is implicated in the development of pathology (13).”
BackgroundSelf-citationCan accelerated ageing models inform us on age‐related tauopathies?
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“Unsurprisingly, reduced genomic stability has been a widely reported feature in Alzheimer's disease (reviewed by Lin et al., 2020).”
BackgroundHuang, J., Song, Z., Wei, B., Li, Q., Lin, P., Li, H., & Dong, K. (2023) · BMC Psychiatry · doi:10.1186/s12888-023-04634-x · Cited by 9
“DNA damage is a critical pathological cause of AD [34].”
BackgroundDhillon, V. S., Deo, P., & Fenech, M. F. (2024) · European Journal of Nutrition · doi:10.1007/s00394-024-03449-0 · Cited by 8
“Accumulation of DNA damage can elicit excessive apoptosis or cell death of neurons thereby leading to neurological diseases [21–24].”
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“Moreover, oxidative DNA damage [20,21] in the AD brain, tightly connected with Aβ and TAU pathologies [12], seem to occur prior to disease onset [22,23].”
BackgroundNovel molecular mechanisms in Alzheimer’s disease: The potential role of DEK in disease pathogenesis
Greene, A. N., Solomon, M. B., & Vinnedge, L. M. P. (2022) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2022.1018180 · Cited by 8
“Finally, DNA damage is a well-accepted trigger of cell death and apoptosis in AD (Lin et al., 2020).”
BackgroundFISHing for Chromosome Instability and Aneuploidy in the Alzheimer’s Disease Brain
Yurov, Y. B., Vorsanova, S. G., & Iourov, I. Y. (2022) · Methods in molecular biology · doi:10.1007/978-1-0716-2655-9_10 · Cited by 8
Exome sequence analysis of rare frequency variants in Late-Onset Alzheimer Disease
Sundarrajan, S., Venkatesan, A., Kumar, S. U., Gopikrishnan, M., Tayubi, I. A., Aditya, M., Siddaiah, G. B., Doss, C. G. P., & Zayed, H. (2023) · Metabolic Brain Disease · doi:10.1007/s11011-023-01221-7 · Cited by 8
“Defects in DNA damage and repair enzymes such as RAD54B may facilitate the disease pathogenesis (Murzik et al. 2008; Lin et al. 2020).”
BackgroundYan, Y., Yin, Y., Feng, X., Chen, Y., Shi, J., Weng, H., & Wang, D. (2020) · International Journal of Medical Sciences · doi:10.7150/ijms.49246 · Cited by 8
“In mature brains, neural cells are also prone to DNA damage caused by metabolites including oxygen free radicals, homocysteine and amyloid β-peptide (Aβ) [4,17,19,21].”
BackgroundCellular Reprogramming and Its Potential Application in Alzheimer’s Disease
Zhou, C., Ni, W., Zhu, T., Dong, S., Sun, P., & Hua, F. (2022) · Frontiers in Neuroscience · doi:10.3389/fnins.2022.884667 · Cited by 8
Zhong, A., Cai, Y., Zhou, Y., Ding, N., Yang, G., & Chai, X. (2023) · Computational and Mathematical Methods in Medicine · doi:10.1155/2023/8072369 · Cited by 8
“Studies have revealed that DNA damage and enzyme system repair defects are associated with the pathogenesis of pulmonary hypertension, systemic lupus erythematosus, Alzheimer ’ s disease, atherosclerosis, aortic disease, and many other diseases [7, 9 – 12].”
Araya, P., Niemeyer, B., Schade, K., Dunn, L. N., Waugh, K., Busquet, N., Brindley, C., Brown, C., Winkler, C., Lyford, H. R., et al. (2025) · iScience · doi:10.1016/j.isci.2025.113130 · Cited by 7
Marmolejo-Garza, A., Châtre, L., Croteau, D. L., Herrón-Bedoya, A., Luu, M. D. A., Bernay, B., Pontin, J., Bohr, V. A., Boddeke, E., & Dolga, A. M. (2024) · Neurobiology of Disease · doi:10.1016/j.nbd.2024.106645 · Cited by 9
“DNA damage and impaired DNA repair mechanisms have been implicated in the pathogenesis of AD (Lin et al., 2020; Weissman et al., 2007) leading to genomic instability and neuronal death.”
The Biological Intersection Between Chemotherapy-Related Cognitive Impairment and Alzheimer Disease
Torre, M., Zanella, C. A., & Feany, M. Β. (2025) · American Journal Of Pathology · doi:10.1016/j.ajpath.2024.12.013 · Cited by 8
“57 e 59 Brie fl y, AD patients and AD-relevant model systems show elevated oxidative stress, DNA damage, and evidence of mitochondrial dysfunction in the brain, 57 e 59 and these processes are tightly linked and occur early in AD.”
Cacabelos, R. (2025) · International Journal of Molecular Sciences · doi:10.3390/ijms26157175 · Cited by 8
Drug repurposing using meta-analysis of gene expression in Alzheimer’s disease
Jang, H. Y., Oh, J. M., & Kim, I. (2022) · Frontiers in Neuroscience · doi:10.3389/fnins.2022.989174 · Cited by 8
“For instance, some anti-neoplastic agents can cause DNA damage, which is a critical pathological cause of Alzheimer’s disease (Lin et al., 2020).”
BackgroundLi, T., Kang, X., Zhang, S., Wang, Y., He, J., Li, H., Shao, C., & Kang, J. (2025) · Frontiers in Immunology · doi:10.3389/fimmu.2025.1561544 · Cited by 6
Wang, Z., Liu, J., Chen, F., Wang, W. K., Xu, Y., Lu, F., Li, Y., & Gao, J. (2025) · Biomedical Signal Processing and Control · doi:10.1016/j.bspc.2025.107926 · Cited by 7
Revol, R., Koistinen, N. A., Menon, P. K., Chicote‐González, A., Iverfeldt, K., & Ström, A. (2023) · Molecular and Cellular Neuroscience · doi:10.1016/j.mcn.2023.103903 · Cited by 5
“These histone modifications are early events, and key for a successful DNA repair (Aricthota et al., 2022; Dhar et al., 2017; Lin et al., 2020).”
BackgroundMicroglial inflammation in genome instability: A neurodegenerative perspective
Maliar, N. L., Talbot, E., Edwards, A. R., & Khoronenkova, S. V. (2024) · DNA repair · doi:10.1016/j.dnarep.2024.103634 · Cited by 6
The many connections of UFMylation with Alzheimer’s disease: a comprehensive review
Yan, T., Clarkson, B. D. S., Lou, Z., Springer, W., & Fiesel, F. C. (2025) · Molecular Neurodegeneration · doi:10.1186/s13024-025-00855-8 · Cited by 4
Iourov, I. Y., Vorsanova, S. G., & Yurov, Y. B. (2024) · Methods in molecular biology · doi:10.1007/978-1-0716-3946-7_3 · Cited by 4
Development of a Novel, Automated High-Throughput Device for Performing the Comet Assay
Karbaschi, M., Ji, Y., Mujawar, M. A., Mendoza, M., Marquez, J. S., Sonawane, A., Shah, P., Ross, C., Bhansali, S., & Cooke, M. S. (2023) · International Journal of Molecular Sciences · doi:10.3390/ijms24087187 · Cited by 4
Hou, J., Hess, J., Zhang, C., van Rooij, J., Hearn, G. C., Fan, C. C., Faraone, S. V., Fennema‐Notestine, C., Lin, S., Escott‐Price, V., et al. (2024) · American Journal of Medical Genetics Part B Neuropsychiatric Genetics · doi:10.1002/ajmg.b.33019 · Cited by 6
“Additionally, we observed downregulated homologous recombination and non-homologous end-joining, which are the DNA double- strand-break repair pathways (Lin et al. 2020) that mainly activate during the cell cycle.”
Naffaa, M. M. (2025) · Lifespan development and mental health. · doi:10.70322/ldmh.2025.10005 · Cited by 3
Kashif, O., & Said, M. (2025) · Discover Medicine · doi:10.1007/s44337-025-00455-x · Cited by 4
“BRCA1 knockdown led to increased neuronal DSBs, elevated cell death, and deficits in learning and memory [32].”
InfluentialMechanism, measurement and significance of oxidative DNA damage - a tribute to Miral Dizdaroglu
Halliwell, B. B. (2026) · International Journal of Radiation Biology · doi:10.1080/09553002.2026.2620569 · Cited by 3
Dai, W., Wang, H., Ji, H., Xiao, X., Li, Y., Jiang, D., Luo, Y., Xiao, X., Yan, B., Yu, J. Z., et al. (2025) · The Analyst · doi:10.1039/d5an00009b · Cited by 3
Synaptic potentiation requires PARP1 activation: prevailing concepts are revisited
Cohen‐Armon, M., & Segal, M. (2026) · Molecular Psychiatry · doi:10.1038/s41380-025-03426-x · Cited by 2
“This widely accepted therapeutic potential of PARP1 inhibitors in neurodegenera-tion causing cognitive impairment [27, 29], is challenged by more recent fi ndings.”
Gerónimo‐Olvera, C., Scheeler, S. M., Aguirre, C. G., Hormazabal, G. V., Garcia, D., Wu, L., Murad, N. F., Schneider, K., Wilson, K. A., Markov, N. T., et al. (2026) · Aging Cell · doi:10.1111/acel.70494 · Cited by 2
“Defects in the DDR contribute to AD pathogenesis, leading to increased DNA damage and neurodegeneration (Lin et al. 2020; Nelson and Xu 2023).”
COMET Assay for Detection of DNA Damage During Axolotl Tail Regeneration
Medina, B. A. C., Álvarez, J., Santa-González, G. A., & Delgado, J. P. (2022) · Methods in molecular biology · doi:10.1007/978-1-0716-2659-7_12 · Cited by 2
Mansouri, Z., Khodagholi, F., Zaringhalam, J., Abbaszadeh, F., Ghasemi, R., & Maghsoudi, N. (2023) · EXCLI journal · doi:10.17179/excli2023-6818 · Cited by 2
“Many researchers are of the opinion that aging and AD may result from the accumulation of unre-paired DNA damages (Lin et al., 2020; Shanbhag et al., 2019; Welch and Tsai, 2022).”
BackgroundQuach, T., & Duchemin, A. (2025) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2025.106212 · Cited by 1
Forged in O2: Transition metal ions and the rise of aerobic life
Uyeda, K. S., & Borovik, A. S. (2025) · Journal of Inorganic Biochemistry · doi:10.1016/j.jinorgbio.2025.113147 · Cited by 1
Wu, Z., Jia, R., Zhang, Q., Huang, L.-Y., Yan, J.-T., Zhang, Y. H., & Fan, Y. (2026) · Biomarker Research · doi:10.1186/s40364-026-00906-2 · Cited by 2
Bao, W., Bi, H., Chao, L., Jiang, Y., Yu, X., Ruan, F., Wu, D., Chen, Z., & Le, K. (2025) · Journal of Alzheimer s Disease · doi:10.1177/13872877251333811 · Cited by 1
“2,3 Moreover, when genetic defects occur in the genes responsible for maintaining the normal function of the genome and involved in the repair of DNA double-strand breaks (DSB) and DNA single-strand breaks (SSB), it can lead to transcriptional stalling in neurons and the activation of cell death…”
Interphase Chromosomes of the Human Brain
Yurov, Y. B., Vorsanova, S. G., & Iourov, I. Y. (2020) · Springer eBooks · doi:10.1007/978-3-030-62532-0_4
Giti, Z., Banaeifar, A., Arshadi, S., & Azarbayjani, M. A. (2021) · Gene Cell and Tissue · doi:10.5812/gct.113871
DNA repair factor-encoding gene promoters
Uchiumi, F. (2022) · Elsevier eBooks · doi:10.1016/b978-0-12-818787-6.00012-6
Lou, Y. (2022) · American Journal of Biomedical Science & Research · doi:10.34297/ajbsr.2022.15.002170
Ono, R. M. D. S. (2022) · Digital Library of Theses and Dissertations (Universidade de São Paulo) · doi:10.11606/d.17.2022.tde-10042023-084601
Strath, L. J., Meng, L., Zhang, Y., Rani, A., Huo, Z., Foster, T. C., Fillingim, R. B., & Cruz‐Almeida, Y. (2024) · Journal of Alzheimer s Disease Reports · doi:10.1177/25424823241289376
“41 As such, a substantial amount of evidence points to DNA damage as a critical player in the pathogenesis AD.”
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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